Home About us Contact
|
Home About us Contact | ||
|
|
||
OVA-specific IgE (ova-specific + ige)
Selected AbstractsNKT cells are dispensable in the induction of oral tolerance but are indispensable in the abrogation of oral tolerance by prostaglandin EEUROPEAN JOURNAL OF IMMUNOLOGY, Issue 1 2003Ryotaro Ishimitsu Abstract NK1.1+ ,,, T cells (NKT cells) regulate the Th1/Th2 balance in response to dietary Ag, which may be involved in regulation of oral tolerance. OVA-specific IgE and IgG1 Ab levels were significantly lower following an i.p. injection of OVA (in CFA) in C57BL/6 mice orally given a single, high dose (25,mg) of OVA than in those orally given PBS. The oral tolerance was normally induced in J,281,/, mice which lack V,14+ NKT cells, suggesting that NKT cells are dispensable for induction of oral tolerance. Treatment with PGE1 or PGE2 abrogated the oral tolerance in J,281+/+ mice; this abrogation was accompanied by an OVA-specific Th2-dominant response. The abrogation of oral tolerance by PGE1 was not evident in J,281,/, mice. Treatment with PGE1 induced an early increase in IL-4 production by liver NKT cells in normal mice and neutralization of the early IL-4 by administration of anti-IL-4 mAb abolished PGE1 -induced abrogation of oral tolerance. These results suggest that liver NKT cells producing IL-4 are responsible for the down-regulation of oral tolerance that is caused by the PGE molecules. [source] The anti-allergenic properties of milk kefir and soymilk kefir and their beneficial effects on the intestinal microfloraJOURNAL OF THE SCIENCE OF FOOD AND AGRICULTURE, Issue 15 2006Je-Ruei Liu Abstract Food allergy is now recognized as a worldwide problem, and like other atopic disorders its incidence appears to be increasing. Kefir is reported to possess the ability to reduce intestinal permeation of food antigens; however, no experimental study has clearly evaluated the relationships between kefir consumption, allergen-specific IgE response, and intestinal microflora. The aim of this study was to evaluate the effect of oral consumption of milk kefir and soymilk kefir on in vivo IgE and IgG1 production induced by ovalbumin (OVA) in mice. The effects of kefir administration on the murine intestinal microflora were also examined. Oral administration of milk kefir and soymilk kefir for 28 days significantly increased the fecal populations of bifidobacteria and lactobacilli, while it significantly decreased those of Clostridium perfringens. Milk kefir and soymilk kefir also significantly decreased the serum OVA-specific IgE and IgG1 levels for both groups, but not those of the IgG2a analogues. Consumption of milk kefir and soymilk kefir suppressed the IgE and IgG1 responses and altered the intestinal microflora in our supplemented group, suggesting that milk kefir and soymilk kefir may be considered among the more promising food components in terms of preventing food allergy and enhancement of mucosal resistance to gastrointestinal pathogen infection. Copyright © 2006 Society of Chemical Industry [source] Effects of Dexamethasone on the Expression of Transforming Growth Factor-, in the Mouse Model of Allergic RhinitisTHE LARYNGOSCOPE, Issue 8 2007Seung-Sin Lee MD Abstract Objectives/Hypothesis: This study aimed to evaluate the effect of dexamethasone on the expression of transforming growth factor (TGF)-, in the mouse model of allergic rhinitis. Study Design: Female BALB/c mice were randomly assigned to four groups, including two control groups and two treatment groups. Methods: 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-,1 and CD4 in nasal mucosa, and TGF-,1 and OVA-specific immunoglobulin E (IgE) in sera were analyzed. Results: Dexamethasone administration before general sensitization reduced the symptom score, OVA-specific IgE, and eosinophil infiltration and increased the serum level of TGF-,1 significantly. Dexamethasone administration before local challenge reduced only the eosinophil infiltration significantly. Immunoreactivity of TGF-,1 and CD4 was lower in both treatment groups. Conclusion: 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-,, and the other by suppressing late allergic reactions through the inhibition of proliferation and chemotaxis of inflammatory cells such as eosinophils. [source] Dose-dependent effects of endotoxins on allergen sensitization and challenge in the mouseCLINICAL & EXPERIMENTAL ALLERGY, Issue 11 2004C. Delayre-Orthez Summary Background Levels of endotoxins greatly differ according to environmental settings. Objective To study the effect of lipopolysaccharide (LPS) at increasing doses (0.1,1000 ng) on allergen sensitization and challenge in the mouse. Methods Mice were sensitized systemically and challenged locally with ovalbumin (OVA) in the presence or absence of LPS. Inflammation was assessed by determining total and differential cell counts and T-helper type 2 (Th)2 cytokine (IL-4 and IL-5) levels in bronchoalveolar lavage fluid (BALF). Total and OVA-specific IgE levels were quantified in serum. Airway hyper-responsiveness (AHR) was assessed by whole-body barometric plethysmography. Results Administered prior to sensitization, LPS at 100 or 1000 ng dose-dependently decreased allergen- induced total and OVA-specific IgE, airway eosinophilia and Th2 cytokines in BALF, without changing AHR. Administered during OVA challenge, LPS at 1 ng (an infra-clinical dose) or 100 ng (a dose triggering neutrophilia) enhanced airway eosinophilia, without affecting IgE levels or AHR. Conclusion Our data clearly demonstrate that exposure to LPS influences allergen-induced IgE production and airway eosinophilia in a time and dose-dependent manner, preventing IgE production and development of eosinophilia when administered during allergen sensitization at high doses, and inducing exacerbation of eosinophilia when administered upon allergen challenge at low doses, including infra-clinical doses. [source] | ||||||||||