Environmental Allergens (environmental + allergen)

Distribution by Scientific Domains
Distribution within Medical Sciences


Selected Abstracts


Susceptibility and reactivity in polysensitized individuals following controlled induction

CONTACT DERMATITIS, Issue 1 2010
Nannie Bangsgaard
Background: It is uncertain whether polysensitized patients acquire multiple allergies only because of a high degree of exposure to environmental allergens, or because of being highly susceptible to developing contact allergy. Objectives: The aim of this study was to investigate and compare susceptibility and reactivity in polysensitized and monosensitized individuals, and in healthy controls. Patients/methods: We sensitized 66 adult individuals (21 polysensitized, 22 monosensitized, and 23 healthy controls) with diphenylcyclopropenone and assessed challenge responses with visual scoring and ultrasound. We compared sensitization rates using a chi-square test and logistic regression analyses, and calculated linear regression lines of the elicitation responses for each individual. The mean values of the slopes and the intercepts for each group were used to measure the strength of the elicitation response, and were compared using the Mann,Whitney test. Results: Sensitization ratio was equal in the three groups: 57% for the polysensitized, 59% for the monosensitized, and 65% for the healthy control group. There was a lowered elicitation threshold in the polysensitized group compared with that in the monosensitized and healthy control groups and, although not statistically significant, a stronger elicitation response was observed in the polysensitized group. Conclusion: Increased reactivity was found in the polysensitized group, demonstrated by a lowered elicitation threshold, compared with that in the monosensitized and healthy control groups. [source]


Mechanisms of immune suppression by interleukin-10 and transforming growth factor-,: the role of T regulatory cells

IMMUNOLOGY, Issue 4 2006
Alison Taylor
Summary Specific immune suppression and induction of tolerance are essential processes in the regulation and circumvention of immune defence. The balance between allergen-specific type 1 regulatory (Tr1) cells and T helper (Th) 2 cells appears to be decisive in the development of allergy. Tr1 cells consistently represent the dominant subset specific for common environmental allergens in healthy individuals. In contrast, there is a high frequency of allergen-specific interleukin-4 (IL-4)-secreting T cells in allergic individuals. Allergen-specific immunotherapy can induce specific Tr1 cells that abolish allergen-induced proliferation of Th1 and Th2 cells, as well as their cytokine production. Tr1 cells utilize multiple suppressor mechanisms, such as IL-10 and transforming growth factor-, (TGF-,) as secreted cytokines and various surface molecules, such as cytotoxic T-lymphocyte antigen 4 and programmed death-1. IL-10 only inhibits T cells stimulated by low numbers of triggered T-cell receptors, which depend on CD28 costimulation. IL-10 inhibits CD28 tyrosine phosphorylation, preventing the binding of phosphatidylinositol 3-kinase p85 and consequently inhibiting the CD28 signalling pathway. In addition, IL-10 and TGF-, secreted by Tr1 cells skew the antibody production from immunoglobulin E (IgE) towards the non-inflammatory isotypes IgG4 and IgA, respectively. Induction of antigen-specific Tr1 cells can thus re-direct an inappropriate immune response against allergens or auto-antigens using a broad range of suppressor mechanisms. [source]


Atopic xerosis: employment of noninvasive biophysical instrumentation for the functional analyses of the mildly abnormal stratum corneum and for the efficacy assessment of skin care products

JOURNAL OF COSMETIC DERMATOLOGY, Issue 2 2006
Hachiro Tagami MD
Summary The subtle dryness of the skin surrounding the lesions of atopic dermatitis (AD) is called atopic dry skin or atopic xerosis (AX). AX is more susceptible to the development of AD skin lesions under various environmental stimuli than the clinically normal skin of the people who have or have had or will have AD, which might be called normal atopic skin (NAS) that shows no functional differences as compared to the skin of normal individuals. Routine histopathologic studies of AX that involve the invasive procedures of biopsy are not so helpful in clarifying the underlying pathogenesis. Modern, noninvasive biophysical instrumentation provides rich and quantitative information about various functional aspects of skin. The stratum corneum (SC) of AX reveals not only decreased hydration but also mildly impaired barrier function demonstrable as an increase in transepidermal water loss, elevated pH values, and an increased turnover rate of the SC consisting of thick layers of smaller-sized corneocytes. These data suggest that AX is related to mildly increased epidermal proliferation as a result of the presence of subclinical cutaneous inflammation. Although AX skin does not display any impairment in the recovery of barrier function after physical skin irritation by tape-stripping, it produces a much more severe, long-lasting inflammatory response together with a delay in barrier repair after chemical irritation such as that induced by sodium lauryl sulphate. The SC of AX is biochemically characterized by reduction in the amounts of ceramides, especially ceramide I, sebum lipids, and water-soluble amino acids. None of these changes in SC functions are seen in NAS, which includes not only the normal-looking skin of AD patients long after regression of all active lesions but also of latent atopic skin such as neonates who later develop AD. This suggests that all of the observed functional as well as biochemical abnormalities of AX are a reflection of subclinical inflammation. The presence of the underlying inflammation in AX also differentiates it from senile xerosis. The mildly impaired SC functions of AX can be improved by daily repeated applications of effective moisturizers, i.e., corneotherapy, which is effective in preventing the exacerbating progression of AX to AD resulting from inadvertent scratching of the skin that facilitates the penetration of environmental allergens into the skin. The biophysical confirmation of such efficacy of moisturizers, including cosmetic bases on the mildly impaired barrier function and decreased water-holding capacity of the SC of AX, definitely substantiates the importance of skin care for the cosmetic skin problems that affect every individual in the cold and dry season ranging from late autumn to early spring. [source]


Lactobacillus strains stabilize intestinal microbiota in Japanese cedar pollinosis patients

MICROBIOLOGY AND IMMUNOLOGY, Issue 4 2009
Akira Kubota
ABSTRACT A randomized double-blind, placebo-controlled trial was conducted to ascertain the intestinal microbiota-altering properties of LGG and L. gasseri TMC0356 (TMC0356) in Japanese cedar Cryptomeria japonica pollinosis patients. Fecal bacteria communities were examined before and after fermented milk administration using culture, FISH and T-RFLP methods. Test group subjects showed the presence of LGG and TMC0356 along with a significant increase in fecal lactobacilli (P < 0.001) after giving LGG and TMC0356 fermented milk. Culture and FISH analysis revealed no significant changes in other intestinal bacterial groups. Each subject exhibited a characteristic T-RFLP profile pattern that varied quantitatively and qualitatively with JCP shedding. Profile changes were observed in 53% of placebo group subjects and in 21% of test group subject's post-administration, indicating that LGG and TMC0356 suppressed intestinal microbiota changes in JCPsis patients. The results suggest that intestinal microbiota might be more sensitive to exposure to environmental allergens than expected from the results of general culture method studies. Stabilization of intestinal microbiota by selected probiotic strains such as LGG and TMC0356 could be beneficial to homeostasis of the intestinal microbiota and useful in the management of JCPsis. [source]


Low prevalence of the intrinsic form of atopic dermatitis among adult patients

ALLERGY, Issue 5 2006
R. Fölster-Holst
Background:, Atopic dermatitis (AD) is a chronic inflammatory skin disease commonly associated with respiratory allergies such as rhinitis and asthma, and a high serum level of IgE. In contrast to the ,classic' IgE-mediated allergic (extrinsic) form of AD, approximately 20% of the patients are reported to show normal IgE levels, lack of sensitizations towards environmental allergens, and absence of associated respiratory allergies. Accordingly, these patients are assigned to a nonallergic (intrinsic) form of the disease. Objectives:, In order to define these two forms of AD more closely, 259 adult patients with AD were investigated. Results:, After a thorough diagnostic workup there were 18 patients (6.9%), who fulfilled the criteria of intrinsic AD. After follow-up, four additional patients had developed respiratory allergies or IgE-mediated sensitizations resulting in an overall proportion for intrinsic AD of 5.4%. Conclusions:, Based on these figures the nature and relevance of the intrinsic form of AD deserves further evaluation. [source]


The course of eczema in children aged 5,7 years and its relation to atopy: differences between boys and girls

BRITISH JOURNAL OF DERMATOLOGY, Issue 3 2006
M. Möhrenschlager
Summary Background, The role of atopy in the pathophysiology of eczema is still under debate. The concept and analyses of the nonatopic and atopic subtypes of eczema have gained increasing interest in recent studies. The course of these subtypes and differences between boys and girls have not been investigated so far. Objectives, To examine the course of nonatopic and atopic eczema in preschool children from Germany with regard to sex. Methods, Repeated cross-sectional studies were performed in 5,7-year-old preschool children from Germany between 1994 and 2000. Individuals with eczema were identified by a dermatological examination. In addition to a questionnaire, skin prick tests and analyses of serum IgE antibodies against seven and five environmental allergens, respectively, were performed. Atopy was defined by sensitization to at least one of five common aeroallergens (birch, grass and mugwort pollen, house dust mites, cat dander). In part of the study population investigations of spare time behaviour and skin function were carried out (including stratum corneum hydration and skin surface pH). Results, A total of 2693 girls and 2783 boys underwent a full dermatological examination of the skin and determination of sensitization. Among the girls, 8·7% demonstrated eczema clinically at the day of investigation in contrast to 6·1% of the boys. In girls, early onset eczema (< 2 years of age) was strongly related to atopy at age 5,7 years [odds ratio (OR) 3·7; 95% confidence interval (CI) 2·7,5·1], whereas late-onset eczema (, 2 years of age) was not (OR 1·0; 95% CI 0·7,1·5). Boys were more often atopic at the age of 5,7 years than girls (28·3% vs. 20·6%), and early and late-onset eczema were related to atopy without such a difference (OR 2·8, 95% CI 2·0,4·0; OR 1·9, 95% CI 1·3,2·8, respectively). The excess of current eczema in 5,7-year-old girls compared with boys was related to the nonatopic type. The higher susceptibility of girls in that age group to develop eczema was reflected by the skin physiological examination: even girls without eczema had significantly higher skin surface pH and lower stratum corneum hydration than boys. Additionally, questionnaire data revealed that girls more often than boys predominantly played indoors, which was associated with more eczema. Conclusions, Atopy and eczema develop differently in boys and girls. Boys are more often atopic, whereas girls suffer significantly more often from eczema without relation to atopy. The nonatopic type of eczema in preschool girls is noticed predominantly after their second birthday. Genetic and lifestyle factors may contribute to this difference. [source]


Phenotyping of epidermal dendritic cells allows the differentiation between extrinsic and intrinsic forms of atopic dermatitis

BRITISH JOURNAL OF DERMATOLOGY, Issue 6 2000
T. Oppel
Atopic dermatitis (AD) is a clinically characteristic, chronic inflammatory skin disease of unknown origin. IgE-mediated uptake and antigen focusing of environmental allergens by dendritic cells (DCs) is assumed to be a central immunopathogenetic event. A so-called intrinsic type of AD (IAD) has been delineated from the more common extrinsic AD (EAD) by normal serum IgE levels, negative RAST tests and negative immediate-type skin reactions towards environmental allergens. The recently characterized human autoantigen Hom S 1 has been proposed to play a part in the pathogenesis of IAD. Objectives,To compare clinical and laboratory data between patients with IAD and EAD, and to investigate potential differences in the inflammatory micromilieu of the epidermal compartment in IAD and EAD lesions. Methods,Epidermal DC phenotyping, a recently validated technique based on the three-colour flow cytometric analysis of Langerhans cells and the so-called inflammatory dendritic epidermal cells from epidermal single-cell suspensions, was performed on samples from 69 patients with AD (seven with IAD and 62 with EAD) and 94 controls. Results,Patients with EAD tended to have an earlier onset of disease but similar disease duration and family history of atopic diseases. Quantitative analysis of CD36 expression on DCs as a marker of inflammation, as well as the percentage of inflammatory dendritic epidermal cells in the CD1a+ epidermal DC pool, indicated a comparable disease activity in IAD and EAD. EAD was characterized by a significantly higher Fc,RI expression on the CD1a+ epidermal DCs than IAD. Using the Fc,RI/Fc,RII expression ratio as a disease marker for AD, values for IAD fell below the diagnostic cut-off level of 1·5 for this ratio. Conclusions,While IAD is clinically similar to EAD, the inflammatory microenvironment in this condition seems different from classical EAD and can be distinguished by phenotyping of epidermal DCs. [source]


Regulatory T cells and asthma

CLINICAL & EXPERIMENTAL ALLERGY, Issue 9 2009
D. S. Robinson
Airway inflammation in asthma is characterized by activation of T helper type-2 (Th2) T cells, IgE production and eosinophilia. In many cases, this process is related to an inappropriate T cell response to environmental allergens, and other T cell-dependent pathways may also be involved (such as Th17). Regulatory T cells (Tregs) are T cells that suppress potentially harmful immune responses. Two major subsets of Treg are CD25hi, Foxp3+Tregs and IL-10-producing Tregs. There is evidence that the numbers or function of both subsets may be deficient in patients with atopic allergic disease. Recent work has extended these findings into the airway in asthma where Foxp3 expression was reduced and CD25hi Treg-suppressive function was deficient. In animal models of allergic airways disease, Tregs can suppress established airway inflammation and airway hyperresponsiveness, and protocols to enhance the development, recruitment and function of Tregs have been described. Together with studies of patients and in vitro studies of human T cells, these investigations are defining potential interventions to enhance Treg function in the airway in asthma. Existing therapies including corticosteroids and allergen immunotherapy act on Tregs, in part to increase IL-10 production, while vitamin D3 and long-acting ,-agonists enhance IL-10 Treg function. Other possibilities may be enhancement of Treg function via histamine or prostanoid receptors, or by blocking pro-inflammatory pathways that prevent suppression by Tregs (activation of Toll-like receptors, or production of cytokines such as IL-6 and TNF-,). As Tregs can also suppress the potentially beneficial immune response important for controlling infections and cancer, a therapeutic intervention should target allergen- or site-specific regulation. [source]


A rapid test for detection of mite allergens in homes

CLINICAL & EXPERIMENTAL ALLERGY, Issue 11 2002
A. Tsay
Summary Background International guidelines recommend allergen avoidance for asthma management, but do not include making assessments of allergen exposure. Mite allergen exposure cannot be assumed, especially in geographical regions where climatic conditions vary. Objective To develop a rapid test that would enable consumers to detect mite allergen in the home. Methods A lateral flow test using gold labelled antibody for mite group 2 allergen was developed as part of a detection kit incorporating the MITEST dust sampling device. Dust samples were assayed by ELISA for group 1 and group 2 allergens and by using the rapid test. The tests were compared as indices of mite allergen exposure. Results There was a good correlation between group 1 and group 2 levels by ELISA (n = 349, r = 0.60, P < 0.001). In a multi-centre study of 65 homes (263 dust samples) in five countries, there was a strong correlation between ELISA and the rapid test. Most samples with high scores in the test (43/48, 90%) contained > 1 µg/m2 group 2 allergen, whereas most low samples contained < 1 µg/m2 (50/64, 78%). Differences between mean group 2 levels of samples that scored low (0.28 µg/m2), medium (1.68 µg/m2) or high (3.18 µg/m2) on the test were highly significant (P 0.007 to < 0.001). Conclusions A simple rapid test has been developed that detects mite allergen in the home within 10 min. The mite screening test should educate consumers about allergen exposure and encourage compliance with allergen-avoidance procedures. This technology has applications for the detection of other common environmental allergens. [source]


Airborne endotoxin exposure and the development of airway antigen-specific allergic responses

CLINICAL & EXPERIMENTAL ALLERGY, Issue 3 2000

Background and objective Repeated exposure of aerosolized antigen via respiratory tract can induce immunoglobulin (Ig) E isotype-specific tolerance to this antigen. However, the atopic individuals often produce a higher titre of IgE in response to airborne environmental allergens. The mechanisms of this differential regulation of airway allergen-specific immune responses are not fully understood. This study investigated the role of airborne endotoxin on the initiation of antigen-specific airway allergic responses. Methods ELISA methods for detection of isotypes of antigen-specific antibodies and competitive reverse transcription polymerase chain reaction for detection mRNA of cytokines were used. In addition, Liu stain method was used to analyse the amounts of eosinophils in bronchoalveolar lavage fluid. Results Mice pre-exposed with airborne endotoxin mounted significantly higher amounts of OVA-specific IgE antibody responses to inhaled OVA than those OVA-only sensitized mice. Inhaled endotoxin could downregulate repeated airway antigen exposure-induced IgE isotype-specific tolerance and increase antigen-induced lung eosinophils infiltration. Conclusions These data show that airborne endotoxin exposure could potentiate allergen-specific airway inflammation. The results should have potential implications for understanding the development of allergen-induced airway allergic responses. [source]