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PubMed2005

[T regulatory lymphocytes, atopy and asthma: a new concept in three dimensions].

BACKGROUND: Allergic inflammation is considered to be the result of a pattern of Th2 lymphocyte activation. However this inflammation, relevant for atopy and infiltration of affected tissues by eosinophils, is insufficient by itself to explain the clinical features of asthma. Several studies have demonstrated that Th2 type inflammation was also associated in asthma with a Th1 response, with production of gamma interferon. It has recently been shown that the regulatory T lymphocytes (Treg) which produce IL-10 and/or TGF-beta and induce tolerance are defective in allergic patients. In addition, these lymphocytes increase during specific immunotherapy. Their decrease could explain the Th2 activation found in atopic patients. PERSPECTIVE: We review the potential importance of Treg cells in atopy and also asthma, and propose a concept whereby the allergic inflammatory response would not be due to a Th1/Th2 imbalance, but rather to a Treg deficiency progressively rising from normal to atopic, from atopy to asthma and from asthma to acute exacerbations. CONCLUSION: Three dimensions of inflammation need therefore to be taken into account: Th1, Th2 and Treg.

Animals↗
PubMed2003

What proportion of rhinitis symptoms is attributable to atopy?

The aim of this study was to assess what proportion of patients with rhinitis symptoms (unrelated to infection) in population-based studies is attributable to atopy. We assessed the relevance of atopy in rhinitis in different countries and populations and between different age groups by performing a Medline search from 1980 onward on population-based studies. In the 22 identified population-based studies found, the overall proportion of rhinitis cases that were atopic was 61%, the proportion of noncases that were atopic was 20%, and the proportion of rhinitis cases that were attributable to atopy was 53%. There is variation between studies but little evidence of systematic geographic variation. For future research on the prevalence and possible increase of atopic rhinitis, it seems to be of major importance to differentiate between atopic and other forms of rhinitis.

Adolescent↗
PubMed2000

Atopy is a risk factor for non-steroidal anti-inflammatory drug sensitivity.

BACKGROUND: There is scarce information in the literature about a possible association between atopy and certain clinical manifestations of NSAID sensitivity. OBJECTIVES: (1) To evaluate the prevalence of atopy in patients proved to be sensitive to cyclooxygenase inhibitors. (2) To assess cross-reactivity to two alternative NSAIDs, paracetamol (acetaminophen) and nimesulide. METHODS: NSAID-sensitive patients attending an allergy clinic and unselected controls were prick tested with inhalant allergens. Oral challenges with NSAIDs were carried out by the single-blinded (SBOC) method. Clinical data about personal and family history of allergic and atopic diseases were obtained by a careful review of the medical records and by direct questioning by experienced allergists. RESULTS: Fifty patients had positive SBOCs to the suspected NSAID and only these were studied. A personal history of atopic diseases was present in 41 patients (82%) and 7 controls (14.5%), and a family history in 24 patients (48%) and 6 controls (12.5%). Prick skin tests with aeroallergens were positive in 39 of 45 patients tested (86.6%) and in 14 of 48 controls (29.1%), (P = .0001). Skin test positivity rates were higher in patients with cutaneous challenge reactions who responded to only one NSAID (single reactors) in comparison to cross-reactors (P = .04). The most frequent clinical manifestations of NSAID sensitivity were (1) cutaneous (angioedema, urticaria) in 34 patients, (2) blended (cutaneous plus respiratory) in 12, (3) respiratory in 3, and (4) anaphylactoid in 1. Aspirin, pyrazolone, paracetamol, and ibuprofen were the drugs more frequently implicated in these reactions. Cross-sensitivity with paracetamol and nimesulide were 32% and 25%, respectively. CONCLUSIONS: The prevalence of atopy is increased in challenge-proven NSAID-intolerant patients. The atopic condition may represent an important risk factor for developing reactions to these drugs. Paracetamol and nimesulide are relatively safe alternative choices in those patients, although their use still carries some risk of unwanted reactions.

Adult↗
PubMed2000

The association between atopy and asthma in a semirural area of Tanzania (East Africa).

BACKGROUND: Atopy is consistently associated with asthma, except in a study in Africa. We assessed the association between atopy and asthma in women from a semirural area of Tanzania (East Africa). METHODS: All pregnant women delivering at the district hospital during a 1-year period were recruited (n = 658, 60.6% of those selected). Asthma was investigated by a standard questionnaire and atopy by specific IgE (immunoglobulin E) antibodies to Dermatophagoides pteronyssinus (Der p 1) and cockroach. RESULTS: The prevalence of wheezing chest was 10.7%; of asthma, 3.5%. Levels of specific IgE of >0.35 kU/l (73%) and high levels of total IgE (62% higher than 1000 kU/l) were highly prevalent. Specific IgE antibody levels in sera were not associated with asthma (3.8% of women with negative specific IgE to any antigen had asthma in comparison to 4.0% of women with positive specific IgE; odds ratio [OR] = 1.06, 0.35-3.22). Total IgE was not different between women with asthma and women without asthma (P=0.36). CONCLUSIONS: In tropical regions, the association between allergy and asthma is complex, and specific IgE reactivity to environmental allergens may not be related to asthma.

Adolescent↗
PubMed2001

No linkage and association of atopy to chromosome 16 including the interleukin-4 receptor gene.

BACKGROUND: Several susceptibility genes for atopy have been suggested in recent years. Few have been investigated as intensively as the interleukin-4-receptor alpha (IL4Ralpha) gene on chromosome 16. The results remain in dispute. Therefore, in a robust design, we tested for association of type I allergy to the IL4R variations I50V and Q576R, and investigated chromosome 16 for atopy candidate regions in general. METHODS: We identified 100 Danish allergy sib-pair families. Five conservative phenotypes for type I allergy were defined and evaluated. The IL4R variations were genotyped in trios and evaluated by the transmission disequilibrium test (TDT). Multipoint linkage analysis and exclusion mapping were conducted with sib-pairs analyzed for 17 microsatellite markers. RESULTS: No evidence for association or linkage to the IL4R polymorphisms was found (P values: 0.12-0.90). Linkage analysis did not support linkage of any of the phenotypes to chromosome 16. Major parts of chromosome 16 were excluded as candidate regions harboring oligogenes for type I allergy. CONCLUSION: We found chromosome 16 unlikely to harbor strong candidate genes for type I allergy. The role of the IL4Ralpha gene in the inheritance of atopy was insignificant in the Danish population. The use of conservative allergy phenotypes in the search for genes predisposing to atopic disease was discussed.

Child↗
PubMed2002

Asthma and atopy - a total genome scan for susceptibility genes.

BACKGROUND: Allergic asthma is an increasingly common disease of complex inheritance. Several studies have suggested candidate regions, but genetic heterogeneity, ethnic differences and varying study designs may in part explain the lack of identified and confirmed susceptibility genes. Investigation of different populations will further clarify the topic. We therefore evaluated allergic asthma and increased total and specific IgE in 39, 45 and 57 sib-pairs from 100 Danish allergy families. METHODS: Affected sib-pairs meeting a narrow phenotype definition were selected for the three phenotypes atopy, allergic asthma and increased total IgE. We performed a total genome scan using 446 microsatellite markers and obtained nonparametric linkage results from the MAPMAKER/SIBS computer program. RESULTS: Our study revealed four candidate regions (MLS > 2) on chromosome 1p36, 3q21-q22, 5q31 and 6p24-p22, and 15 candidate regions (1 < MLS < 2) that may contain susceptibility genes for asthma and atopy. We did not find linkage to the candidate genes TNF-beta, FcER1beta and Il4R-alpha, except for weak support for linkage of the asthma phenotype to TNF-beta (MLS = 1.18). CONCLUSIONS: We found evidence for two new asthma and atopy loci, 1p36 and 3q21-q22, and supported linkage in the Danish population to seven previously reported candidate regions.

Asthma↗
PubMed2003

Rhinoconjunctivitis, bronchial responsiveness, and atopy as determinants for incident non-work-related asthma symptoms in apprentices exposed to high-molecular-weight allergens.

OBJECTIVE: The aim of this study was to explore the role of rhinoconjunctivitis (RC), taking into account atopy and the level of bronchial responsiveness to methacholine, on the incidence of respiratory symptoms and in the development and/or worsening of asthma. METHODS: We examined data from a prospective study in 769 students starting exposure to high-molecular-weight occupational allergens and who were serially followed for up to 44 months. RESULTS: The presence of RC symptoms at baseline was significantly associated with an increased risk of developing shortness of breath and wheezing in atopic subjects regardless of PC20 level and in subjects with a PC20 <or= 32 mg/ml regardless of atopic status. RC symptoms were significantly associated with the development of exercise-induced respiratory symptoms. Multivariate analyses indicated that having a measurable PC20 was significantly associated with the incidence of all respiratory symptoms studied, whereas baseline seasonal RC was associated only with incident exercise-induced respiratory symptoms; atopy played a minimal role, and only through an interaction with seasonal RC. CONCLUSION: Of the three potential factors for the development of respiratory symptoms that we considered, i.e. RC symptoms, having a measurable PC20 and atopy, having a measurable PC20 is the most significant one.

Adolescent↗
PubMed2001

Urinary eosinophil protein X in children with asthma: influence of atopy and airway infections.

It has been suggested that urinary eosinophil protein X (U-EPX) can be used to monitor bronchial inflammation in childhood asthma. However, the influence of atopy and airway infections is not well elucidated. To determine the clinical value of measuring U-EPX in children with asthma and to evaluate the influence of atopy and airway infections, U-EPX was measured in 170 children with asthma (mean age 69 months, range 12-179 months), in 79 children with lower or upper respiratory tract infections (mean age 41 months, range 1-165 months), and in 64 controls. U-EPX was elevated in children with acute asthma (median 132 microg/mmol of creatinine, quartiles 77-195 microg/mmol of creatinine, n = 51, p <0.001) and chronic asthma (median 93 microg/mmol of creatinine; quartiles 46-149 microg/mmol of creatinine, n = 119, p <0.01) compared with controls (median 54 microg/mmol of creatinine, quartiles 40-89 microg/mmol of creatinine, n = 39). Atopic children had higher levels of U-EPX than non-atopics with acute asthma (median 155 microg/mmol of creatinine, quartiles 113-253 microg/mmol of creatinine, n = 27, vs. median 102 microg/mmol of creatinine, quartiles 56-168 microg/mmol of creatinine, n = 24, p <0.05), as well as with chronic asthma (median 110 microg/mmol of creatinine, quartiles 65-162 microg/mmol of creatinine, n = 63, vs. median 60 microg/mmol of creatinine, quartiles 39-123 microg/mmol of creatinine, n = 56, p <0.01). In chronic asthma, children without atopy had levels of U-EPX similar to values of controls; levels were similar in symptomatic and asymptomatic patients, and not influenced by treatment with inhaled corticosteroids. Moreover, U-EPX levels were higher in children with pneumonia (median 207 microg/mmol of creatinine, quartiles 111-280 microg/mmol of creatinine, n = 35, p <0.001), laryngitis (median 109 microg/mmol of creatinine, quartiles 65-161 microg/mmol of creatinine, n = 24, p <0.01), and rhinitis (median 172 microg/mmol of creatinine, quartiles 123-254 microg/mmol of creatinine, n = 19, p <0.001) than in controls (median 62 microg/mmol of creatinine, quartiles 41-93 microg/mmol of creatinine, n = 64). There was significant overlap among all groups of children with disease, as well as between children with disease and controls. Hence, U-EPX may reflect differences in eosinophil involvement and activation between children with atopic and non-atopic asthma, but the individual spread within groups and the influence of airway infections limits the clinical value of U-EPX in childhood asthma.

Adolescent↗
PubMed2003

Bronchial hyper-responsiveness and atopy in urban, peri-urban and rural South African children.

Twenty years ago, the prevalence of atopic sensitization and bronchial hyper-responsiveness (BHR) in Xhosa children in a rural location in South Africa was very low. The aim of this study was to document the current prevalence of these two indices by comparing traditional rural Xhosa children, recently urbanized Xhosa children and established city white children, and to consider factors that may account for the observed increase in all of these groups. One thousand four hundred and fifty-seven school children aged 10-14 years from the rural Transkei, from a recently urbanized peri-urban area and from urban Cape Town areas were studied using a questionnaire. Four hundred and eighteen children had histamine challenges, and 492 tests for atopy were also conducted. As determined by bronchial challenge with histamine, 17% of rural and 34.4% of recently urbanized Xhosa children had increased BHR, a marked increase from the 0.03% and 3.17% prevalence of increased BHR previously found using the exercise challenge. The prevalence of increased BHR in white urban children was 33%. Sensitization to one or more aero-allergens, as indicated by CAP RAST tests, was present in 36.6% of the rural Xhosa children with normal BHR and in 62.5% of those with increased BHR, a striking increase from that of previous studies. Atopic sensitization to one or more aero-allergens, as indicated by a skin prick test (SPT), was found in 42.3% of the recently urbanized Xhosa children and 45% of urbanized white children. We have also documented sensitization to house dust mites in the rural Xhosa children for the first time. Passive cigarette smoking was not identified as a risk factor for increased BHR or atopy. Wood smoke in the indoor environment did not play a role in the rural Xhosa children's BHR. Ascaris infection does not appear to play any modifying role in the development of increased BHR in the rural or urban children. We have found that increases in BHR in the rural and recently urbanized Xhosa children develop independently of increases in atopy. Our results challenge the 'hygiene' hypothesis as a complete explanation for the recent dramatic worldwide increases in allergic diseases.

Adolescent↗
PubMed1980

HLA, atopy, and cyclophosphamide in steroid-responsive childhood nephrotic syndrome.

In a study designed to confirm our preliminary report of associations between HLA-B12, atopy, and relapse following cyclophosphamide treatment in steroid-responsive nephrotic syndrome (SRNS), we again found a higher incidence of HLA-B12 in SRNS children (44%) than we did in controls (24%). The association of HLA-B12 with short time-to-relapse after cyclophosphamide treatment of SRNS was also confirmed, but that with atopy in SRNS children was not, though we observed a similarly high incidence of atopy in them as before.

Asthma↗
PubMed1994

Association between atopy and variants of the beta subunit of the high-affinity immunoglobulin E receptor.

The beta-subunit of the high-affinity IgE receptor (Fc epsilon RI-beta) on chromosome 11 is maternally linked to atopy, the state of enhanced IgE responsiveness underlying allergic asthma and rhinitis. We have identified a common variant of Fc epsilon RI-beta, lle181Leu within the 4th transmembrane domain. Leu181 shows significant association with positive IgE responses in a random patient sample. Amongst 60 unrelated nuclear families with allergic asthmatic probands, Leu181 is identified in 10 (17%), is maternally inherited in each, and shows a strong association with atopy. Our data indicate that Fc epsilon RI-beta, subject to maternal modification, may be the atopy-causing locus on chromosome 11q.

Amino Acid Sequence↗
PubMed2002

Positive association to IgE levels and a physical map of the 13q14 atopy locus.

Linkage of atopy and associated traits to a locus on chromosome 13q14 has been identified by several studies in diverse populations. We have previously shown the putative atopy gene to be contained within an interval of approximately 5 Mb flanked by D13S328 and D13S1269 and centred on D13S273. We have now extended this work using a top-down approach to physical mapping. A YAC contig was constructed covering the D13S328 and D13S1269 interval. Thirty-one ESTs were mapped to the contig. We constructed a BAC and PAC contig flanking D13S273 by approximately 750 kb in either direction. The interval contained 27 of the 31 ESTS from the YAC contig. Seven previously unknown microsatellites were recovered and then typed in two subject panels. A positive association between the total serum Immunoglobulin E concentration and the novel USAT24G1 microsatellite was discovered (P(corrected)<0.005) and replicated in a second panel of families. The discovery of a region of positive association within the BAC/PAC contig will permit identification of the atopy gene from this locus.

Adolescent↗
PubMed2006

Variation in the type I interferon gene cluster on 9p21 influences susceptibility to asthma and atopy.

A genome-wide screen for asthma and atopy susceptibility alleles conducted in the Hutterites, a founder population of European descent, reported evidence of linkage with a short tandem repeat polymorphism (STRP) within the type I interferon (IFN) gene cluster on chromosome 9p21. The goal of this study was to identify variation within the IFN gene cluster that influences susceptibility to asthma and atopic phenotypes. We screened approximately 25 kb of sequence, including the flanking sequence of all 15 functional genes and the single coding exon in 12, in Hutterites representing different IFNA-STRP genotypes. We identified 78 polymorphisms, and genotyped 40 of these (in 14 genes) in a large Hutterite pedigree. Modest associations (0.003<P<0.05) with asthma, bronchial hyper-responsiveness (BHR), and atopy were observed with individual variants or genes, spanning the entire 400 kb region. However, pairwise combinations of haplotypes between genes showed highly significant associations with different phenotypes (P<10(-5)) that were localized to specific pairs of genes or regions of this cluster. These results suggest that variation in multiple genes in the type I IFN cluster on 9p22 contribute to asthma and atopy susceptibility, and that not all genes contribute equally to all phenotypes.

Adolescent↗
PubMed2003

Atopy and depression: results from the Northern Finland 1966 Birth Cohort Study.

Several studies have suggested an association between IgE-mediated atopic allergies and depression. The present study extends our understanding about putative gender differences of this association and provides further epidemiological evidence for our previous finding that the association between atopy and depression may be characteristic for females only. In order to clearly determine the presence of atopic disorders and depression, we used more valid tools than had been employed earlier and we had access to a database (the Northern Finland 1966 Birth Cohort), in which individuals were followed up prospectively until the age of 31 years. The information on allergic symptoms, verified by skin-prick tests and comprising data of 5518 individuals, was used to ascertain the presence of atopy. Depression was assessed with the help of Hopkins' Symptom Checklist-25 and self-reported doctor-diagnosed depression. After adjusting for a father's social class, mother's parity, and place of residence, logistic regression analyses showed that the risk of developing depression increased in parallel with the increasing severity of depression and, when compared with nonatopic subjects, was 3.0 to 4.7-fold up in atopic females and statistically significant. In atopic males, the association between atopy and depression was statistically significant only in the highest depression scores, the odds ratio being 6.3-fold. The results indicate that females suffering from atopic diseases might possess an elevated risk of developing depression already during early adulthood. In males, the association between these two disorders is evident only among the most severe manifestations of depression. Possible background theories, that is, genetic abnormalities in serotonin metabolism, HPA-axis dysfunction, and histamine theory are discussed.

Adult↗
PubMed1998

Phenotype stability in asthma and atopy in childhood.

The asthma phenotype can be described using a combination of the following: symptom type, pattern and severity; markers of atopy; and measurement of bronchial responsiveness. Because of the very nature of the disease, symptoms of asthma are variable in both the short-and the long-term, and the natural history of the disease is such that symptoms in an individual may evolve over time through different patterns. Although atopy appears to be a life-long attribute resulting from an early life switching to a TH2 immune response, the surrogate markers of atopy each are subject to their own time-related determinants and patterns of change with age. Bronchial responsiveness in childhood is neither specific nor sensitive for asthma, and although showing good short-term repeatability, can vary widely when measured over a period of months or years. Stimuli for responsiveness testing should be chosen which can be inhaled safely in high doses so as to allow an end point to be reached by as many subjects within a population as possible, and individuals may have to be tested repeatedly over time so as to avoid misclassification.

Asthma↗
PubMed2000

Cord blood levels of immunoglobulin G subclass antibodies to food and inhalant allergens in relation to maternal atopy and the development of atopic disease during the first 8 years of life.

BACKGROUND: Factors that either protect from or enhance the development of atopic disease appear to be acting early in life. The gestational environment, including maternal immune responses, such as transplacentally transferred immunoglobulin (Ig) G antibodies to allergens, may be of importance in this respect, since allergen-specific immunity has been demonstrated to develop in utero. OBJECTIVE: To evaluate the relation between cord blood IgG subclass antibodies to allergens, maternal atopy and development of atopic disease in the children. MATERIAL AND METHODS: The study group comprised a cohort of 96 children participating in a prospective study up to 8 years of age. Cord blood IgG subclass antibodies to ovalbumin, beta-lactoglobulin, Bet v 1 and cat dander were analysed by ELISA. RESULTS: The levels of all IgG subclass antibodies to ovalbumin and rBet v 1 were higher in newborn infants with an atopic mother, as compared with babies with nonatopic mothers. IgG1 antibody levels to cat and IgG4 antibody levels to beta-lactoglobulin and cat were also higher in atopic than in nonatopic mothers, whereas the other subclass antibody levels to those allergens were similar. High levels of cord blood IgG antibodies to cat and birch, but not to the food allergens, were associated with less atopic symptoms in the children during the first 8 years of life. Moreover, children who developed IgE antibodies to cat had lower levels of IgG antibodies to that allergen at birth. CONCLUSIONS: High levels of cord blood IgG subclass, especially IgG4, antibodies to food and inhalant allergens are associated with maternal atopy. High levels of IgG antibodies to inhalant, but not food, allergens are associated with less development of atopy in the children.

Administration, Inhalation↗
PubMed2000

Studies on linkage and association of atopy with the chromosomal region 12q13-24.

BACKGROUND: Several studies have shown linkage of bronchial asthma, allergic rhinitis and total serum IgE concentration to the chromosomal region 12q13-24 in ethnical diverse populations. This region harbours a number of candidate genes for asthma and atopy, including stem cell factor (SCF), leukotriene A4 hydrolase (LTA4H), thyroid receptor 2 (TR2), and signal transducer and activator of transcription 6 (STAT6). However, the same region was shown as well to be linked to other diseases with inflammatory character. So far no variants in any of these genes have been published which would allow association studies and confirm the pathogenicity of any of these genes. OBJECTIVE: We wanted to test for linkage of the chromosomal region 12q13-24 with the atopic phenotype without regard to clinical manifestations. Furthermore we screened for common nucleotide polymorphisms in candidate genes to enable association studies. METHODS: We employed sib-pair linkage analysis and transmission disequilibrium testing with regard to four highly polymorphic microsatellite markers in 12q13-24 in atopic nuclear families. In addition, we looked for polymorphisms in the genes coding for SCF, LTA4H, TR2 and STAT6 performing SSCP-analysis and direct genomic sequencing. RESULTS: We found no evidence for linkage of the genomic region 12q13-24 to elevated total serum IgE levels, specific sensitization to common inhalant allergens or atopy. Furthermore we identified three nucleotide polymorphisms including one common variant in the gene coding for SCF. No association of this polymorphism and any of the atopic phenotypes was seen. CONCLUSION: We conclude from our data that genes in the chromosomal region 12q13-24 and in particular SCF are unlikely to exert a major effect on the induction of the atopic phenotype in our Caucasian population. However, we did not focus on the asthmatic and thereby inflammatory aspect of atopy which might explain these results in contradiction to previous studies.

Chromosomes, Human, Pair 12↗
PubMed2002

Association of body mass index with respiratory symptoms and atopy: results from the European Community Respiratory Health Survey.

BACKGROUND: There are several reports showing that obese adults report more respiratory symptoms suggestive of asthma than those who are not obese. OBJECTIVE: To determine the association of body mass index with respiratory symptoms and atopy in young adults METHOD: Information collected from 15,454 participants in the European Community Respiratory Health Survey, a multicentre cross-sectional survey of young adults, was analysed to determine the association of body mass index with respiratory symptoms and atopy. RESULTS: Men and women with a body mass index of greater than 30 were at an increased risk of wheeze with shortness of breath compared with those with a body mass of 20-24.99 (OR in men 1.85, 95% confidence interval 1.41-2.42; OR in women 2.03, 95% confidence interval 1.59-2.58). Similar associations were observed for other symptoms suggestive of asthma. Body mass index was not associated with 'hayfever or nasal allergies', specific IgE to house dust mite, grass or cat or with total IgE in men or women. CONCLUSION: Reported associations of body mass index with symptoms suggestive of asthma are unlikely to be explained by a higher risk of atopy in the obese. Alternative explanations must be sought.

Adult↗