ovalbumin and Respiratory-Tract-Infections

Topics: Allergens; Animals; Asthma; Biopsy; Blood Proteins; Bronchi; Cell Adhesion; Crosses, Genetic; Dendritic Cells; Eosinophil Granule Proteins; Eosinophils; Epithelial Cells; Fibroblasts; Humans; Inflammation Mediators; Matrix Metalloproteinase 9; Mice; Mice, Transgenic; Muscle, Smooth; Ovalbumin; Pulmonary Eosinophilia; Respiratory Tract Infections; Ribonucleases; Th1 Cells; Th2 Cells; Tissue Inhibitor of Metalloproteinase-1; Transgenes; Virus Diseases

Infants with respiratory syncytial virus (RSV)-associated bronchiolitis are at increased risk of childhood asthma. Recent studies demonstrated that certain infections induce innate immune memory (also termed trained immunity), especially in macrophages, to respond more strongly to future stimuli with broad specificity, involving in human inflammatory diseases. Metabolic reprogramming increases the capacity of the innate immune cells to respond to a secondary stimulation, is a crucial step for the induction of trained immunity. We hypothesize that specific metabolic reprogramming of lung trained macrophages induced by neonatal respiratory infection is crucial for childhood allergic asthma.. To address the role of metabolic reprogramming in lung trained macrophages induced by respiratory virus infection in allergic asthma.. Neonatal mice were infected and sensitized by the natural rodent pathogen Pneumonia virus of mice (PVM), a mouse equivalent strain of human RSV, combined with ovalbumin (OVA). Lung CD11b. Proline metabolism reprogramming of trained macrophages induced by early respiratory infection combined with allergen sensitization contributes to development of allergic asthma in childhood. Proline metabolism could be a well target for prevention of allergic asthma in childhood.

Topics: Allergens; Animals; Asthma; Humans; Hypersensitivity; Macrophages; Mice; Mice, Inbred BALB C; Ovalbumin; Proline; Respiratory Syncytial Virus Infections; Respiratory Tract Infections

Asthma is an airway inflammatory disease and a major health problem worldwide. Anti-inflammatory steroids and bronchodilators are the gold-standard therapy for asthma. However, they do not prevent the development of the disease, and critically, a subset of asthmatics are resistant to steroid therapy.. To elucidate the therapeutic potential of human β-defensins (hBD), such as hBD2 mild to moderate and severe asthma.. We investigated the role of hBD2 in a steroid-sensitive, house dust mite-induced allergic airways disease (AAD) model and a steroid-insensitive model combining ovalbumin-induced AAD with C muridarum (Cmu) respiratory infection.. In both models, we demonstrated that therapeutic intranasal application of hBD2 significantly reduced the influx of inflammatory cells into the bronchoalveolar lavage fluid. Furthermore, key type 2 asthma-related cytokines IL-9 and IL-13, as well as additional immunomodulating cytokines, were significantly decreased after administration of hBD2 in the steroid-sensitive model. The suppression of inflammation was associated with improvements in airway physiology and treatment also suppressed airway hyper-responsiveness (AHR) in terms of airway resistance and compliance to methacholine challenge.. These data indicate that hBD2 reduces the hallmark features and has potential as a new therapeutic agent in allergic and especially steroid-resistant asthma.

Topics: Airway Resistance; Animals; Asthma; beta-Defensins; Bronchoalveolar Lavage Fluid; Chlamydia Infections; Chlamydia muridarum; Disease Models, Animal; Inflammation; Interleukin-13; Interleukin-9; Lung; Lung Compliance; Mice; Ovalbumin; Pyroglyphidae; Respiratory Hypersensitivity; Respiratory Tract Infections

Mycoplasma pneumoniae, an atypical human pathogen, has been associated with asthma initiation and exacerbation. Asthmatic patients have been reported to have higher carriage rates of M pneumoniae compared with nonasthmatic subjects and are at greater risk for invasive respiratory infections.. We sought to study whether prior allergen sensitization affects the host response to chronic bacterial infection.. BALB/cJ and IL-4 receptor α. Anti-M pneumoniae antibody responses were decreased in allergen-sensitized, M pneumoniae-infected animals compared with control animals, but OVA-specific IgG responses were unaffected. Similar decreases in anti-S pneumoniae antibody levels were found in OVA-sensitized animals. However, M pneumoniae, but not S pneumoniae, infection augmented anti-OVA IgE antibody responses. Loss of IL-4 receptor signaling partially restored anti-M pneumoniae antibody responses in IgG. An established type 2-biased host immune response impairs the host immune response to respiratory bacterial infection in a largely pathogen-independent manner. Some pathogens, such as M pneumoniae, can augment ongoing allergic responses and inhibit pulmonary type 2 cytokine responses and allergic airway hyperreactivity.

Topics: Allergens; Animals; Asthma; Cytokines; Immunoglobulin G; Lung; Mice, Inbred BALB C; Mice, Knockout; Ovalbumin; Pneumococcal Infections; Pneumonia, Mycoplasma; Receptors, Cell Surface; Respiratory Tract Infections

Pidotimod is a synthetic dipeptide with biological and immuno‑modulatory properties. It has been widely used for treatment and prevention of recurrent respiratory infections. However, its impact on the regulation of allergic pulmonary inflammation is still not clear. In the current study, an ovalbumin (OVA)‑induced allergic asthma model was used to investigate the immune‑modulating effects of pidotimod on airway eosinophilia, mucus metaplasia and inflammatory factor expression compared with dexamethasone (positive control). The authors determined that treatment with pidotimod exacerbated pulmonary inflammation as demonstrated by significantly increased eosinophil infiltration, dramatically elevated immunoglobulin E production, and enhanced T helper 2 response. Moreover, treatment failed to attenuate mucus production in lung tissue, and did not reduce OVA‑induced high levels of FIZZ1 and Arg1 expression in asthmatic mice. In contrast, administration of dexamethasone was efficient in alleviating allergic airway inflammation in OVA‑induced asthmatic mice. These data indicated that pidotimod as an immunotherapeutic agent should be used cautiously and the effectiveness for controlling allergic asthma needs further evaluation and research.

Topics: Animals; Arginase; Asthma; Bronchoalveolar Lavage Fluid; Cell Differentiation; Disease Models, Animal; Down-Regulation; Eosinophils; Female; Hypersensitivity; Immunoglobulin E; Intercellular Signaling Peptides and Proteins; Lung; Metaplasia; Mice, Inbred C57BL; Mucus; Ovalbumin; Pyrrolidonecarboxylic Acid; Respiratory Tract Infections; Th2 Cells; Thiazolidines

Previous studies have demonstrated that S. mansoni infection and inoculation of the parasite eggs and antigens are able to modulate airways inflammation induced by OVA in mice. This modulation was associated to an enhanced production of interleukin-10 and to an increased number of regulatory T cells. The S. mansoni schistosomulum is the first stage to come into contact with the host immune system and its tegument represents the host-parasite interface. The schistosomula tegument (Smteg) has never been studied in the context of modulation of inflammatory disorders, although immune evasion mechanisms take place in this phase of infection to guarantee the persistence of the parasite in the host.. The aim of this study was to evaluate the Smteg ability to modulate inflammation in an experimental airway inflammation model induced by OVA and to characterize the immune factors involved in this modulation. To achieve the objective, BALB/c mice were sensitized with ovalbumin (OVA) and then challenged with OVA aerosol after Smteg intraperitoneal inoculation. Protein extravasation and inflammatory cells were assessed in bronchoalveolar lavage and IgE levels were measured in serum. Additionally, lungs were excised for histopathological analyses, cytokine measurement and characterization of the cell populations. Inoculation with Smteg led to a reduction in the protein levels in bronchoalveolar lavage (BAL) and eosinophils in both BAL and lung tissue. In the lung tissue there was a reduction in inflammatory cells and collagen deposition as well as in IL-5, IL-13, IL-25 and CCL11 levels. Additionally, a decrease in specific anti-OVA IgE levels was observed. The reduction observed in these inflammatory parameters was associated with increased levels of IL-10 in lung tissues. Furthermore, Smteg/asthma mice showed high percentage of CD11b+F4/80+IL-10+ and CD11c+CD11b+IL-10+ cells in lungs.. Taken together, these findings demonstrate that S. mansoni schistosomula tegument can modulates experimental airway inflammation.

Topics: Animals; Antibodies, Helminth; Bronchoalveolar Lavage Fluid; Cytokines; Disease Models, Animal; Female; Immunoglobulin E; Inflammation Mediators; Interleukin-10; Lung; Mice; Monocytes; Ovalbumin; Respiratory Tract Infections; Schistosoma mansoni; Schistosomiasis mansoni

It has been reported that adoptive transfer of γδ T cells increases the cellular infiltration, especially eosinophils, in the lungs of allergic mice, suggesting that γδ T cells may play a proinflammatory role in allergic airway inflammation. Respiratory syncytial virus (RSV) infection can decrease the number of Th2-type γδ T cells. However, the underlying mechanisms remain unknown.. BALB/c mice were inoculated intranasally with RSV before or after sensitization to OVA. The amounts of Th1/Th2 cytokines as well as the levels of specific antibodies were determined by ELISA. The apoptotic death of pulmonary γδ T cells was analyzed by flow cytometry.. Adoptive transfer of γδ T cells increased the production of Th2 cytokines in the lungs and allergy-related antibodies in the serum, further confirming that γδ T cells act as pro-inflammatory cells or a promoter for the development of allergic asthma. RSV infection before sensitization to OVA enhanced apoptotic death of pulmonary γδ T cells. The percentage and absolute number of FasL-expressing γδ T cells in the lungs of allergic mice were elicited significantly by prior RSV infection. Blocking FasL with monoclonal antibody diminished apoptotic death of γδ T cells, suggesting that FasL is important for RSV-induced apoptosis of pulmonary γδ T cells.. This work provides evidence that RSV infection suppresses the subsequent development of OVA-induced allergic responses partly by enhancing FasL-mediated apoptosis of pulmonary γδ T cells.

Topics: Allergens; Analysis of Variance; Animals; Apoptosis; Cytokines; Disease Models, Animal; Fas Ligand Protein; Female; Immunization; Mice; Mice, Inbred BALB C; Ovalbumin; Pneumonia; Random Allocation; Reference Values; Respiratory Syncytial Virus Infections; Respiratory Syncytial Viruses; Respiratory Tract Infections; Risk Assessment; Sensitivity and Specificity; Th2 Cells

Cystic echinococcosis (CE) is a near cosmopolitan zoonosis caused by the larval stage of the dog tapeworm Echinococcus granulosus. E. granulosus infection induces a polarized T-helper type 2 (Th2) systematic immune response in its intermediate hosts. However, it is not known whether the infection modulates lung inflammation by regulating local immune response. In this study, we examined the effects of E. granulosus infection on mouse ovalbumin (OVA)-induced asthma model.. BALB/c mice were intraperitoneally transplanted with 50 small E. granulosus cysts cultured in vitro. At 3 months post-inoculation, the mice were sensitized and challenged with ovalbumin (OVA). For histopathological studies, hematoxylin eosin and periodic acid schiff staining was used to examine the inflammatory cells infiltration and goblet cells hyperplasia, respectively. Cytokine levels were measured by mouse cytometric bead array (CBA) Kit and quantitative RT-PCR and other molecular biological approaches. Airway hyperresponsiveness was assessed in response to increasing doses of methacholine. Serum immunoglobulins were determined by ELISA.. E. granulosus infection significantly increased Th2 and Treg cytokine levels in serum and lung tissues, but down-regulated the expression of IL-5 in the lungs and IL-17A in serum and lung tissues of asthmatic mice sensitized and challenged with OVA. Histological staining of lung tissues showed that E. granulosus infection significantly reduced the severity of OVA-induced airway inflammation including reduction of eosinophil cell infiltration and mucus production. The E. granulosus infection also reduced eosinophil accumulation induced by OVA in bronchoalveolar lavage fluid (BALF) and also ameliorated airway hyperresponsiveness, a hallmark symptom of asthma.. E. granulosus infection remarkably reduces the severity of OVA-induced airway inflammation likely through enhancing IL-10 and down-regulation of IL-5 and IL-17A.

Topics: Animals; Echinococcosis; Echinococcus granulosus; Eosinophils; Female; Gene Expression Regulation; Inflammation; Interleukin-10; Interleukin-17; Interleukin-5; Mice; Mice, Inbred BALB C; Ovalbumin; Respiratory Tract Infections; Specific Pathogen-Free Organisms

Infant rats primed during the first week of life with soluble antigen displayed adult-equivalent levels of T-helper 2 (Th2)-dependent immunological memory development as revealed by production of secondary immunoglobulin G1 (IgG1) antibody responses to subsequent challenge, but in contrast to adults failed to prime for Th1-dependent IgG2b responses. We demonstrate that this Th2 bias in immune function can be redressed by oral administration to neonates of a bacterial extract (Broncho-Vaxom OM-85) comprising lyophilized fractions of several common respiratory tract bacterial pathogens. Animals given OM-85 displayed a selective upregulation in primary and secondary IgG2b responses, accompanied by increased gamma interferon and decreased interleukin-4 production (both antigen specific and polyclonal), and increased capacity for development of Th1-dependent delayed hypersensitivity to the challenge antigen. We hypothesize that the bacterial extract functions via enhancement of the process of postnatal maturation of Th1 function, which is normally driven by stimuli from the gastrointestinal commensal microflora.

Topics: Adjuvants, Immunologic; Animals; Antibodies, Bacterial; Antigens, Bacterial; Bacteria; Bacterial Infections; Cell Extracts; Disease Models, Animal; Hypersensitivity, Delayed; Immunization; Immunocompromised Host; Immunoglobulin G; Ovalbumin; Rats; Respiratory Tract Infections; T-Lymphocytes; Th1 Cells

We recently described a murine model of atopic asthma in which a marked, extensive hyperplasia of airway goblet cells is induced by repeated challenge of ovalbumin (OA)-sensitized mice with intratracheally administered allergen (Am. J. Respir. Cell Mol. Biol. 1996;14:425-438). We report here the time course of the duration of this feature and of its spontaneous resolution in the absence of further allergen exposure. Induction of severe neutrophilic inflammation in the airways by repeated intratracheal administration of lipopolysaccharide failed to induce goblet cell hyperplasia (GCH) to as great a degree as that induced by allergen, suggesting that nonallergic inflammation is a relatively poor inducer of this phenotype change in mice. When a "subclinical" infection of the lungs with the human A2 strain of respiratory syncytial virus was superimposed on the model of atopic asthma, recruitment of monocytes and lymphocytes to the airways was enhanced and a discharge of goblet cell mucin contents was observed. This may partly explain the respiratory difficulty that typifies virally induced exacerbations of asthma in humans. Daily systemic treatment of sensitized mice with dexamethasone during the period of allergen challenge produced a dose-related suppression of developing GCH, while similar treatment during the period following the establishment of extensive hyperplasia induced an accelerated resolution toward a normal epithelial phenotype. These results confirm and extend the relevance of this model as a representation of the human disease.

Topics: Allergens; Animals; Anti-Inflammatory Agents; Asthma; Bronchoalveolar Lavage Fluid; Dexamethasone; Eosinophils; Epithelial Cells; Hyperplasia; Leukocyte Count; Lipopolysaccharides; Lung; Lymphocytes; Macrophages; Male; Mice; Mice, Inbred BALB C; Neutrophils; Ovalbumin; Respiratory Syncytial Virus Infections; Respiratory Tract Infections

Virus infections frequently exacerbate asthma, and in some cases may even precipitate its onset. Although this association is well known, experimental investigation has been hampered by the lack of adequate models.. The effects of acute respiratory virus infection on sensitization to aereoallergen were investigated in this study.. Nebulized ovalbumin was used as an aeroantigen in normal mice, and in those infected with respiratory syncytial virus or influenza A.. Both viruses caused transient illness. Ovalbumin inhalation did not induce specific serum antibodies unless the mice were infected at the time of nebulization. In exposed uninfected mice cutaneous challenge with ovalbumin caused no response, but caused acute systemic illness and collapse if previous pulmonary exposure had occurred during respiratory infection. Mice that collapsed in response to cutaneous ovalbumin were found to have IgG1 specific to ovalbumin that was not found in the other mice. Intracellular cytokine staining of splenocyte cultures showed ovalbumin-specific production of IL-4 was enhanced by virus infection during exposure. In CD8+ T cells, ovalbumin-specific interferon-gamma production was also enhanced by co-infection with influenza. Both viruses were equally associated with the induction of anaphylaxis.. These results show that infection with respiratory viruses powerfully augments cellular and humoral immune responses to aeroantigen and provide an experimental model that allows such effects to be investigated.

Topics: Administration, Inhalation; Allergens; Anaphylaxis; Animals; Bronchial Hyperreactivity; Female; Flow Cytometry; Immunoglobulin E; Immunoglobulin G; Influenza A virus; Injections, Intradermal; Mice; Orthomyxoviridae Infections; Ovalbumin; Respiratory Syncytial Virus Infections; Respiratory Syncytial Viruses; Respiratory Tract Infections; Spleen; Weight Loss

A key rate-limiting step in the adaptive immune response at peripheral challenge sites is the transmission of antigen signals to T cells in regional lymph nodes. Recent evidence suggests that specialized dendritic cells (DC) fulfill this surveillance function in the resting state, but their relatively slow turnover in most peripheral tissues brings into question their effectiveness in signaling the arrival of highly pathogenic sources of antigen which require immediate mobilization of the full range of host defenses for maintenance of homeostasis. However, the present report demonstrates that recruitment of a wave of DC into the respiratory tract mucosa is a universal feature of the acute cellular response to local challenge with bacterial, viral, and soluble protein antigens. Consistent with this finding, we also demonstrate that freshly isolated respiratory mucosal DC respond in vitro to a variety of CC chemokines as well as complementary cleavage products and N-formyl-methionyl-leucine-phenylalanine. This suggests that rapid amplification of specific antigen surveillance at peripheral challenge sites is an integral feature of the innate immune response at mucosal surfaces, and serves as an "early warning system" to alert the adaptive immune system to incoming pathogens.

Topics: Animals; Antigens; Bordetella pertussis; Chemokines; Dendritic Cells; Epithelium; Inflammation; Moraxella catarrhalis; Mucous Membrane; N-Formylmethionine Leucyl-Phenylalanine; Neisseriaceae Infections; Ovalbumin; Rats; Rats, Inbred Strains; Respiratory Tract Infections; Respirovirus; Respirovirus Infections; T-Lymphocytes; Whooping Cough

1. We investigated whether virus-induced airway hyperresponsiveness in guinea-pigs could be modulated by pretreatment with capsaicin and whether viral respiratory infections could potentiate ovalbumin-aerosol-induced tracheal hyperresponsiveness. 2. Animals were inoculated intratracheally with bovine parainfluenza-3 virus or control medium 7 days after treatment with capsaicin (50 mg kg-1, s.c.). Four days after inoculation, tracheal contractions were measured to increasing concentrations of substance P, histamine and the cholinoceptor agonist, arecoline. 3. In tracheae from virus-infected guinea-pigs, contractions in response to substance P, histamine and arecoline were significantly enhanced (P < 0.01) by 144%, 46% and 77%, respectively. Capsaicin pretreatment inhibited the hyperresponsiveness to substance P partly (62%) and to histamine and arecoline completely. 4. In another series of experiments animals were first sensitized with ovalbumin (20 mg kg-1, i.p.). After 14 days animals were exposed to either saline or ovalbumin aerosols for 8 days. After 4 aerosol exposures (4 days) animals were inoculated with either parainfluenza-3 virus or control medium. One day after the last ovalbumin aerosol, tracheal contraction in response to increasing concentrations of substance P, histamine and arecoline was measured. 5. Tracheae from ovalbumin-aerosol-exposed control inoculated animals showed a similar degree of airway hyperresponsiveness to saline-aerosol-exposed virus-treated guinea-pigs. Virus inoculation of ovalbumin-treated animals significantly potentiated the tracheal contractions to substance P compared to either of the treatments alone. The contractions in response to histamine and arecoline were only slightly enhanced. 6. In conclusion, sensory nerves and/or tachykinins are involved in virus-induced airway hyperresponsivenessin guinea-pigs and viral respiratory infections can potentiate the increase in tracheal responsiveness to bronchoconstrictor agonists after ovalbumin exposure.

Topics: Animals; Arecoline; Capsaicin; Dose-Response Relationship, Drug; Guinea Pigs; Histamine; Hypersensitivity; Male; Ovalbumin; Respiratory Tract Infections; Substance P; Tachykinins; Trachea; Virus Cultivation

Induced interleukin 2 (IL2) responsiveness in allergen-stimulated lymphocytes from children with post respiratory syncytial virus (RSV) infection was studied. Induction of IL2 responsiveness in the patients lymphocytes was observed upon stimulation with allergens such as Dermatophgoides farinae (Df) antigen, ovalbumin (OVA) and alpha-casein. Such responses were not induced in age-matched normal lymphocytes. Maximum response was shown in lymphocytes from children who had been suffering from the infection for approximately one month, and the response gradually decreased over the course of eight months. The frequency of induced IL2 responsiveness was unrelated to family history of atopic diseases, although there was a high incidence (67%) of family history among the patients. These results indicate that RSV-sensitized lymphocytes from the patients have acquired hypersensitivity to allergens such as food and mite antigens, factors which are commonly involved in the onset of atopic diseases.

Topics: Animals; Caseins; Cells, Cultured; Child, Preschool; Female; Humans; Infant; Infant, Newborn; Interleukin-2; Lymphocytes; Male; Mites; Ovalbumin; Respiratory Syncytial Viruses; Respiratory Tract Infections; Respirovirus Infections

Groups of BALB/c mice were sham infected or inoculated intranasally (IN) with live RSV. From Day 4 to 8 after infection, the animals were exposed IN to ovalbumin (OVA) with or without alum adjuvant. At different intervals, levels of OVA concentration in serum, IgG-anti-OVA antibody activity in serum, and IgA-anti-OVA antibody activity in bronchial washings were determined, employing the ELISA technique. IgE-anti-OVA antibody titers in serum and bronchial washings were assessed by PCA. OVA concentrations in serum were significantly higher in RSV-infected animals compared to uninfected controls. The use of alum adjuvant also increased OVA uptake in uninfected animals but to a lesser extent than RSV infection. RSV-infected animals developed significantly higher OVA-specific antibody titers of IgG isotype in serum and IgA isotype in bronchial washings than the uninfected controls, while alum enhanced the immune response less markedly but still significantly in uninfected mice. An IgE antibody response to OVA in serum was demonstrable in 50% of RSV-infected mice immunized IN with OVA and alum, while all uninfected animals and RSV-infected animals immunized with OVA alone (without adjuvant) failed to develop a detectable IgE response. These findings suggest that infections with viral agents such as RSV may function as adjuvants for other antigens inhaled during acute respiratory infection. These observations may explain the alterations in the immune response to other antigens in patients with acute viral-induced bronchopulmonary diseases.

Topics: Adjuvants, Immunologic; Administration, Inhalation; Alum Compounds; Aluminum; Animals; Antigens; Bronchoalveolar Lavage Fluid; Immunoglobulin A; Immunoglobulin E; Immunoglobulin G; Lung; Male; Mice; Mice, Inbred BALB C; Ovalbumin; Respiratory Syncytial Viruses; Respiratory Tract Infections; Respirovirus Infections; Sulfates

Guinea pigs, actively sensitized to ovalbumin, were inoculated by nasal insufflation with parainfluenza 3 or virus growth medium 4 d before performing in vitro pharmacological studies on tracheal and bronchial smooth muscle. In each airway segment, cumulative dose-response effects of ovalbumin were obtained in the absence and presence of a maximally effective concentration of a beta adrenergic receptor agonist, sulfonterol. Sulfonterol shifted the dose-response curve to the right and reduced the maximum smooth muscle contractile response to ovalbumin. Virus infection did not alter the dose-response effects of ovalbumin. However, the magnitude of the inhibitory effects of sulfonterol was smaller in segments taken from animals inoculated with virus. Blockade by virus infection of the inhibitory effect of sulfonterol was reversed when the concentrations of beta agonist were increased. Sulfonterol did not alter the dose-response effects of histamine at any of the concentrations that markedly antagonized the effects of ovalbumin. Virus infection did not alter the sensitivities to sulfonterol or papaverine in producing relaxation in either airway segment. The magnitude of relaxation produced by papaverine was significantly larger in bronchial rings taken from animals infected with virus for 4 d, but there was no alteration by virus of the dose-response effects of histamine or carbachol. In experiments measuring antigen-induced release of slow reacting substance of anaphylaxis and histamine from minced lung, virus infection did not alter the sensitivity or the maximum effects of ovalbumin. Also, the ability of sulfonterol to inhibit the release of slow reacting substance of anaphylaxis and histamine was not affected by virus infection.These results demonstrate that infection of guinea pigs with respiratory virus results in a selective blockade of the beta adrenergic-mediated inhibition of antigen-induced contraction of airway smooth muscle. The guinea pig may serve as a useful model in physiological studies of virus-induced asthma.

Topics: Adrenergic beta-Agonists; Animals; Asthma; Benzyl Alcohols; Benzyl Compounds; Bronchi; Carbachol; Female; Guinea Pigs; Histamine; In Vitro Techniques; Models, Biological; Muscle Contraction; Muscle, Smooth; Ovalbumin; Parainfluenza Virus 3, Human; Paramyxoviridae Infections; Respiratory Tract Infections; Trachea

Guinea pigs sensitized to ovalbumin exhibit signs of respiratory impairment when exposed to an aerosol of the antigen. This response was investigated in anesthetized guinea pigs by determining forced pulmonary mechanics to derive peak expiratory flow rate, forced vital capacity, forced expiratory volume in 0.1 sec, maximal mid-expiratory flow rate and respiratory rate. Measurement of these parameters allows qualitative comparisons to be made with changes that are routinely determined during investigations of human asthma. Exposure of anesthetized guinea pigs to a 3% ovalbumin aerosol for 2 min produced an increase in respiratory rate, a 20% fall in peak expiratory flow rate and maximal mid-expiratory flow rate, a 50% fall in forced vital capacity and a 40% fall in forced expiratory volume in 0.1 sec. This response was reversed by aminophylline. In these respects the response appears to be similar to the acute asthmatic response in humans.

Topics: Aminophylline; Anaphylaxis; Animals; Asthma; Disease Models, Animal; Female; Forced Expiratory Volume; Guinea Pigs; Male; Maximal Midexpiratory Flow Rate; Ovalbumin; Peak Expiratory Flow Rate; Respiration; Respiratory Tract Infections; Vital Capacity