High Levels Of Allergen-specific IgE Research Articles

Effect of Lactobacillus rhamnosus GG immunopathologic changes in chronic mouse asthma model.

Asthma is a heterogeneous inflammatory disorder of the airway. A Th2 response usually contributes to high levels of allergen-specific IgE and eosinophilic airway inflammation. Several findings have demonstrated that neutrophils, not eosinophils, are the major inflammatory cells in chronic asthma patients with steroid-resistance. Lactobacillus rhammosus GG (LGG) exhibits anti-inflammatory properties on OVA-induced acute airway inflammation. We hypothesized that orally administrated LGG should reduce airway remodeling in chronic experimental models. Female Balb/c mice were sensitized with OVA. LGG was used to investigate whether oral administrations of LGG inhibited OVA-induced airway inflammation in a chronic asthma model and the different intervention times between LGG pre-treatment and post-treatment groups. BALF was analyzed with Liu's stain and ELISA assay. Lung histopathology was assayed with HE, IHC and Masson's trichrome staining. Lung tissues were assayed with PCR (T-bet, GATA3, RORrt and Foxp3). Many cytokines were detected in the serum and BALF. LGG significantly decreased the number of infiltrating inflammatory cells. We also found that the oral LGG group suppressed not only Th2 cytokine, but also IL-17, TNF-α and HMGB1 in the BALF levels. However, GATA3 and RORrt decreased significantly in the RNA level in the LGG groups, but the T-bet and Foxp3 increased in the RNA level. LGG not only had anti-inflammatory effects on OVA-induced airway inflammation, but also improved airway remodeling and collagen expression in the chronic asthma mouse model. Moreover, LGG might be an additional or supplementary therapy for allergic airway diseases.

Transmission of allergen-specific IgG and IgE from maternal blood into breast milk visualized with microarray technology

Transmission of allergen-specific IgG and IgE from maternal blood into breast milk visualized with microarray technology

Preterm birth reduces the incidence of atopy in adulthood

Immunologic pathways are primed in early life. Preterm birth can influence this process and thereby affect whether a person will have atopy later in life. Previous studies on the effects of preterm birth on atopy in adulthood have been inconclusive and limited to children or subjects born moderately preterm. Our aim was to compare the incidence of atopy among young adults who were born preterm and at very low birth weight (≤ 1500 g) with that of term-born young adults (control subjects). The study comprised 166 adults who were born preterm and at very low birth weight and 172 control subjects, all of whom were from the Helsinki Study of Very Low Birth Weight Adults. We assessed atopic predisposition at ages 18 to 27 years using skin prick tests for 6 common aeroallergens and measurements of serum concentrations of total IgE and 3 types of allergen-specific (cat, birch, and timothy) IgE. We asked the subjects whether they had been given a diagnosis of asthma or allergic rhinitis or had atopic eczema and analyzed data by using logistic or linear regression, adjusting for potential confounding factors. The risk for having at least 1 positive reaction on a skin prick test was reduced (adjusted odds ratio, 0.43; 95% CI, 0.23-0.79, P = .007), and the concentration of cat-specific IgE was less (25% less; 95% CI, 43% to 2.3% less; P = .033) in sera from very-low-birth-weight subjects compared with that seen in sera from control subjects. Within the very-low-birth-weight group, those born at an earlier gestational age were less likely to have positive skin prick test reactions (adjusted odds ratio for 1 week, 0.82; 95% CI, 0.68-0.98, P = .029) and less likely to have high levels of allergen-specific IgE. Cumulative incidences of atopic disease were similar between adults of very low birth weight and control subjects. Young adults born prematurely and at very low birth weight have a lower incidence of atopy than adults who were born full term. This finding supports the hypothesis that the risk for atopy is determined during early stages of development.

High allergen‐specific serum immunoglobulin E levels in nonatopic West Highland white terriers

Human and canine atopic dermatitis (AD) share an association with IgE specific to environmental allergens, but few studies have evaluated serum allergen-specific IgE in nonatopic dogs. This study compared serum allergen-specific IgE levels in 30 atopic and 18 nonatopic West Highland white terriers. Atopic dermatitis was confirmed using standard criteria. Nonatopic dogs were over 5 years of age and had no clinical signs or history of AD. Serum allergen-specific IgE levels were measured with Allercept(®) IgE ELISAs using a 48-allergen Australian panel. Positive reactions were defined as ≥150 ELISA absorbance units. Intradermal tests were performed in 16 atopic dogs, either at the time of or at various times prior to serum collection. In atopic dogs, the most common positive ELISA and intradermal test results were to Dermatophagoides farinae (11 of 30 dogs), but there were no statistically significant correlations between results from the two methods for any allergen. In nonatopic dogs, multiple high-positive ELISA reactions were reported to 45 of 48 allergens, most commonly D. farinae and Tyrophagus putrescentiae (17 of 18 dogs each). Positive ELISA results in nonatopic dogs were statistically significantly higher than those in atopic dogs for 44 of 48 allergens, including two allergens (D. farinae and Dermatophagoides pteronyssinus) commonly regarded as significant in canine AD. In conclusion, positive allergen-specific IgE ELISAs were not specific for canine AD, and high allergen-specific IgE levels were seen in nonatopic dogs. The clinical significance of this and whether it characterizes a protective phenotype is unclear.

CD23 Trimers Are Preassociated on the Cell Surface Even in the Absence of Its Ligand, IgE

Allergic disease is mediated by high levels of allergen-specific IgE. IgE binding to CD23, the low affinity receptor for IgE, results in a negative feedback signal leading to a decrease in IgE production. Previous studies have shown that CD23 associates as an oligomer and that cooperative binding of at least two lectin domains is required for high affinity IgE binding to CD23. We have previously shown that cooperative binding is required for regulation of IgE production. This study describes the production of several mAbs that bind the stalk region of murine CD23. One of the Abs, 19G5, inhibited the IgE/CD23 interaction at 37 degrees C, but not at 4 degrees C. Analysis of the binding properties of these Abs revealed that CD23 dissociates at high temperatures, such as 37 degrees C; however, the N terminus is constitutively associated, indicating partial, rather than complete, dissociation. A novel finding was that the stalk region, previously thought to mediate trimer association, was not required for oligomerization. These data reveal important information about the structure of CD23 that may be useful in modulating IgE production.

Inhibition of human airway sensitization by a novel monoclonal anti-IgE antibody, 17-9.

We investigated the effect of a novel mouse IgG2b nonanaphylactogenic anti-human IgE antibody, 17-9, on allergen and histamine responses in passively sensitized human airways in vitro to determine the specific contribution of IgE to the sensitization process. Bronchial rings were sensitized with serum containing high levels of allergen-specific IgE (Dermatophagoides farinae), or with a hapten-specific chimeric humanized IgE (JW8). There was a concentration-dependent contraction of serum-sensitized bronchial rings to D. farinae (517 +/- 188 mg tension at 10 U/ml, n = 8) that was not observed in nonsensitized controls. This response was practically abolished when tissues were sensitized in the presence of 100 microg/ml anti-IgE antibody 17-9 (54 +/- 20 mg). In tissues sensitized with the anti-NIP IgE, JW8, there was a concentration-dependent contraction to the specific antigen NIP-BSA (560 +/- 154 mg at 0.3 microg/ml, n = 5) that was not observed in nonsensitized control subjects and that was substantially inhibited when 17-9 was present in the sensitization buffer (124 +/- 109 mg). The inhibition with 17-9 was specific, as pretreatment with a non-IgE-specific IgG2b antibody did not affect allergen responses. Potency and maximal contractions to histamine in serum-sensitized tissues were significantly elevated compared with nonsensitized controls; this was not affected by the presence of 17-9 during sensitization (pEC50 = 5.1 +/- 0.2 versus 5.0 +/- 0.3 in tissues sensitized in the absence of 17-9). In tissues sensitized with JW8 there was no significant increase in responsiveness to histamine. We conclude that allergen responses in sensitized human airways are dependent on IgE levels in the sensitizing serum while nonspecific (hyper)responsiveness depends on serum factors other than IgE. Nonanaphylactogenic anti-human IgE antibodies effectively inhibit allergen responses of human airways in vitro but may not affect other factors inducing hyperresponsiveness.

THE INVESTIGATION OF WHEEZING INFANTS

We investigated the allergic factors affecting wheezing before the age of first year and their relation to asthma at three years of age.35 wheezing infants (recurrent episodes of afebril wheezing) underwent allergic testing before the age of first year (6.4±3.6 months old). Total serum IgE levels increased 43%. Allergen specific IgE levels elevated 49%. Eosinophyllia was noted 23%. Positive food challenge test (egg or milk) suggest food allergy was noted 49%. Only 26% had all negative. 91% of the infants had allergic family histories.Evaluation of each factor according to relative risk suggest that the high allergen specific IgE levels, positive food challenge test, hospitalization because of severe wheezing and allergic family histories are asthmatic risk factors at three years of age.

Role of IgE in hyperresponsiveness induced by passive sensitization of human airways.

Incubation of airways from nonatopic patients with serum from patients with high IgE levels confers responsiveness to "specific" (allergen) and hyperresponsiveness to "nonspecific" (histamine) stimuli. We have tested the hypothesis that the level of IgE determines the degree of specific and nonspecific responsiveness. Bronchial rings from nonatopic patients were sensitized overnight with serum containing high levels of allergen-specific IgE, or with an allergen-specific chimeric IgE (JW8) in physiologic buffer. In vitro responsiveness to allergen and histamine was evaluated and compared with non-sensitized tissues from the same patients. Responses to specific allergen were demonstrated in all tissues sensitized with atopic serum or chimeric IgE, but not in nonsensitized tissues. Allergen responses were specific, since tissues sensitized using serum containing high Dermatohagoides farinae-specific IgE only, did not respond to either horse or dog allergens. The potency and magnitude of the maximal contraction to histamine was significantly (p < 0.05) increased in tissues sensitized using atopic serum with high total IgE concentrations compared with nonsensitized preparations, but was unchanged in tissues sensitized using chimeric IgE or serum with low total IgE levels. Therefore, specific IgE determines allergen responsiveness in passively sensitized human airways, but histamine hyperresponsiveness is independent of specific IgE and appears to be related to some other factor associated with serum containing high concentrations of total IgE.