ovalbumin and Rhinitis--Allergic--Seasonal

Sublingual immunotherapy has been considered to be a painless and effective therapeutic treatment for allergic rhinitis, and is known as type 1 allergy of the nasal mucosa. So far, its mechanism of action has been elucidated employing peripheral blood serum and lymphocytes in an antigen-specific fashion. Because of the limitations in sampling human materials, there is still controversy among many reports between clinical efficacy and laboratory data. Therefore, its mechanism of action needs to be investigated further by using promising animal models such as rodents and monkeys. Bearing this in mind, in our present study, we successfully constructed an effective murine model for sublingual immunotherapy in allergic rhinitis in which mice were administered ovalbumin (OVA) sublingually followed by intraperitoneal sensitization and nasal challenge.

Topics: Administration, Sublingual; Humans; Immunotherapy; Nasal Mucosa; Ovalbumin; Rhinitis, Allergic, Seasonal; Treatment Outcome

Gyokuheifusan (GHS, Jade Windscreen Powder in English, Yupingfengsan in Chinese) is an herbal formula in traditional Kampo medicine which consolidates superficial resistance to protect against invasion by external pathogens. This review describes the immunopharmacologic properties of GHS as a holistic Kampo medicine, which can affect human homeostasis and constitution of human beings. Oral treatment with GHS has preventive and curative effects in allergic rhinitis induced by Japanese cedar pollen in guinea pigs. Since these effects do not occur with authentic antiallergic agents, GHS appears to have holistic effects on allergic rhinitis. In another study, the effects of GHS on murine antibody production against ovalbumin (OVA) were evaluated. When mice were sensitized intraperitoneally to OVA, the concentration of OVA-specific immunoglobulins in the sera significantly increased with GHS treatment. When they were sensitized intranasally to OVA, GHS significantly reduced the concentration of OVA-specific antibodies in the sera. It was suggested that GHS stimulates immune responses when the antigen had already invaded the body, and that GHS might consolidate the resistance of nasal mucosa to protect from OVA invasion, and then OVA-specific antibodies in sera might be suppressed. These results suggest that traditional medicines have own characteristics different from those of modern medicines, and that original pharmacologic experiments are important to evaluate traditional medicines scientifically.

Topics: Administration, Oral; Animals; Antibody Formation; Depression, Chemical; Disease Models, Animal; Drugs, Chinese Herbal; Guinea Pigs; Medicine, Kampo; Mice; Ovalbumin; Phytotherapy; Pollen; Rhinitis, Allergic, Seasonal

Topics: Adolescent; Adult; Allergens; Animals; Antibody Formation; Asthma; Binding Sites, Antibody; Cattle; Child; Chromosome Mapping; Disease Models, Animal; Diseases in Twins; Eczema; Female; gamma-Globulins; Genes, MHC Class II; Genotype; Haploidy; Histocompatibility Antigens; Humans; Hypersensitivity, Immediate; Immunity; Immunoglobulin E; Immunoglobulin G; In Vitro Techniques; Male; Mice; Mice, Inbred Strains; Middle Aged; Ovalbumin; Passive Cutaneous Anaphylaxis; Pedigree; Penicillin G; Pollen; Reagins; Rhinitis, Allergic, Seasonal

Eligibility to immunotherapy is based on the determination of IgE reactivity to a specific allergen by means of skin prick or in vitro testing. Biomarkers predicting the likelihood of clinical improvement during immunotherapy would significantly improve patient selection.. Proteins were differentially assessed by using 2-dimensional differential gel electrophoresis and label-free mass spectrometry in pretreatment sera obtained from clinical responders and nonresponders within a cohort of 82 patients with grass pollen allergy receiving sublingual immunotherapy or placebo. Functional studies of Fetuin-A (FetA) were conducted by using gene silencing in a mouse asthma model, human dendritic cell in vitro stimulation assays, and surface plasmon resonance.. Analysis by using quantitative proteomics of pretreatment sera from patients with grass pollen allergy reveals that high levels of O-glycosylated sialylated FetA isoforms are found in patients exhibiting a strong decrease in rhinoconjunctivitis symptoms after sublingual immunotherapy. Although FetA is involved in numerous inflammatory conditions, its potential role in allergy is unknown. In vivo silencing of the FETUA gene in BALB/c mice results in a dramatic upregulation of airway hyperresponsiveness, lung resistance, and T. As a reflection of the patient's inflammatory status, pretreatment levels of sialylated FetA in the blood are indicative of the likelihood of clinical responses during grass pollen immunotherapy.

Topics: Allergens; alpha-2-HS-Glycoprotein; Animals; Biomarkers; Dendritic Cells; Double-Blind Method; Gene Silencing; Humans; Lipopolysaccharides; Mice, Inbred BALB C; Ovalbumin; Poaceae; Pollen; Rhinitis, Allergic, Seasonal; Sublingual Immunotherapy

Ceylon cinnamon has been shown to possess anti-inflammatory properties in many diseases including allergic inflammation.. The aim of this study was to analyse in more detail the effects of cinnamon extract (CE) and its major compounds p-cymene and trans-cinnamaldehyde (CA) on allergen-specific immune responses in vitro and in vivo.. Addition of CE, p-cymene or CA, but not ethanol significantly inhibited DC maturation and subsequent allergen-specific T cell proliferation as well as Th1 and Th2 cytokine production. Sulphidoleukotriene release and CD63 expression by basophils were also significantly diminished after addition of CE. In vivo, treatment of OVA-sensitized mice with CE led to a significant shift from OVA-specific IgE towards IgG2a production and to a strong inhibition of OVA-specific proliferation. Moreover, airway inflammation as well as anaphylaxis after intranasal or systemic allergen challenge was significantly reduced in CE-treated mice. Furthermore, topical application of CE prevented calcipotriol-induced atopic dermatitis-like inflammation in these mice.. Taken together, our data indicate that the anti-inflammatory effect of cinnamon might be exploited for treatment of allergic inflammation, which needs to be further investigated.

Topics: Acrolein; Animals; Basophils; Betula; CD4-Positive T-Lymphocytes; Cell Proliferation; Cinnamomum zeylanicum; Coculture Techniques; Cymenes; Cytokines; Dendritic Cells; Dermatitis, Atopic; Disease Models, Animal; Humans; Hypersensitivity, Immediate; Mice; Mice, Inbred BALB C; Ovalbumin; Plant Extracts; Plethysmography, Whole Body; Poaceae; Pollen; Respiratory Hypersensitivity; Rhinitis, Allergic, Seasonal

Although there have been many studies revealing the mechanism and establishing the therapeutical method for allergic rhinitis, no suitable animal models for allergic rhinitis, especially for pollen allergy, are currently available. We therefore aimed in this study to develop a murine model producing IgE in response to an inhaled antigen without using any adjuvants. Ovalbumin (OVA)-specific T cell receptor transgenic mice (DO11.10) inhaled an OVA solution for one h, twice a week, for six weeks. The resulting increase of OVA-specific IgE in the serum was observed depending on the times of inhalation. Spleen cells from mice that had inhaled the antigen produced more IL-4 and less IFN-γ than those from the control mice in vitro. These results indicate that inhaled antigen enhanced the Th2-type responses and induced IgE production in a T cell-mediated manner. Our findings would contribute to studies on prevention and treatment of pollen allergy.

Topics: Allergens; Animals; Antigens; Disease Models, Animal; Humans; Immunoglobulin E; Interferon-gamma; Interleukin-4; Male; Mice; Mice, Transgenic; Ovalbumin; Receptors, Antigen, T-Cell; Rhinitis, Allergic; Rhinitis, Allergic, Seasonal; Th2 Cells

Th2 cytokines play a pivotal role in the pathogenesis of allergic rhinitis. To investigate the effect of p38 mitogen-activated protein kinase (MAPK) on the production of Th2 cytokines such as IL-4 and IL-5 in allergic rhinitis, a model of allergic rhinitis was established in SD rats. The expression level of p38 MAPK mRNA in PBMCs was detected by means of real time quantitative RT-PCR. The p38 MAPK activity in PBMCs was detected by Western blotting. PBMCs were cultured with various concentrations of p38 MAPK inhibitor SB 239063 or without the treatment, and then IL-4, IL-5 levels of the supernatant were determined by using sandwich ELISA. The results showed that mRNA expression and activity of p38 MAPK in PBMCs were significantly higher in allergic rhinitis rats than in control rats (P<0.05). The p38 MAPK inhibitor SB 239063 decreased the production of IL-4 and IL-5 in a dose-dependent manner. It is concluded that p38 MAPK plays an important role in the pathogenesis of allergic rhinitis which is associated with Th2 cytokines release.

Topics: Animals; Cytokines; Female; Imidazoles; Interleukin-4; Interleukin-5; Leukocytes, Mononuclear; Male; Ovalbumin; p38 Mitogen-Activated Protein Kinases; Pyrimidines; Rats; Rats, Sprague-Dawley; Rhinitis, Allergic, Seasonal; RNA, Messenger; Th2 Cells

Transforming growth factor-beta (TGF-beta) levels are elevated in the nasal mucosa in allergic rhinitis. However, because TGF-beta is secreted extracellulary in latent complexes, it remains unclear whether the local TGF-beta expression actually drives active signaling and affects the pathophysiology of allergic rhinitis. The objective of this study is to investigate whether TGF-beta signaling is activated in allergic rhinitis and plays a role in the pathophysiology of allergic rhinitis.. An ovabumin (OVA)-sensitized and -nasally challenged mouse model of allergic rhinitis was established and phosphorylation of Smad2 in the nasal mucosa was examined by immunohistochemistry. In addition, the effects of the pharmacological inhibition of endogenous TGF-beta signaling on the allergic rhinitis model were histologically examined. Furthermore, phosphorylation of Smad2 in the nasal mucosa samples obtained from patients with allergic rhinitis was also evaluated.. In the mouse model of allergic rhinitis, OVA challenge induced phosphorylation of Smad2 predominantly in epithelial cells in the nasal mucosa. In addition, the administration of an inhibitor of TGF-beta type I receptor kinase activity during OVA challenge suppressed goblet cell hyperplasia in the nasal mucosa. Furthermore, phosphorylated Smad2 expression increased in nasal epithelial cells in patients with allergic rhinitis.. These results suggest that TGF-beta signaling is activated in epithelial cells in the nasal mucosa in allergic rhinitis and may contribute to the development of goblet cell hyperplasia.

Topics: Animals; Cell Proliferation; Disease Models, Animal; Goblet Cells; Humans; Hyperplasia; Immunization; Mice; Nasal Mucosa; Ovalbumin; Phosphorylation; Protein Serine-Threonine Kinases; Pyrazoles; Quinolines; Receptor, Transforming Growth Factor-beta Type I; Receptors, Transforming Growth Factor beta; Rhinitis, Allergic, Perennial; Rhinitis, Allergic, Seasonal; Signal Transduction; Smad2 Protein; Transforming Growth Factor beta

Epidemiological and clinical studies report higher incidences of anxiety and increased emotional reactivity in individuals suffering from respiratory allergies. To evaluate if respiratory allergies are capable of promoting anxiety-like behavior in rodents, we used models of allergic rhinitis and behavioral evaluations followed by assessment of mRNA for cytokines in relevant brain regions. Mice and rats were sensitized to ovoalbumin or pollen, respectively, following standard sensitization and challenge protocols. After challenge, the animals were evaluated in the open field, elevated plus-maze and resident-intruder tests. Cytokines and corticotropin-releasing factor expression were assessed in several brain regions by real-time RT-PCR and plasma corticosterone concentrations by radioimmunoassay. Mice and rats sensitized and exposed to allergen showed increased anxiety-like behavior and reduced social interaction without any overt behavioral signs of sickness. T-helper type 2 (T(H)2) cytokines were induced in both rats and mice in the olfactory bulbs and prefrontal cortex and remained unchanged in the temporal cortex and hypothalamus. The same results were found for CRF mRNA expression. No differences were observed in corticosterone concentrations 1h after the last behavioral test. These results show that sensitization and challenge with allergens induce anxiety across rodent species and that these effects were paralleled by an increased expression of T(H)2 cytokines and CRF in the prefrontal cortex. These studies provide experimental evidence that sensitized rodents experience neuroimmune-mediated anxiety and reduced social interaction associated with allergic rhinitis.

Topics: Aggression; Allergens; Animals; Anxiety; Body Weight; Brain Chemistry; Corticosterone; Corticotropin-Releasing Hormone; Cytokines; Interpersonal Relations; Mice; Mice, Inbred BALB C; Ovalbumin; Pollen; Radioimmunoassay; Rats; Rats, Inbred BN; Reverse Transcriptase Polymerase Chain Reaction; Rhinitis, Allergic, Seasonal; T-Lymphocytes, Helper-Inducer

There is growing speculation that the impairment in regulatory-T-cell (Treg)-mediated dominant tolerance may play an important role in the pathogenesis of allergic rhinitis (AR). The aim of this study was to investigate whether the changes in the forkhead transcription factor 3 (Foxp3) gene expression may aggravate nasal mucosal inflammation in allergic mice, and whether or not these features result from the loss of Tregs.. AR was induced by both intraperitoneal injection and intranasal administration of ovalbumin in BALB/c mice, while the control mice were treated with saline. A comparison of the frequency of CD4+CD25+Foxp3+ Tregs in peripheral blood mononuclear cells of the AR and control mice was made by flow cytometry. Spleen mononuclear cells were used for RNA extraction and RT-PCR was used to measure Foxp3 mRNA expression.. The expression of the Foxp3 gene was significantly reduced in spleen mononuclear cells in AR mice compared with the control. Moreover, a significant decrease in the percentage of CD4+CD25+Foxp3+ Tregs was exhibited in peripheral blood mononuclear cells of AR mice compared with the control mice.. The insufficiency of Tregs and the Foxp3 gene may contribute to the development of AR in mice.

Topics: Animals; CD4 Antigens; Disease Models, Animal; Female; Flow Cytometry; Forkhead Transcription Factors; Gene Expression; Interleukin-2 Receptor alpha Subunit; Lymphocyte Count; Mice; Mice, Inbred BALB C; Nasal Mucosa; Ovalbumin; Rhinitis, Allergic, Seasonal; RNA, Messenger; Spleen; T-Lymphocytes, Regulatory

Increased cough reflex sensitivity is found in patients with allergic rhinitis and may contribute to cough caused by rhinitis. We have reported that cough to citric acid is enhanced in the guinea pig model of allergic rhinitis. Here we address the hypothesis that the cough reflex sensitivity is increased in this model. The data from our previous studies were analyzed for the cough reflex sensitivity. The allergic inflammation in the nose was induced by repeated intranasal instillations of ovalbumin in the ovalbumin-sensitized guinea pigs. Cough was induced by inhalation of doubling concentrations of citric acid (0.05-1.6 M). Cough threshold was defined as the lowest concentration of citric acid causing two coughs (C2, expressed as geometric mean [95% confidence interval]). We found that the cough threshold was reduced in animals with allergic rhinitis. C2 was 0.5 M [0.36-0.71 M] and 0.15 M [0.1-0.23 M] prior and after repeated intranasal instillations of ovalbumin, respectively, P<0.01, n=36). C2 was not affected in control animals (n=29). We have reported that the selective leukotriene cys-LT1 receptor antagonist montelukast inhibited cough enhancement in this model. We found that this was accompanied by inhibition of the changes in cough reflex sensitivity. C2 was reduced in animals with allergic rhinitis treated orally with vehicle (0.57 M [0.28-1.1] vs. 0.09 M [0.04-0.2 M], P<0.05, n=8), but not in animals treated with montelukast (0.57 M [0.22-1.4 M] vs. 0.52 M [0.17-1.6 M], NS, n=8). We conclude that the cough reflex sensitivity is increased in the guinea pig model of allergic rhinitis. Our results suggest that guinea pig is a suitable model for mechanistic studies of increased cough reflex sensitivity in rhinitis.

Topics: Acetates; Allergens; Animals; Anti-Asthmatic Agents; Citric Acid; Cough; Cyclopropanes; Guinea Pigs; Inflammation; Leukotriene Antagonists; Male; Nasal Mucosa; Ovalbumin; Quinolines; Reflex; Rhinitis, Allergic, Seasonal; Sulfides

Different drugs from various pharmacological classes were compared for their ability to protect against the nasal effects of acute allergen challenge in a guinea pig model. In the model, sneezing and nose rubbing were recorded after an initial allergen challenge in guinea pigs previously sensitized to egg albumin. Four days later the same guinea pigs were re-challenged a second time when anesthetised. In these anaesthetized animals, nasal airway pressure, pulmonary inflation pressure and cellular infiltration into nasal lavage fluid were measured. The drug tested were autacoid antagonists (mepyramine--3mg/kg, cetirizine--3mg/kg and montelukast--10mg/kg), L-NAME (10 or 20mg/kg), heparin (20mg/kg) and dexamethasone (20mg/kg) given either intraperitoneally or intravenously; all were given shortly before challenge. Sneezing induced by allergen challenge was statistically significantly reduced by mepyramine, cetirizine and dexamethasone whereas only cetirizine reduced nose rubbing. Changes in nasal airway pressure due to allergen exposure were reduced by cetirizine, montelukast, L-NAME, and heparin, but not by mepyramine, nor dexamethasone. In the presence of L-NAME, nasal airway pressure actually changed in the opposite direction. Cellular infiltration, as assessed by cytometry in nasal lavage fluid 60min after acute allergen challenge, was reduced by montelukast and heparin but not by antihistamines, L-NAME nor dexamethasone. This pattern of effects of the drugs, given by doses and routes previously described in the literature as being effective was not completely consistent with expected responses. The lack of effect of dexamethasone probably reflects the fact that it was given acutely whereas in the clinic chronic administration is used. The two antihistamines were not identical in their actions, presumably reflecting the fact that cetirizine has therapeutic actions not entirely confined to blockade of H1 receptors. Montelukast has not been reported to have major effects on sneezing and itching in the clinic but reduces nasal obstruction (lower nasal airway pressure or nasal patency). Montelukast's effects on cellular infiltration indicate the possible involvement of leukotrienes. Heparin has actions on inflammatory cell infiltration. This could explain its profile of reducing both cellular infiltration, and increased nasal airway pressure.

Topics: Acetates; Acute Disease; Animals; Cetirizine; Cyclopropanes; Dexamethasone; Disease Models, Animal; Guinea Pigs; Heparin; Histamine H1 Antagonists; Male; Nasal Obstruction; NG-Nitroarginine Methyl Ester; Ovalbumin; Pyrilamine; Quinolines; Rhinitis, Allergic, Seasonal; Sneezing; Sulfides

It has been suggested that human hepatitis A virus cellular receptor, also known as T-cell immunoglobulin and mucin domain-1 (TIM-1), plays an important role in the development of allergic diseases on the basis of epidemiologic data, but the molecular mechanism has been unclear. In a murine model of ovalbumin (OVA)-sensitized allergic rhinitis (AR), we examined the expression of TIM-1 and its correlation with T helper1-associated transcription factor, T-bet, as a potential mediator of T-cell immunoglobulin expression.. Mice were challenged intranasally with OVA to elicit AR. The expression of TIM-1 in nasal tissues was examined by real-time reverse-transcription polymerase chain reaction (RT-PCR), and the surface expression of TIM-1 in peripheral blood mononuclear cells was evaluated by means of flow cytometry. In addition, the expression of TIM-1 as well as T-bet in splenic lymphocytes was examined by Western blotting.. TIM-1 mRNA was increased significantly in nasal tissues (P < .05) as seen by real-time RT-PCR. Flow cytometry indicated a differential TIM-1 expression of 135.5 +/- 34.2 in the AR group versus 51.1 +/- 10.9 in the control group (P < .05). The mean values of normalized TIM-1 were 0.43 +/- 0.18 and 0.21 +/- 0.10 in AR and control groups, respectively, whereas the mean values of normalized T-bet were 0.22 +/- 0.13 and 0.67 +/- 0.17 in the AR and control groups, respectively. There was a significant difference in the production of TIM-1 as well as T-bet in AR mice versus control mice (P < .05). The increased production of TIM-1 correlated significantly with the decreased T-bet in spleen tissue of AR mice (r = -0.52, P < .05).. Our experimental model recapitulates an increase in lymphocyte TIM-1 expression seen in AR both locally and systemically. Our results also demonstrate an inverse relationship between lymphocyte TIM-1 and T-bet expression, suggesting a possible mechanism that TIM-1 influences the development of AR.

Topics: Animals; Blotting, Western; Disease Models, Animal; DNA Primers; Female; Flow Cytometry; Hepatitis A Virus Cellular Receptor 1; Leukocytes, Mononuclear; Membrane Proteins; Mice; Mice, Inbred BALB C; Mucins; Ovalbumin; Protein Structure, Tertiary; Reverse Transcriptase Polymerase Chain Reaction; Rhinitis, Allergic, Seasonal; RNA, Messenger; T-Box Domain Proteins

The present study was undertaken to investigate the involvement of chemical mediators in nasal allergic responses using histidine decarboxylase knockout (HDC-KO) mice. An allergic rhinitis model was developed in HDC-KO and wild-type mice by the intraperitoneal injection of ovalbumin, aluminum hydroxide gel and pertussis toxin. Five days later, they were boosted by a subcutaneous injection of ovalbumin into the back. From day 18 after the first immunization to day 39, intranasal sensitization with ovalbumin was performed every day and the severity of allergic rhinitis was observed by measuring nasal allergic responses and total IgE levels. It was found that the intranasal administration of antigen caused a significant increase of nasal sneezing and rubbing from day 25 to day 39 both in sensitized HDC-KO and wild-type mice. In addition, a significant elevation of total IgE levels in serum was also found both in sensitized HDC-KO and wild-type mice from day 18 to day 39 after the first immunization. L-733,060, a tachykinin NK(1) receptor antagonist at a dose of 10 mg/kg (s.c.), resulted in the dose-dependent inhibition of nasal allergic responses induced by antigen in both HDC-KO and wild-type mice. In addition, both chlorpheniramine at doses of 3 and 10 mg/kg (p.o.) and BW A868C at doses of 0.3 and 1 mg/kg (i.v.) also showed a dose-related reduction of the nasal allergic responses induced by antigen in sensitized wild-type mice. On the other hand, they had no effects on the nasal signs induced by antigen in HDC-KO mice. From these results, it was revealed that substance P induces nasal allergic responses in the mouse model of chronic allergic rhinitis through the activation of tachykinin NK(1) receptors. Therefore, it can be concluded that not only histamine, but also substance P and prostaglandin D(2), participated in the nasal allergic responses induced by antigen in mice.

Topics: Animals; Behavior, Animal; Chlorpheniramine; Histamine H1 Antagonists; Histidine Decarboxylase; Hydantoins; Immunization; Immunoglobulin E; Inflammation Mediators; Male; Mice; Mice, Inbred C57BL; Mice, Knockout; Neurokinin-1 Receptor Antagonists; Ovalbumin; Piperidines; Receptors, Immunologic; Receptors, Prostaglandin; Rhinitis, Allergic, Seasonal; Sneezing; Substance P

The aim of this study was to determine whether intranasal administration of botulinum toxin type A (BTX-A) could relieve the typical symptoms of allergic rhinitis (AR) and alter substance P (SP)- and vasoactive intestinal peptide (VIP)-immunoreactive (IR) expression in nasal mucosa of AR animals sensitized with ovalbumin (OVA).. AR was induced by intraperitoneal injection of OVA followed by its repeated intranasal instillation in female Wistar rats. Some AR animals were intranasally treated with a cotton strip containing BTX-A (10 U per nostril) for 1 h. After BTX-A treatment, OVA was repeatedly instilled in AR and AR + BTX-A groups every 2 days for 10 days. Subsequently, nasal symptoms were evaluated, and nasal secretions collected. Finally, the nasal mucosae of all animals were prepared for histological and immunohistochemical assessment.. BTX-A administration alleviated typical AR symptoms including rhinorrhea, nasal itching and sneezing, and subsequent intranasal repeated challenge with OVA did not trigger AR symptoms. After BTX-A treatment, inflammatory histological characteristics within the nasal mucosa of AR animals were absent, but atrophy of serous glands was observed. BTX-A decreased dense SP-IR and VIP-IR cells and fibers within and beneath the epithelium, around blood vessels and close to serous glands in AR animals.. Local BTX-A treatment is an effective method to reduce AR symptoms. BTX-A decreased the excessive SP-IR and VIP-IR expression induced by OVA. Therefore, BTX-A may affect the nasal mucosa via the suppression of neuropeptides, playing a major role in autonomous mucosal innervation in the pathophysiology of AR.

Topics: Administration, Intranasal; Allergens; Animals; Botulinum Toxins, Type A; Female; Immunohistochemistry; Nasal Mucosa; Ovalbumin; Rats; Rats, Wistar; Rhinitis, Allergic, Seasonal; Substance P; Vasoactive Intestinal Peptide

This study aimed to evaluate the effect of dexamethasone on the expression of transforming growth factor (TGF)-beta in the mouse model of allergic rhinitis.. Female BALB/c mice were randomly assigned to four groups, including two control groups and two treatment groups.. General sensitization and local challenge were performed with ovalbumin (OVA). In the treatment groups, dexamethasone was injected intraperitoneally 3 hours before general sensitization or local challenge. Symptom score, eosinophil infiltration, and immunostaining for TGF-beta1 and CD4 in nasal mucosa, and TGF-beta1 and OVA-specific immunoglobulin E (IgE) in sera were analyzed.. Dexamethasone administration before general sensitization reduced the symptom score, OVA-specific IgE, and eosinophil infiltration and increased the serum level of TGF-beta1 significantly. Dexamethasone administration before local challenge reduced only the eosinophil infiltration significantly. Immunoreactivity of TGF-beta1 and CD4 was lower in both treatment groups.. These results suggest that dexamethasone may play an important role in the regulation of allergic reactions by at least two mechanisms; one by suppressing allergic sensitization through decrease of CD4+ T cells and increase of TGF-beta, and the other by suppressing late allergic reactions through the inhibition of proliferation and chemotaxis of inflammatory cells such as eosinophils.

Topics: Animals; CD4-Positive T-Lymphocytes; Dexamethasone; Disease Models, Animal; Eosinophils; Female; Gene Expression; Glucocorticoids; Immunoglobulin E; Immunohistochemistry; Leukocyte Count; Mice; Mice, Inbred BALB C; Nasal Mucosa; Ovalbumin; Reverse Transcriptase Polymerase Chain Reaction; Rhinitis, Allergic, Seasonal; RNA, Messenger; Transforming Growth Factor beta

Konjac is a traditional Japanese food with a peculiar texture, and it has been suggested that its main ingredient, konjac glucomannan (KGM), ameliorates metabolic disorders such as diabetes and hypercholesteremia. We have found that feeding with pulverized KGM (PKGM) prevents skin inflammation in a murine model of atopic dermatitis. Here, we show that dietary PKGM suppresses allergic rhinitis-like symptoms in mice upon immunization and nasal sensitization with ovalbumin (OVA). The PKGM-fed mice showed a much lower frequency of sneezing than in control animals. We also found that PKGM supplementation exclusively suppressed OVA-specific IgE response without affecting IgG1/IgG2a responses as well as systemic Th1/Th2 cytokine production. These results suggest that PKGM can be a beneficial foodstuff in preventing nasal allergy such as seasonal pollinosis.

Topics: Administration, Oral; Animals; Cells, Cultured; Dietary Carbohydrates; Enzyme-Linked Immunosorbent Assay; Female; Immunoglobulin E; Interferon-gamma; Interleukin-4; Interleukin-5; Mannans; Mice; Mice, Inbred BALB C; Molecular Weight; Monocytes; Ovalbumin; Powders; Rhinitis, Allergic, Seasonal; Sneezing; Spleen; Viscosity

Type I allergic diseases such as allergic rhinitis are caused by IgE-mediated humoral immune responses, while eosinophils also fulfill important roles in the etiology of IgE-mediated allergy. IL-21 regulates growth, differentiation, and function of T, B, and NK cells, while the production of IgE is also influenced by IL-21. In this study we examined whether IL-21 is capable of controlling IgE-mediated allergic reactions in vivo by using the allergic rhinitis mouse model that was established by repetitive sensitization and intranasal challenge with OVA. Intranasal administration with recombinant mouse IL-21 (rmIL-21) significantly reduced the number of sneezes, as well as the serum concentration of OVA-specific IgE, in comparison with that of untreated allergic mice. The rmIL-21 treatment also suppressed germline Cepsilon transcription in the nasal-associated lymphoid tissues, which may have, at least partly, resulted from the up-regulation of Bcl-6 mRNA caused by IL-21. Local expression of IL-4, IL-5, and IL-13 was also inhibited by the intranasal cytokine therapy whereas, in contrast, the expression of endogenous IL-21 mRNA was induced by exogenous rmIL-21. Moreover, IL-21 acted on nasal fibroblasts to inhibit production of eotaxin. This novel function of IL-21 may be associated with the attenuation of eosinophil infiltration into nasal mucosa that was revealed by histopathological observation. These results indicated that IL-21 nasal administration effectively ameliorated allergic rhinitis through pleiotropic activities, i.e., the prevention of IgE production by B cells and eotaxin production by fibroblasts.

Topics: Administration, Intranasal; Animals; Antibody Formation; B-Lymphocytes; Cell Differentiation; Cytokines; DNA-Binding Proteins; Eosinophils; Female; Fibroblasts; Gene Expression Regulation; Immunoglobulin E; Interleukins; Killer Cells, Natural; Mice; Mice, Inbred BALB C; Ovalbumin; Palatine Tonsil; Proto-Oncogene Proteins c-bcl-6; Recombinant Proteins; Rhinitis, Allergic, Seasonal; T-Lymphocytes

Aqueous extract from the fruiting body of Cryptoporus volvatus has been reported to present anti-tumor, anti-allergy, anti-inflammation and immunomodulatory activities. However, the effect mechanisms of anti-allergy and anti-inflammation are poorly understood. The aim of study is to evaluate whether Cryptoporus polysaccharides (CP) extracted from fruiting body of Cryptoporus volvatus decrease the development of nasal symptoms, airway hyperresponsiveness (AHR) to methacholine (MCh) and the infiltration of eosinophils in nasal mucosa in rat model of allergic rhinitis, and investigate a possible action mechanism of CP by detecting the expression of eotaxin mRNA in nasal mucosa and lung tissues. Rats were immunized with ovalbumin and consecutive topical antigen instillation was performed. Repeated intranasal ovalbumin challenge caused rhinitis symptom, AHR to MCh, eosinophil infiltration and histological alterations into the nasal mucosa and increase of eotaxin mRNA expression in nasal mucosa and lung tissue were examined. Pretreatment with CP 3, 9 and 27 mg kg(-1) (ig) decreased the numbers of sneezing 27.4%, 38.4% and 44.3% and nasal rubbing 27.5%, 34.9% and 47.7% comparison with model group, respectively. CP caused a dose-related inhibition of MCh-induced AHR. CP 27 mg kg(-1) decreased the expression of eotaxin mRNA in the nasal mucosa by 35%. These results suggest CP can relieve the symptom, eosinophil infiltration and injury of tissue in nasal mucosa and lung tissue and AHR of allergic rhinitis in rats. Its action mechanism may be associated with the decrease of eotaxin mRNA expression.

Topics: Airway Resistance; Animals; Anti-Allergic Agents; Bronchial Hyperreactivity; Bronchial Provocation Tests; Chemokine CCL11; Chemokines, CC; Chemotaxis, Leukocyte; Disease Models, Animal; Eosinophils; Fruiting Bodies, Fungal; Gene Expression Regulation; Lung; Lung Compliance; Methacholine Chloride; Nasal Mucosa; Ovalbumin; Polyporaceae; Polysaccharides; Rats; Rats, Sprague-Dawley; Rhinitis, Allergic, Seasonal; RNA, Messenger

Studies show that children in rural environments develop less asthma and allergic rhinitis than their urban counterparts. This may be a result, in part, of neonatal exposure to environmental antigens such as LPS and/or early exposure to allergens.. This study examined the effects of neonatal allergen and/or LPS exposure on subsequent immune responses to allergen.. Newborn mice were exposed to LPS and/or ovalbumin. At age 6 weeks, these animals were sensitized and challenged with ovalbumin, and airway inflammation, hyperresponsiveness, and cytokine expression were assessed.. Animals exposed to LPS in the neonatal period developed T cells expressing CD25 and IL-10 on sensitization and challenge. They demonstrated abrogation of airway hyperresponsiveness and significant decreases in IL-13 from bronchoalveolar lavage fluid and in specific IgE. IL-4-expressing spleen cells were also significantly decreased. Mice exposed in the neonatal period to ovalbumin demonstrated airway hyporesponsiveness after subsequent ovalbumin sensitization and challenge and did not produce specific IgE. In contrast, these animals showed increases in IFN-gamma. Animals exposed to both LPS and ovalbumin developed a response characterized by IL-10 and IFN-gamma-expressing T cells.. This suggests that mucosal antigen exposure in the neonatal period results in inhibition of allergic responses to environmental allergens. Early LPS exposure directs mucosal responses toward tolerance, whereas ovalbumin exposure follows the T(H)1-type response on subsequent sensitization.. This study suggests that prevention of airways allergy may be best achieved by appropriate exposure of the airway mucosa early in life to environmental antigens.

Topics: Allergens; Animals; Animals, Newborn; Asthma; Cytokines; Environment; Female; Immune Tolerance; Interleukin-10; Lipopolysaccharides; Mice; Mice, Inbred BALB C; Ovalbumin; Rhinitis, Allergic, Perennial; Rhinitis, Allergic, Seasonal; T-Lymphocytes, Regulatory

The pathophysiology of the early- and late-phase nasal response to allergen challenge is not completely defined. Recent technical advances enable direct monitoring of these responses in mice.. IL-13 is detected in the nasal membranes of both human beings and mice with allergic rhinitis, but its role in disease pathogenesis is unclear. We measured early and late nasal allergic responses after treatment with soluble IL-13Ralpha2-IgG fusion protein (sIL-13Ralpha2-Fc), and in IL-13-deficient mice (IL-13(-/-)).. IL-13(-/-) mice (BALB/c background) and wild-type mice were sensitized to ovalbumin by intraperitoneal injection and then challenged intranasally with ovalbumin without sedation. The sIL-13Ralpha2-Fc or control human IgG was administered by intraperitoneal (i.p.) injection 24 hours and 1 hour before each ovalbumin challenge. Early nasal responses after the 4th ovalbumin challenge and late nasal responses 24 hours after the 6th ovalbumin challenge were assessed.. Sensitized/challenged wild-type mice treated with sIL-13Ralpha2-Fc or IL-13(-/-) mice demonstrated significantly reduced late nasal responses in face of persistent nasal tissue eosinophilia; the early nasal response was little affected by targeting IL-13. Goblet cell hyperplasia was not detected in nasal membranes.. The data indicate that IL-13 is a major contributor to the development of a late nasal response with little influence on the early response, and without affecting nasal eosinophilic inflammation. Inhibition of IL-13 may have an important therapeutic application in preventing the persistent nasal blockage in allergic rhinitis.. Current therapies for allergic rhinitis may not take into account the important differences in the pathophysiology of the early and late responses and the important role of IL-13 in sustaining chronic nasal congestion and obstruction.

Topics: Animals; Eosinophils; Injections, Intraperitoneal; Interleukin-13; Interleukin-13 Receptor alpha2 Subunit; Mice; Mice, Inbred BALB C; Mice, Knockout; Ovalbumin; Rhinitis, Allergic, Perennial; Rhinitis, Allergic, Seasonal; Time Factors

Allergic rhinitis is an inflammation involving T(H)2-type cytokine production, with pathologic eosinophil infiltration in the nasal mucosa. Although TNF-alpha is thought to be a pro-inflammatory cytokine, the relationship between TNF-alpha and allergic rhinitis has not been clarified.. The role of TNF-alpha in a murine model of ovalbumin (OVA)-sensitized allergic rhinitis was investigated by using mice deficient in the gene encoding TNF-alpha (TNF-alpha(-/-) mice).. Both wild-type (TNF-alpha(+/+)) and TNF-alpha(-/-) mice were sensitized with OVA by means of intraperitoneal injection. They were then challenged with intranasal OVA, and various allergic responses were assessed.. The production of OVA-specific IgE in the serum (P <.05) and the frequency of sneezes (P <.05) and nasal rubs (P <.05) decreased significantly in TNF-alpha(-/-) mice after OVA sensitization compared with that in TNF-alpha(+/+) mice (P <.05). The mRNA expression of IL-4, IL-10, and eotaxin in nasal mucosa in TNF-alpha(-/-) mice was also significantly suppressed compared with that in TNF-alpha(+/+) mice after OVA sensitization (P <.05). Furthermore, the expression of both endothelial-leukocyte adhesion molecule 1 and vascular cell adhesion molecule 1 mRNA in the nasal mucosa was significantly suppressed (P <.05), although intercellular adhesion molecule 1 mRNA expression did not decrease significantly in TNF-alpha(-/-) mice compared with that in TNF-alpha(+/+) mice after OVA sensitization. In addition, the effect of TNF-alpha on endothelial-leukocyte adhesion molecule 1 and vascular cell adhesion molecule 1 expression by means of Western blot analysis was compatible with the mRNA results. Pathologically, eosinophil infiltration in nasal mucosa was significantly restricted in TNF-alpha(-/-) mice compared with in TNF-alpha(+/+) mice after OVA sensitization (P <.05).. TNF-alpha is necessary for antigen-specific IgE production and for the induction of T(H)2-type cytokines and chemokines. Furthermore, TNF-alpha might be important for the expression of adhesion molecules to recruit eosinophils to the allergic inflammatory site. We conclude that the lack of TNF-alpha inhibited the development of allergic rhinitis.

Topics: Animals; Cell Adhesion Molecules; Chemokines; Cytokines; Eosinophilia; Male; Mice; Mice, Inbred BALB C; Mice, Inbred C57BL; Ovalbumin; Rhinitis, Allergic, Perennial; Rhinitis, Allergic, Seasonal; RNA, Messenger; Th2 Cells; Tumor Necrosis Factor-alpha

TAK-427 (2-[6-[[3-[4-(diphenylmethoxy)piperidino]propyl]amino]imidazo[1,2-b]pyridazin-2-yl]-2-methylpropionic acid dihydrate) is a novel anti-allergic agent that has both histamine H1-receptor antagonist and anti-inflammatory activities. In this study, we evaluated the efficacy of TAK-427 on acute nasal responses and nasal obstruction using various guinea pig models of allergic rhinitis. TAK-427 inhibited the histamine-induced nasal reactions with an ID50 value of 0.633 mg/kg, p.o. TAK-427 (0.1-10 mg/kg, p.o.) and most histamine H1-receptor antagonists tested inhibited the increase in intranasal pressure, nasal hypersecretion, sneezing and nasal itching caused by a single antigen challenge in sensitized guinea pigs. In addition, TAK-427 (0.3, 30 mg/kg, p.o.) significantly inhibited the development of nasal obstruction when sensitized guinea pigs were repeatedly challenged via inhalation with Japanese cedar pollen, whereas the histamine H1-receptor antagonist, azelastine (1 mg/kg, p.o.), and ketotifen (1 mg/kg, p.o.) were without effect. These results suggest that TAK-427 might not only suppress acute nasal symptoms but also ameliorate nasal obstruction via the effects other than those as a histamine H1-receptor antagonist.

Topics: Acute Disease; Animals; Anti-Inflammatory Agents; Disease Models, Animal; Guinea Pigs; Histamine; Histamine H1 Antagonists; Imidazoles; Male; Nasal Obstruction; Ovalbumin; Pollen; Pyridazines; Rhinitis, Allergic, Perennial; Rhinitis, Allergic, Seasonal; Sneezing

The purpose of this study was to investigate the involvement of chemical mediators other than histamine in nasal allergic signs using histamine H(1) receptor-deficient mice. In passively sensitized mice, antigen instillation into the nasal cavity induced significant increases in sneezing and nasal rubbing in wild-type mice, but no such increases were observed in histamine H(1) receptor-deficient mice. In actively sensitized mice, both sneezing and nasal rubbing were also significantly increased in a dose-dependent manner in both wild-type and histamine H(1) receptor-deficient mice. Histamine H(1) receptor antagonists such as cetirizine and epinastine significantly inhibited antigen-induced nasal allergic signs in wild-type mice, although the effects were incomplete. In addition, the thromboxane A(2) receptor antagonist ramatroban also inhibited these responses in wild-type mice. However, the leukotriene receptor antagonist zafirlukast showed no effects in wild-type mice. These results suggested that in the acute allergic model (passive sensitization), only histamine H(1) receptors are related to nasal signs induced by antigen, whereas in the chronic allergic model (active sensitization), both histamine H(1) receptors and thromboxane A(2) receptors were involved in the responses.

Topics: Animals; Anti-Allergic Agents; Antigens; Behavior, Animal; Carbazoles; Cetirizine; Dose-Response Relationship, Drug; Female; Histamine H1 Antagonists; Immunization; Immunoglobulin E; Indicators and Reagents; Indoles; Leukotriene Antagonists; Mice; Mice, Knockout; Ovalbumin; Passive Cutaneous Anaphylaxis; Phenylcarbamates; Receptors, Histamine H1; Rhinitis, Allergic, Seasonal; Sneezing; Sulfonamides; Thromboxane A2; Tosyl Compounds

The presence of nitric oxide (NO) in the nose is well documented; however, the role of this molecule in nasal physiology is still poorly understood. Our laboratory has previously demonstrated that NO is a mediator of the immediate secretory response to an intranasal histamine challenge in a rat model of nasal allergy. Histamine challenge, however, does not elicit a late-phase response (LPR). To study the role of NO in the LPR, we developed a model of nasal allergy in which brown Norway rats are actively sensitized to the allergen ovalbumin and later challenged intranasally with either phosphate-buffered saline solution (vehicle), ovalbumin in vehicle, or ovalbumin and the NO synthase inhibitor N -nitro-l -arginine methyl ester. In each experiment, nasal lavage samples were collected 30, 120, 240, and 360 minutes after challenge. Lavage samples were analyzed for albumin content by ELISA, inflammatory cell concentration with a hemocytometer, and evidence of inflammation by light microscopy. Blocking NO synthesis with N -nitro-l -arginine methyl ester significantly inhibited both albumin exudation and inflammatory cell influx into the nasal cavity during the LPR. These data suggest that NO plays a role in the LPR of nasal allergy.

Topics: Albumins; Allergens; Animals; Enzyme Inhibitors; Histamine; Inflammation Mediators; Nasal Lavage Fluid; Nasal Mucosa; Nasal Provocation Tests; NG-Nitroarginine Methyl Ester; Nitric Oxide; Nitric Oxide Synthase; Ovalbumin; Passive Cutaneous Anaphylaxis; Rats; Rats, Inbred BN; Rhinitis, Allergic, Perennial; Rhinitis, Allergic, Seasonal

Eosinophils are found in the nasal lavage fluid (NLF) and nasal biopsies of patients with allergic rhinitis after a nasal antigen challenge, and associated not only with a late-phase allergic reaction (LPR) but also an early phase allergic reaction (EPR). Numerous studies have been carried out to clarify the participation of eosinophils in LPR or airway hyperresponsiveness. However, there has been no published report describing in detail the role of eosinophils during EPR. To better understand the involvement of eosinophils in EPR, we studied the effects of repeated antigen challenges on nasal airway responsiveness and eosinophilic inflammation in EPR using a guinea pig rhinitis model.. Nasal airway responsiveness was measured as the nasal airway resistance (NAR) after nasal antigen provocation. Eosinophilic inflammation during EPR was assessed by nasal lavage and histopathological examination using two groups of animals: those in group 1 were subjected to a sensitization pretreatment only, and those in group 2 were subjected to a pretreatment of sensitization followed by repeated nasal challenges.. Repeated antigen challenges induced nasal hyperresponsiveness as indicated by a decrease in the antigen provocation dose and a significant increase in NAR. Furthermore, significant increases in eosinophil counts, eosinophil peroxidase (EPO) activity and protein content in NLF during EPR were observed following antigen provocation in group 2. There were significant correlations between the levels of these parameters, and albumin was the most prevalent of the proteins in NLF. Histopathological examination showed that the degree of eosinophil infiltration into the lamina propria of the nasal mucosa of the animals in group 2 was significantly and apparently higher than in group 1. Particularly, epithelial disruption and mucosal edema were significantly elevated after antigen provocation in group 2.. These results suggest that chronic eosinophil accumulation is induced by repeated antigen challenges in the nasal tissue, and that once antigen provocation occurs, eosinophils in the tissue are activated and responsible for the amplification of EPR such as vascular permeability and mucosal edema.

Topics: Animals; Disease Models, Animal; Eosinophil Peroxidase; Eosinophils; Guinea Pigs; Male; Nasal Lavage Fluid; Nasal Mucosa; Nasal Provocation Tests; Ovalbumin; Peroxidases; Proteins; Rhinitis, Allergic, Seasonal

The time course of changes in absorption of horseradish peroxidase (HRP) through the nasal mucosa after antigen challenge was evaluated in a guinea pig model of allergic rhinitis immunized with ovalbumin. Before and at 5 minutes, 4 hours, and 24 hours after nasal antigen challenge, both nasal cavities were filled with 5% HRP solution for 30 minutes, and blood was obtained to measure serum HRP levels by enzyme-linked immunosorbent assay. In immunized animals, the serum HRP levels were 2.3 times higher than those of normal controls (p<.05) before antigen challenge, which was performed 7 days after a series of nasal antigenic sensitizations. At 5 to 35 minutes after antigen challenge, the HRP levels decreased to one sixth of the prechallenge levels (p<.05), and they did not show a difference from the control levels. However, they increased markedly at 4 and 24 hours after antigen challenge (p<.01). The present study suggests that the absorption of macromolecules through the allergic nasal mucosa is enhanced markedly, depending upon the time course after antigen challenge, although it shows no apparent difference from normal controls during the dominant exudative process.

Topics: Absorption; Animals; Cell Membrane Permeability; Disease Models, Animal; Enzyme-Linked Immunosorbent Assay; Guinea Pigs; Horseradish Peroxidase; Injections, Intraperitoneal; Male; Nasal Mucosa; Nasal Provocation Tests; Ovalbumin; Rhinitis, Allergic, Seasonal; Time Factors

We have previously demonstrated that pyrene in diesel-exhaust particles (DEP) has an adjuvant activity on immunoglobulin E (IgE) antibody production in mice immunized with Japanese cedar pollen allergen (JCPA) or ovalbumin (OA) intraperitoneally. The present study is concerned with the adjuvant activity in IgE antibody production against JCPA of pyrene or DEP inoculated intranasally in mice. We show that anthracene, fluoranthene and benzo(a)pyrene in DEP have the ability to enhance anti-JCPA IgE antibody production in mice by intranasal immunization. Mice were grouped, immunized with 10 micrograms of JCPA plus 400 micrograms of pyrene, 10 micrograms of JCPA plus 100 micrograms of DEP, 10 micrograms of JCPA plus 2 mg of aluminum hydroxide and 10 micrograms of JCPA alone intranasally 7 times at 2 week intervals. Mice were also grouped, and immunized with JCPA (10 micrograms) plus 40 micrograms of anthracene, JCPA (10 micrograms) plus 400 micrograms of fluoranthene, JCPA (10 micrograms) plus 40 micrograms of benzo(a)pyrene, and JCPA (10 micrograms) plus 400 micrograms of pyrene and JCPA (10 micrograms) alone. We found that the IgE antibody responses to JCPA in mice immunized with JCPA plus pyrene, JCPA plus DEP or JCPA plus the three chemical organic compounds mentioned above were significantly enhanced compared with those immunized with JCPA alone. In addition, when the intraperitoneal macrophages obtained from the normal mice (unimmunized mice) were incubated with pyrene, anthracene, fluoranthene or benzo(a)pyrene in vitro, an enhanced chemiluminescence (CI) response and interleukin-1 alpha (IL-1 alpha) production of the macrophages was observed in each instance. These results suggest that in the production of IgE antibody to JCPA the adjuvancy of polycyclic aromatic hydrocarbons (PAHs) in DEP may be important in an attack of Japanese cedar pollinosis.

Topics: Adjuvants, Immunologic; Administration, Intranasal; Air Pollutants; Allergens; Aluminum Hydroxide; Animals; Anthracenes; Antibodies, Anti-Idiotypic; Benzo(a)pyrene; Female; Fluorenes; Food Contamination; Humans; Immunization; Immunoglobulin E; Interleukin-1; Luminescent Measurements; Macrophages, Peritoneal; Male; Mice; Ovalbumin; Pollen; Polycyclic Aromatic Hydrocarbons; Pyrenes; Rats; Rats, Wistar; Rhinitis, Allergic, Seasonal; Trees; Urban Population; Vehicle Emissions

Allergoids have been used successfully for immunotherapy of allergic disorders. It has appeared to us that the effect of allergoids could be potentiated by their coupling to an immunomodulator. In the present study we show that a conjugate made up of the coupling of ovalbumin through glutaraldehyde action to the C. granulosum-derived immunomodulator P40 is completely devoid of antigenicity and of cross-reactivity with ovalbumin. This conjugate was found to significantly inhibit mast cell degranulation. It also proved to be capable of protecting against the lethal systemic anaphylactic shock sensitized mice. Immunotherapy was performed in patients hypersensitive to either the pollen of Dactylis glomerata or to the house dustmite allergens using the conjugates made of the specific allergens and of the P40. Clinical improvement was observed in a significant percentage of the patients subjected to immunotherapy. Administration of the conjugates did not result in untoward reactions in any of the patients.

Topics: Allergens; Animals; Antigens, Bacterial; Cells, Cultured; Corynebacterium; Cross Reactions; Desensitization, Immunologic; Female; Humans; Mast Cells; Mice; Mites; Ovalbumin; Poaceae; Pollen; Rhinitis, Allergic, Seasonal

Topics: Animals; Bordetella pertussis; Chromatography, Gas; Chromatography, Gel; Guinea Pigs; Ileum; Immune Sera; Infrared Rays; Lung; Male; Mass Spectrometry; Muscle Contraction; Ovalbumin; Phospholipids; Rats; Rhinitis, Allergic, Seasonal; Silicon Dioxide; Spectrum Analysis; SRS-A; Ultraviolet Rays

Topics: Agar; Allergens; Asthma; Chromatography; Chymotrypsin; Dermatitis, Atopic; Egg White; Electrophoresis; Gels; Glycoproteins; Hexosamines; Hexoses; Humans; Immune Sera; Immunochemistry; Immunoelectrophoresis; Muramidase; Neuraminic Acids; Ovalbumin; Proteins; Rhinitis, Allergic, Seasonal; Skin Tests; Starch; Trypsin; Trypsin Inhibitors

Topics: Anaphylaxis; Animals; Antigens; Benzopyrans; Dinitrophenols; Ferritins; Haplorhini; Histamine H1 Antagonists; Histamine Release; Humans; Hypersensitivity, Immediate; Immunity, Active; Immunity, Maternally-Acquired; Immunoglobulin E; Leukocytes; Lung; Ovalbumin; Rabbits; Rhinitis, Allergic, Seasonal; Skin Tests

Topics: Adolescent; Child; Child, Preschool; Humans; Ovalbumin; Pollen; Rhinitis, Allergic, Seasonal; Skin Tests; Statistics as Topic