Aspirin-induced asthma and HLA-DRB1 and HLA-DPB1 genotypes

DEKKER, J. W.; NIZANKOWSKA, E.; SCHMITZ-SCHUMANN, M.; PILE, K.; BOCHENEK, G.; DYCZEK, A.; COOKSON, W. O. C. M.; SZCZEKLIK, A.

doi:10.1046/j.1365-2222.1997.540848.x

Cited by 57 publications

(68 citation statements)

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“…11 A later study 12 could not prove this in its patient group, although they saw a significant decrease in the incidence of DPB1*0401 in both aspirin-tolerant and aspirinintolerant subjects with asthma. Another study group 13 has investigated the connection of aspirin-intolerant asthma and HLA-DPB1 and -DRB1 antigens. Their results, in agreement with the previously mentioned study, showed that the frequency of DPB1*0401 in aspirinintolerant asthma patients was decreased.…”

Section: Discussionmentioning

confidence: 99%

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2000

The Laryngoscope

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Objectives/Hypothesis: Genetic etiology is suspected in the development of nasal polyposis on the basis of familial aggregation. This study investigated whether there is an association between HLA-DRB1, -DQA1, and -DQB1 alleles and developing nasal polyposis. Study Design: Data from 50 polypectomized patients were compared with data from 50 healthy randomly selected controls. Polyp score, possible asthma, aspirin sensitivity, and ASA triad were also recorded. Methods: Genotyping of HLA-DRB1 alleles was carried out with the Dynal RELI SSO HLA-DRB, a direct DNA probe test that utilizes a polymerase chain reaction (PCR) and nucleic acid hybridization for the differentiation of 70 HLA-DRB alleles and 9 supertypes. For DQA1* genotyping PCR-RFLP (restriction fragment length polymorphism) was used, differentiating eight alleles. The DQB1* typing was carried out using a INNO-LiPA DQB PCR-reverse hybridization kit, allowing the discrimination of 30 alleles. Results: People carrying the HLA-DR7-DQA1*0201, and -DQB1*0202 haplotype were found to have a two to three times higher odds ratios (ORs) for developing the disease, compared with controls. Patients with ASA triad carried the above-mentioned DR7 allele with the linked alleles significantly more often (P < .001). Subjects carrying HLA-DR5 allele and the linked alleles had lower odds ratio values. Conclusion: These results underline that allergy is not conditional for the formation of nasal polyps as thought before. Nasal polyposis associated with asthma and aspirin sensitivity is probably a unique form of nasal polyps. The authors plan further investigations in this field.

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Section: Discussionmentioning

confidence: 99%

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2000

The Laryngoscope

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“…[21][22][23] . Nos pacientes deste estudo, não se observou diferenças estatisticamente significativas na tipificação de HLA-A, B e DR quando se comparou os grupos IA e TA.…”

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“…A seguir, Dekker et al 22 detectaram uma forte associação entre AIA e HLA-DPB1*0301, o qual difere do DPB1*1401 por apenas um aminoácido, o que sugere que estes alelos apresentam uma função semelhante. Molnar-Gabor et al 23 , utilizando PCR, demonstraram que pacientes com HLA-DR7-DQA1*0201 e DQB1*0202 apresentaram risco duas a três vezes maior de desenvolverem a PNS e observaram, também, uma relação estatisticamente significante entre IA e HLA-DR7, sugerindo que a IA e PNS representava uma forma particular de PNS.…”

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Perfil de citocinas e tipificação de HLA em pacientes com polipose nasossinusal tolerantes e intolerantes a aspirina

Becker

Guimarães

Nascimento

et al. 2003

Rev. Bras. Otorrinolaringol.

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A infiltração eosinofílica do pólipo nasossinusal (PNS) associado à intolerância aspirínica (IA) é característica relevante. Diversos mediadores participam da migração dos eosinófilos para os tecidos. A IA decorre do aumento da síntese de leucotrienos em indivíduos geneticamente susceptíveis. OBJETIVO: Analisar o perfil de citocinas e a tipificação de HLA-A, B e DR em pacientes com PNS tolerantes e intolerantes à aspirina. FORMA DE ESTUDO: Estudo de coorte transversal. MATERIAL E MÉTODO: selecionando-se 45 pacientes: 15 portadores de PNS eosinofílica tolerantes à aspirina (grupo TA); 15 de PNS eosinofílica associada à intolerância aspirínica, manifestada por broncoespasmo (grupo IA) e 15 sem PNS, que apresentavam desvio de septo nasal (grupo controle). O perfil de citocinas (IL-2; IL-4; IL-5; IL-6; IL-8; IL-10; IFN-gama e TNF-alfa) foi pesquisado nos fragmentos de pólipo nasal ou de mucosa de concha média (grupo controle) através da reação reversa da cadeia de polimerase (RT-PCR). A tipificação de HLA-A, B e DR foi realizada através de teste sorológico de microcitotoxicidade ou por amplificação de DNA pela reação em cadeia da polimerase (PCR). RESULTADOS: A expressão de RNAm para as interleucinas 4, 5, 6, 8, 10, IFN-gama e TNF-alfa foi semelhante nos três grupos. A expressão de RNAm para IL-2 associou-se com a IA. Os pacientes portadores dos antígenos A11, B49, DR15 e DR13 apresentaram uma maior probabilidade de desenvolver polipose nasossinusal não relacionada à IA, enquanto os portadores de DR17 apresentaram uma maior probabilidade de desenvolver polipose nasossinusal associada à intolerância aspirínica (Tríade Aspirínica). CONCLUSÃO: A polipose nasossinusal associada à intolerância aspirínica (Tríade Aspirínica) mostrou associação significante com HLA- DR17 e IL-2, sugerindo um perfil de citocinas TH1.

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“…8). In addition, specific HLA-DR and DQ molecules have been shown to be implicated in house dust mite asthma (9,10), aspirin-induced asthma (11), soybean epidemic asthma (12), and occupational asthma and atopy involving isocyanates (13) or acid anhydrides (14). However, the role and contribution of specific HLA class II molecules in the development of allergic asthma are unknown and are difficult to assess in humans because of their genetic heterogeneity.…”

Section: Introductionmentioning

confidence: 99%

Short ragweed allergen induces eosinophilic lung disease in HLA-DQ transgenic mice

Chapoval¹,

Nabozny²,

Marietta³

et al. 1999

J. Clin. Invest.

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The familial incidences of allergy and asthma suggest a genetic basis for these diseases. Recently, genome-wide searches and candidate gene approaches have been used to examine the possible involvement of a number of genes in the development of atopy and asthma. The regions of potential linkage to markers were detected with one or more asthma phenotypes on chromosomes 5q, 6p, 11q, 12q, 13q, and 14q, respectively (1-3).Human leukocyte antigen (HLA) molecules are encoded by highly polymorphic gene families located on chromosome 6p. They play a pivotal role in regulating the T-cell immune response and have been implicated in susceptibility to a wide range of diseases with an immunologic basis. The association of HLA haplotypes and ragweed allergy was the first human Ir (immune response) gene to be recognized (4), and HLA-DR2 and HLA-DQ6 restriction of IgE reactions to antigen 5 is well documented (5-7). Recently, strong relationships between the immune response to several highly purified allergens and specific HLA-DR and DQ haplotypes have been published (reviewed in ref. 8). In addition, specific HLA-DR and DQ molecules have been shown to be implicated in house dust mite asthma (9, 10), aspirin-induced asthma (11), soybean epidemic asthma (12), and occupational asthma and atopy involving isocyanates (13) or acid anhydrides (14). However, the role and contribution of specific HLA class II molecules in the development of allergic asthma are unknown and are difficult to assess in humans because of their genetic heterogeneity.Eosinophils play an important role in the pathogenesis of allergic airway inflammation. The infiltration of the airway wall with a large number of activated eosinophils and release of their toxic granule proteins and lipid metabolites cause damage to bronchial epithelial cells (15)(16)(17)(18)(19). It is believed that an airway hyperresponsiveness, the hallmark of asthma, occurs as a result of this eosinophil-mediated damage. In the majority of clinical studies, pulmonary eosinophilia has been shown to correlate with disease severity (15,17), and the resolution of airway eosinophilia correlates with the remission of asthma symptoms (16).Recently, a number of murine models of antigeninduced pulmonary eosinophilia and airway hyperreactivity (AHR) have been developed to study the role of B cells (20,21), T cells (20,(22)(23)(24), mast cells (25), NK cells (20), dendritic cells (26), IgE and its receptor (27, 28), cytokines (29-32), leukotrienes (33), and costimulatory molecules (34,35) in the mechanisms of immune responses in asthma. However, in all of these animal models, MHC class II molecules are mouse derived. We have generated transgenic mice expressing human DQ6 (HLA-DQA1*0103 and HLA-DQB1*0601) and DQ8 (HLA-DQA1*0301 and HLA-DQB1*0302) genes (36-38). These mice lack endogenous class II molecules, and the only functional class II molecules on antigen-presenting cells (APCs) are human DQ6 or DQ8. The human leukocyte antigen (HLA) restriction of the IgE response to different allergens in humans ...

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Aspirin-induced asthma and HLA-DRB1 and HLA-DPB1 genotypes

Abstract: The presence of an HLA association suggests that immune recognition of an unknown antigen may be part of the aetiology of AIA.

Cited by 57 publications

References 21 publications

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Perfil de citocinas e tipificação de HLA em pacientes com polipose nasossinusal tolerantes e intolerantes a aspirina

Short ragweed allergen induces eosinophilic lung disease in HLA-DQ transgenic mice

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