ovalbumin and Intestinal-Diseases

Asthma is a chronic airway inflammatory disease. Current treatment of mainstream medications has significant side effects. There is growing evidence that the refractoriness of asthma is closely related to common changes in the lung and intestine. The lungs and intestines, as sites of frequent gas exchange in the body, are widely populated with gas signaling molecules NO and CO, which constitute NO-CO metabolism and may be relevant to the pathogenesis of asthma in the lung and intestine. The Chinese herbal formula Tingli Dazao Xiefei Decoction (TD) is commonly used in clinical practice to treat asthma with good efficacy, but there are few systematic evaluations of the efficacy of asthma on NO-CO metabolism, and the mode of action of its improving effect on the lung and intestine is unclear.. To investigate the effect of TD on the lung and intestine of asthmatic rats based on NO-CO metabolism.. In vivo, we established a rat asthma model by intraperitoneal injection of sensitizing solution with OVA atomization, followed by intervention by gavage administration of TD. We simultaneously examined alterations in basal function, pathology, NO-CO metabolism, inflammation and immune cell homeostasis in the lungs and intestines of asthmatic rats, and detected changes in intestinal flora by macrogenome sequencing technology, with a view to multi-angle evaluation of the treatment effects of TD on asthmatic rats. In vitro, lung cells BEAS-2B and intestinal cells NCM-460 were used to establish a model of lung injury causing intestinal injury using LPS and co-culture chambers, and lung cells or intestinal cells TD-containing serum was administered to intervene. Changes in inflammatory, NO-CO metabolism-related, cell barrier-related and oxidative stress indicators were measured in lung cells and intestinal cells to evaluate TD on intestinal injury by way of amelioration and in-depth mechanism.. In vivo, our results showed significant basal functional impairment in the lung and intestine of asthmatic rats, and an inflammatory response, immune cell imbalance and intestinal flora disturbance elicited by NO-CO metabolic disorders were observed (P < 0.05 or 0.01). The administration of TD was shown to deliver a multidimensional amelioration of the impairment induced by NO-CO metabolic disorders (P < 0.05 or 0.01). In vitro, the results showed that LPS-induced lung cells BEAS-2B injury could cause NO-CO metabolic disorder-induced inflammatory response, cell permeability damage and oxidative stress damage in intestinal cells NCM-460 (P < 0.01). The ameliorative effect on intestinal cells NCM-460 could only be exerted when TD-containing serum interfered with lung cells BEAS-2B (P < 0.01), suggesting that the intestinal ameliorative effect of TD may be exerted indirectly through the lung.. TD can ameliorate NO-CO metabolism in the lung and thus achieve the indirectly amelioration of NO-CO metabolism in the intestine, ultimately achieving co-regulation of lung and intestinal inflammation, immune imbalance, cellular barrier damage, oxidative stress and intestinal bacterial disorders in asthma in vivo and in vitro. Targeting lung and intestinal NO-CO metabolic disorders in asthma may be a new therapeutic idea and strategy for asthma.

Topics: Animals; Asthma; Disease Models, Animal; Inflammation; Intestinal Diseases; Intestines; Lipopolysaccharides; Lung; Metabolic Diseases; Mice; Mice, Inbred BALB C; Ovalbumin; Oxidative Stress; Rats

Oral immunotherapy (OIT) is a promising treatment of food allergy. To administer an appropriate oral dose of an allergenic component as OIT to individuals sensitized with a food allergen may prevent inducing food allergic inflammation in them. So we attempted to establish a mouse model to evaluate efficacy for oral administration of food allergen after sensitization. In BALB/c mice sensitized by injecting ovalbumin (OVA) with alum twice, OVA was administered before inducing inflammation by feeding the mice with egg white (EW) diet. Severe inflammatory responses, such as enteropathy, weight loss, IL-4 production, and increase of IgE antibody levels, were suppressed by administration with 4 mg of OVA 7 times before feeding EW diet. OVA administration alone induced a slight Th2 response, but no symptoms. The current study demonstrated that severe food allergic enteropathy could be prevented by pre-administration with appropriate dose of OVA to sensitized mice.

Topics: Administration, Oral; Animals; Disease Models, Animal; Dose-Response Relationship, Drug; Female; Food Hypersensitivity; Immunization; Immunoglobulin E; Interleukin-4; Intestinal Diseases; Mice; Mice, Inbred BALB C; Ovalbumin

To improve the efficacy and safety of tolerance induction for food allergies, identifying the tissues responsible for inducing intestinal inflammation and subsequent oral tolerance is important. We used OVA23-3 mice, which express an ovalbumin-specific T-cell receptor, to elucidate the roles of local and systemic immune tissues in intestinal inflammation.. OVA23-3 mice developed marked enteropathy after consuming a diet containing egg white (EW diet) for 10 days but overcame the enteropathy (despite continued moderate inflammation) after receiving EW diet for a total of 28 days. Injecting mice with anti-IL-4 antibody or cyclosporine A confirmed the involvement of Th2 cells in the development of the enteropathy. To assess the individual contributions of Peyer's patches (PPs), mesenteric lymph nodes (MLNs), and the spleen to the generation of effector CD4+ T-cells, we analyzed the IL-4 production, proliferation in response to ovalbumin, and CD4+ T-cell numbers of these tissues. EW feeding for 10 days induced significant IL-4 production in PPs, the infiltration of numerous CD4+ T-cells into MLNs, and a decrease in CD4+ T-cell numbers in spleen. On day 28, CD4+ T-cells from all tissues had attenuated responses to ovalbumin, suggesting tolerance acquisition, although MLN CD4+ T-cells still maintained IL-4 production with proliferation. In addition, removal of MLNs but not the spleen decreased the severity of enteropathy and PP-disrupted mice showed delayed onset of EW-induced inflammatory responses. Disruption of peripheral lymphoid tissues or of both PPs and MLNs almost completely prevented the enteropathy.. PPs and MLNs coordinately promote enteropathy by generating effector T-cells during the initial and exacerbated phases, respectively; the spleen is dispensable for enteropathy and shows tolerogenic responses throughout EW-feeding. The regulation of PPs may suppress the initiation of intestinal inflammation, subsequently restricting MLNs and inhibiting the progression of food-allergic enteropathy.

Topics: Animal Feed; Animals; CD4-Positive T-Lymphocytes; Disease Models, Animal; Egg White; Female; Food Hypersensitivity; Interleukin-4; Intestinal Diseases; Lymph Nodes; Male; Mesentery; Mice; Ovalbumin; Peyer's Patches; Spleen

Anti-allergic efficacy of red ginseng (RG) and fermented red ginseng (FRG) was evaluated. RG or FRG were administered to ovalbumin (OVA)-sensitized mice for 8 weeks. Immunoglobulins (Igs), Th1/Th2 type cytokines, and β-lactoglobulin (BLG) in serum, and intestinal barrier-related molecules in jejunum were measured using enzyme-linked immunosorbent assay or reverse transcription-polymerase chain reaction. Mice sensitized with OVA increased serum IgG₁, IgE, OVA-IgG₁, and OVA-IgE. Both RG and FRG decreased serum IgE, OVA-IgE, and pro-inflammatory cytokines. Serum BLG, a marker of gut permeability, was significantly higher in sensitized animals and was decreased in mice fed RG or FRG. In addition, intestinal barrier-related markers such as MMCP-1, IL-4, TNF-α, COX-2, and iNOS mRNA expressions were decreased by RG or FRG. Our results suggest in vivo anti-allergic activities of RG or FRG, which are associated with the regulation of Th1/Th2 balance, intestinal inflammation and subsequent the suppression of IgE.

Topics: Administration, Oral; Animals; Anti-Allergic Agents; Cytokines; Dietary Proteins; Female; Fermentation; Food Hypersensitivity; Immunoglobulin E; Immunoglobulin G; Inflammation; Inflammation Mediators; Intestinal Diseases; Intestinal Mucosa; Jejunum; Lactoglobulins; Mice; Mice, Inbred BALB C; Ovalbumin; Panax; Permeability; Phytotherapy; Plant Extracts; RNA, Messenger; Th1-Th2 Balance

Modulating early immune response by application of bacteria and their by-products has been suggested as a preventive strategy against the development of allergic diseases. In light of this, the aim of the study was to test the effects of oral administration of bacterial lysates (BL) in a rat model of food allergy.. BL or PBS were administered orally to neonatal Brown Norway rats up to an age of 42 days. Additionally, animals were sensitized 3 times (days 35, 40 and 45) intraperitoneally with ovalbumin (OVA). On days 60 and 61, rats were locally challenged with OVA by gavage feeding.. Detection of increased allergen-specific Ig serum levels and proliferative responses of spleen mononuclear cells confirmed systemic sensitization. In serum of animals that received BL in addition to OVA sensitization, the levels of allergen-specific IgE and IgG were significantly reduced compared to animals which were not exposed to BL. Allergen-stimulated lymphocytes from spleen and mesenteric lymph nodes of BL-treated animals showed a significantly elevated cytokine production of IL-10. To assess local functional changes of the intestinal barrier we measured the intestinal permeability, which was increased in OVA-sensitized and challenged animals compared to nonsensitized controls, yet significantly reduced in sensitized animals which received BL.. These data suggest that local administration of BL (pathogen-associated molecular patterns) in the intestine exhibits immuno-modulating effects. Furthermore, pathophysiological features of food allergy, such as the loss of gut mucosal integrity, might be reduced by the treatment with BL.

Topics: Administration, Oral; Animals; Animals, Newborn; Cell Extracts; Enzyme-Linked Immunosorbent Assay; Food Hypersensitivity; Immunoglobulin E; Immunoglobulin G; Intestinal Diseases; Ovalbumin; Rats; Specific Pathogen-Free Organisms

Clarification of the mechanisms underlying the development of food-sensitive intestinal inflammation will provide an important clue to combating food allergies.. To establish a model of intestinal inflammation caused by oral administration of antigen without additional treatments, we focused on the ovalbumin (OVA) 23-3 T-cell receptor transgenic mouse, which had been reported to have high serum antigen-specific IgE responses to the feeding of an egg white diet.. Changes in body weight of mice fed an egg white diet were monitored throughout the 28-day experimental period. After the 28-day feeding, intestinal tissues were harvested for histologic examination. Endogenous production of cytokines and histamine in the jejunum, and production of cytokines secreted by OVA-specific CD4+ T cells purified from mesenteric lymph nodes, were analyzed.. Egg white diet-fed OVA23-3 mice developed weight loss and inflammation with villous atrophy and goblet cell hyperplasia, especially in the jejunum. A further characteristic feature was evidence of weight recovery and tissue repair. Jejunal inflammation was also observed in egg white diet-fed recombination activating gene (RAG)-2-deficient OVA23-3 mice. In addition, tissue sections revealed significant infiltration of specific IgE-positive cells and IgE-positive degranulating mast cells. Higher levels of IL-4 and significant levels of histamine were detected in the tissues. In the supernatant of OVA-stimulated T cells, IL-10 levels were also markedly elevated.. We report that high-dose and continuous intake of primitive OVA alone induces enteropathy containing regions under repair in OVA23-3 mice. Antigen-specific T cells and inflammatory cells primed by T(H)2 responses play important roles in regulation of development and improvement of the disease.. Long-term antigen intake causes T(H)2-dependent and food-sensitive enteropathy followed by tissue repair.

Topics: Animals; Antigens; Cell Movement; Egg Hypersensitivity; Egg White; Immunoglobulin E; Inflammation; Intestinal Diseases; Intestinal Mucosa; Jejunum; Male; Mast Cells; Mice; Mice, Inbred BALB C; Mice, Transgenic; Ovalbumin; Receptors, Antigen, T-Cell; Th2 Cells; Wasting Syndrome; Wound Healing

Undiagnosed food allergies have been proposed as possible causes of promoting and perpetuating irritable bowel syndrome . Our aim was to find out if sensitization could induce chronic functional motor disturbances in the intestine and the mechanisms implicated. Rats were sensitized to ovalbumin (OVA) following three hypersensitivity induction protocols, two parenteral and one oral. Rat mast cell protease II (RMCP II) release in response to OVA challenge and immunoglobulin E (IgE) concentration were measured in serum. At least 1 week after challenge, small intestinal motility was evaluated using strain gauges. Intestinal tissue samples from orally sensitized rats were checked for in vitro stimulation with OVA. Mucosal mast cells were counted from duodenum sections. All sensitized rats showed intestinal hypermotility. Only rats sensitized by parenteral procedure showed an increase in RMCP II after OVA challenge in serum. IgEs increased only in the Bordetella pertussis sensitized group. Small intestine sections from orally sensitized rats released more RMCP II than sections from control rats. All sensitized rats showed an increase in the number of mucosal mast cells in duodenum. In conclusion, hypersensitivity to food proteins induces chronic motor alteration that persists long after antigen challenge and an excited/activated state of sensitized mucosal mast cells.

Topics: Animals; Bordetella pertussis; Cholecystokinin; Duodenum; Food Hypersensitivity; Gastrointestinal Motility; Ileum; Immunoglobulin E; Immunohistochemistry; Intestinal Diseases; Intestinal Mucosa; Intestine, Small; Male; Mast Cells; Muscle Tonus; Ovalbumin; Rats; Rats, Sprague-Dawley; Serine Endopeptidases

Intestinal anaphylaxis triggers neuronal activation in the nucleus tractus solitarius (nTS) of the rat brain stem. Stress may modulate reflex circuitry in the brain stem and facilitate intestinal inflammatory responses. We hypothesized that stress would modulate central neuronal activation during intestinal anaphylaxis. NTS neurons were activated following intestinal antigen challenge in sensitized Hooded Lister rats but not in negative controls (P < 0.05). The number of Fos-positive neurons following intestinal anaphylaxis decreased in animals exposed to water-avoidance stress (P < 0.05), although serum levels of rat mast cell protease II were not different in stressed and unstressed animals, indicating a similar degree of mast cell degranulation. Stress seems to inhibit neuronal activation in the rat brain stem during intestinal inflammation without modulation of the inflammatory response itself. This may have implications for a potential efferent neuronal modulation of inflammatory responses in the gut.

Topics: Anaphylaxis; Animals; Cell Count; Chickens; Intestinal Diseases; Male; Neural Inhibition; Ovalbumin; Proto-Oncogene Proteins c-fos; Rats; Solitary Nucleus; Stress, Physiological

Morphologic and immunologic changes in the gut mucosa of food-hypersensitive mice, from a study model generated by feeding ovalbumin (OVA) to female BALB/c mice after intraperitoneal injection of cyclophosphamide (CY), were investigated in an effort to clarify the mechanisms of food-sensitive enteropathy. Villous atrophy, crypt hyperplasia, and increased numbers of intraepithelial lymphocytes (IEL) were confirmed in the antigen-challenged OVA-sensitive mice as seen in food-sensitive enteropathy in humans, whereas no significant morphologic changes were observed in the nontreated control group or groups treated with OVA or CY alone. IEL and lamina propria lymphocytes (LPL) were isolated from the intestinal mucosa before and after the antigen challenge, and surface markers were analyzed by FACScan. After the antigen challenge, the numbers of CD8+ cells increased among the IEL, and the occurrence of both CD4+ and CD8+ cells increased among the LPL. The numbers of Thy-1+ cells and TCR- alpha/beta + cells increased among both the IEL and LPL, and LFA-1 expression was enhanced in both of these lymphocyte populations. The proliferative response of IEL and LPL to OVA increased in a dose-dependent manner after the antigen challenge in the OVA-sensitive mouse model. These results indicate that IEL and LPL, possibly those that have migrated from peripheral blood, are activated by orally administered antigens and cause mucosal damage in the food-sensitive enteropathy.

Topics: Animals; Antigens; Atrophy; Disease Models, Animal; Female; Food Hypersensitivity; Hyperplasia; In Vitro Techniques; Intestinal Diseases; Intestinal Mucosa; Jejunum; Lymphocyte Activation; Mice; Mice, Inbred BALB C; Ovalbumin; T-Lymphocyte Subsets

In order to clarify the mechanisms of food-sensitive enteropathy, a food hypersensitive model was generated by feeding ovalbumin to female BALB/c mice after intraperitoneal injection of cyclophosphamide and morphological and immunological changes in the gut mucosa were investigated. Villus atrophy, crypt hyperplasia and increased numbers of intra-epithelial lymphocytes (IEL) were confirmed in this model, as seen in food-sensitive enteropathy in humans. Subpopulations of IEL and lamina propria lymphocytes were enumerated by immunohistochemical observation. CD8-positive cells were increased both in epithelium and lamina propria, whereas CD4-positive cells were decreased in lamina propria. We document here that orally administered food antigen actually induces food-sensitive enteropathy and mucosal damage is generated by lymphocytes that infiltrate the intestinal mucosa. We also investigated the effect of feeding an omega-3 fatty acid-enriched diet in this model and found that it was efficient in attenuating mucosal damage.

Topics: Animals; Fatty Acids, Omega-3; Female; Food Hypersensitivity; Intestinal Diseases; Intestinal Mucosa; Lymphocyte Subsets; Lymphocytes; Mice; Mice, Inbred BALB C; Ovalbumin

Several variables were found to influence enzyme-linked immunosorbent assay (ELISA) measurements of IgG and IgG subclass antibodies to food antigens. Two polyclonal rabbit antibody reagents to human IgG, and two sets of murine monoclonal antibodies to human IgG subclasses, were compared as secondary reagents. The choice of both polyclonal and monoclonal reagents affected significantly the results. High levels of IgA to an antigen depressed the measurements of comparable total IgG antibodies but did not influence the percentages of the four IgG subclass activities. Different ways of expressing the IgG subclass results were compared and the validity of the reference measurements used to obtain them was examined. Information from previous studies, together with the present data, suggests that absolute values cannot be reliably determined. We have therefore chosen to express the results for IgG subclass activities on a relative basis with reference to units of total IgG activity against the same antigen in each subject. This approach is practical and appears scientifically acceptable but limits the use of such determinations to comparisons between groups of subjects studied in the same laboratory.

Topics: Adolescent; Adult; Aged; Antibodies, Monoclonal; Antigens; Caseins; Dose-Response Relationship, Immunologic; Edible Grain; Enzyme-Linked Immunosorbent Assay; Female; Food; Glycine max; Humans; Immunoglobulin A; Immunoglobulin G; Intestinal Diseases; Lactalbumin; Lactoglobulins; Male; Middle Aged; Ovalbumin; Serum Albumin, Bovine

The effect of chronic dietary antigen challenge on the intestine was examined in sensitized rats. Three groups of Hooded-Lister rats were studied: animals sensitized to egg albumin; sham-sensitized animals; and unmanipulated controls. In sensitized rats, serum immunoglobulin E titers to egg albumin were greater than or equal to 1:64, whereas control and pair-fed rats showed no response. Sensitized rats received egg albumin 1 mg/ml in drinking water and rat chow ad libitum. Pair-fed animals also received egg albumin but were pair-fed with sensitized animals. Controls received water and rat chow ad libitum. Chronic antigen challenge resulted in reduced food intake and weight gain in sensitized animals. When the rats were killed after 9 days of antigen exposure, proximal intestine from experimental animals showed decreased disaccharidase activity, brush-border microvillus surface, area, and villus height. Crypt depth and enterocyte migration rate were increased. Mucosal mast cell involvement was suggested by mast cell proliferation, evidence of mast cell degranulation, and increased serum rat mast cell protease II levels. At the time of death, only sensitized jejunum demonstrated an increase in short-circuit current in Ussing chambers in response to antigen challenge. The findings indicate that chronic antigen exposure leads to intestinal injury, reduced food intake, and diminished weight gain.

Topics: Anaphylaxis; Animals; Antigens; Body Weight; Female; Food Hypersensitivity; Immunization; Immunoglobulin E; Intestinal Diseases; Intestinal Mucosa; Intestine, Small; Mast Cells; Microscopy, Electron; Ovalbumin; Peptide Hydrolases; Rats; Rats, Inbred Strains

Antigen challenge of jejunal epithelium from rats sensitized to egg albumin induces an active Cl- secretory process secondary to release of mucosal mast cell mediators. The present study was designed to define the relative role of these mast cell mediators and the enteric nervous system in the transport abnormalities associated with intestinal anaphylaxis. Net ion transport of stripped jejunal tissue from sensitized and sham-treated animals was studied in Ussing chambers. The Cl- secretory response induced by egg albumin during intestinal anaphylaxis was similar to that after addition of 5-hydroxytryptamine (5-HT), histamine, and prostaglandins D2 and E2 to jejunal tissue. Cinanserin, a 5-HT2-receptor antagonist, virtually abolished the response to 5-HT and totally abolished the response to egg albumin. Methysergide, a 5-HT1-receptor antagonist had no effect on either response. Indomethacin, an inhibitor of prostaglandin synthesis, significantly inhibited the 5-HT and egg albumin response. Diphenhydramine, an H1-receptor antagonist and cimetidine, an H2-receptor antagonist both significantly inhibited the histamine response but neither altered the response to egg albumin. Atropine, an anticholinergic, and tetrodotoxin, a nerve blocker, did not inhibit the antigen induced anaphylactic response. These results indicate that 5-HT, acting through 5-HT2 receptors is largely responsible for the transport abnormalities seen in intestinal anaphylaxis induced by egg albumin while prostaglandins appear to play a partial role. The findings do not support a role for the enteric nervous system for the egg albumin induced changes in Cl- secretion.

Topics: Anaphylaxis; Animals; Biological Transport; Cyclooxygenase Inhibitors; Electric Stimulation; Female; Histamine; Histamine Antagonists; Intestinal Diseases; Intestines; Ions; Mast Cells; Ovalbumin; Prostaglandins; Rats; Serotonin; Serotonin Antagonists; Tetrodotoxin

We examined the mucosal barrier function during anaphylaxis induced by the hapten N,N'-di-2,4,dinitrophenyl-lysine (di-DNP-lysine) in BDF1 female mice immunized with dinitrophenylated Ascaris suum extract. Immunized mice were gavaged with 10 mg or 50 mg of ovalbumin (OVA) with or without N,N'-di-2,4,-DNP-lysine (di-DNP-lysine). Animals that received di-DNP-lysine underwent anaphylaxis and were observed to have significantly greater serum concentrations of immunoreactive OVA (iOVA) than control mice. The severity of anaphylaxis, which varied with the dose of di-DNP-lysine administered, influenced the uptake of OVA; greater amounts of iOVA were detected in serum of mice undergoing more severe anaphylaxis. On gel permeation of serum from both groups of mice, immunoreactive OVA was found to have a molecular size similar to native OVA. Di-DNP-lysine is a synthetic hapten that reliably induced anaphylaxis in sensitized animals challenged by gavage. Anaphylaxis resulted in the uptake into the circulation of greater quantities of an unrelated protein antigen present in the intestinal lumen. The protein antigen that was taken up into the circulation appeared to be intact and thus may have an influence on the development of the immune response, or lack thereof, to this bystander antigen.

Topics: Anaphylaxis; Animals; Intestinal Absorption; Intestinal Diseases; Lysine; Mice; Ovalbumin; Permeability

The protein induced modifications of the small bowel mucosa from ovalbumin-sensitised mouse have been studied in organ culture. A decrease in gamma-glutamyl transpeptidase, alkaline phosphatase, lactase, sucrase, and glucoamylase activities was observed in the explants cultured in the presence of ovalbumin. In contrast, a large increase of those enzymatic activities was noted in the culture media, the overall effect observed being a net stimulation of the total enzymatic activities of the culture system. The enzymes accumulated in the particulate fraction of the medium (brush border membrane fraction) suggesting an increased turnover of membrane components by a process of shedding or microvesiculation. This model serves as a useful tool in evaluating the local response of the small bowel mucosa induced by a specific protein.

Topics: Animals; Disease Models, Animal; DNA; Dose-Response Relationship, Immunologic; Immunization; Intestinal Diseases; Intestinal Mucosa; Intestine, Small; Male; Mice; Mice, Inbred ICR; Organ Culture Techniques; Ovalbumin; Thymidine

Humoral responses to ovalbumin (OA) administered i.p. with Al(OH)3 were depressed in C57BL mice immunized 5-13 days after infection with N. dubius, but not N. brasiliensis or T. muris. These two parasites induced elevated IgM responses, possibly as a result of systemic contact with parasite larvae or debris since i.v. administered N. dubius also increased IgM titres to OA. Depression of anti-OA IgG titres by N. dubius was also observed in infected BALB/c and CBA mice given OA-Al(OH)3 (i.p.), but not in C57BL mice given OA-Al(OH)3 (s.c.), OA-FCA (i.p. or s.c.), or OA-B, pertussis (i.p.). These findings suggest that local effects of N. dubius within the peritoneum reduce the adjuvanticity of Al(OH)3, resulting in depressed responses to OA-Al(OH)3.

Topics: Animals; Antibody Formation; Enzyme-Linked Immunosorbent Assay; Helminthiasis; Immunoglobulin G; Immunoglobulin M; In Vitro Techniques; Intestinal Diseases; Mice; Mice, Inbred BALB C; Mice, Inbred C57BL; Mice, Inbred CBA; Ovalbumin; Species Specificity

Serum IgG, IgA and IgM activities to wheat, egg and cow's milk antigens were measured by an ELISA method in children and adults with coeliac disease (CD). In untreated patients, the IgA activity was characteristically raised to gluten antigens but often also to proteins from egg or cow's milk. Setting the upper reference range for gluten antibodies as the highest IgA reading obtained in healthy controls and patients with other intestinal disorders, IgA measurements afforded virtually 100% diagnostic sensitivity and specificity and detected 94% of children and 80% of adults with untreated CD. Such measurements, therefore, represent a valuable adjunct in the diagnosis of this disease. IgA activity to beta-lactoglobulin, casein or ovalbumin higher than the normal 95 percentile was found in 44-89% of untreated patients. Reduction of these antibody titres seemed to reflect relatively well the response to treatment with a gluten free diet, particularly the activity to beta-lactoglobulin. Monitoring of IgA antibodies to dietary antigens other than gluten may therefore be of particular importance in the follow-up of CD patients.

Topics: Adolescent; Adult; Aged; Antigens; Celiac Disease; Child; Child, Preschool; Enzyme-Linked Immunosorbent Assay; Female; Glutens; Humans; Immunoglobulins; Infant; Intestinal Diseases; Male; Middle Aged; Milk Proteins; Ovalbumin

Sera from 111 patients with various gastro-intestinal (GI) diseases were studies for the presence of antibodies to human serum albumin (HSA), bovine serum albumin (BSA) and ovalbumin (OA) by passive haemagglutination assay. The antibody titre to BSA was higher than that to HSA or OA. The anti-BSA antibody was demonstrated in upper GI diseases i.e. esophageal cancer, gastric ulcer, gastric cancer and duodenal ulcer, and not in lower GI disease i.e. Crohn's disease, ulcerative colitis and colon cancer. Both the mean titre and the incidence of the anti-BSA antibody tended to be higher in women than in men, and the titre was in a positive correlation with serum gamma-globulin levels. Sephadex G-200 column chromatography revealed that the anti-BSA antibody was widely distributed between void volume and 7S fraction.

Topics: Adolescent; Adult; Antibodies; Antibodies, Neoplasm; Child; Colonic Neoplasms; Esophageal Neoplasms; Female; Gastric Juice; Gastrointestinal Diseases; Humans; Inflammation; Intestinal Diseases; Male; Middle Aged; Ovalbumin; Peptic Ulcer; Serum Albumin; Serum Albumin, Bovine; Stomach Neoplasms

Experiments are described which demonstrate that intraperitoneal injection of a soluble protein antigen (ovalbumin) in Freund's complete adjuvant (FCA) followed 14 days later by seven days of repeated infusions of an ovalbumin/DEAE-dextran mixture resulted in the appearance of IgA-specific antiovalbumin-containing cells (AOCC) in the intestinal lamina propria and IgA associated specific antibody in intestinal secretion of pigs. Neither intraperitoneal injection alone nor infusion of the antigen mixture alone resulted in a significant local intestinal immune response. In intraperitoneal primed animals the repeated infusion of ovalbumin without DEAE-dextran or a single intraduodenal injection of ovalbumin both resulted in a similar AOCC response in the intestine but, in the absence of DEAE-dextran, IgA was not the predominant class specificity of AOCC. Evidence is also presented for a depression of the intestinal immune response when intraperitoneal immunisation was performed using a large dose of antigen in FCA.

Topics: Animals; Antibody Formation; Antibody-Producing Cells; Female; Immunization; Immunization Schedule; Immunoglobulins; Intestinal Diseases; Intestines; Male; Ovalbumin; Swine; Swine Diseases