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IL33 and IL1RL1 variants are associated with asthma and atopy in a Brazilian population.

Abstract Atopic asthma is a chronic inflammatory disease in airways resulting from genetic and environmental factors, characterized by production of the Th2 cytokines interleukin-4 (IL-4), interleukin-5 (IL-5) and interleukin-13 (IL-13). Interleukin-33 (IL-33) appears to be a potent inducer of Th2 immune response. This occurs when IL-33 binds and activates its receptor, the membrane ST2 (ST2L) in mast cells, dendritic cells, basophils, eosinophils, innate lymphoids and Th2 cells, leading to the release of these cytokines and intensifying allergic inflammation. Polymorphisms in the IL33 and IL1RL1 can act as protective or risk factors for asthma and/or allergy in humans. No study was conducted to replicate such findings in a European and African descendent mixed population. DNA was extracted from peripheral blood from 1223 subjects, and the samples were genotyped using Illumina 2.5 Human Omni Beadchip. We tested for possible associations between SNPs in the IL33 and ST2 with asthma and allergy markers such as specific IgE (sIgE), IL-5 and IL-13 production and skin prick test (SPT). Logistics regressions were performed using PLINK software 1.07. The analyses were adjusted for sex, age, helminth infection and ancestry markers. The G allele of IL33 SNP rs12551256 was negatively associated with asthma (OR 0.71, 95% CI: 0.53-0.94, P = 0.017). In contrast, the A allele of IL1RL1 rs1041973 was positively associated with IL-5 production (OR 1.36, 95% CI: 1.09-1.84, P = 0.044), sIgE levels (OR 1.40, 95% CI: 1.07-1.84, P = 0.013) and positive SPT (OR 1.48, 95% CI: 1.08-2.03, P = 0.014), for Blomia tropicalis mite. The same allele, in atopic subjects, was associated with decreased production of soluble ST2 (sST2) (P < 0.05). Moreover, expression quantitative trait loci (eQTL) analysis suggests that rs1041973 and rs873022 regulate the expression of IL1RL1 gene. This latest SNP, rs873022, the T allele, was also associated with a lower production of sST2 in plasma of Brazilians. The genetic risk score for rs1041973 and rs16924161 demonstrated a higher risk for SPT positivity against B. tropicalis, the greater the number of risk alleles for both SNPs. Our findings demonstrate a robust association of genetic variants in IL1RL1 and IL33 SNPs with allergy markers and asthma.
PMID
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Authors

Mayor MeshTerms

Genetic Association Studies

Keywords
Journal Title international journal of immunogenetics
Publication Year Start




PMID- 28266165
OWN - NLM
STAT- MEDLINE
DA  - 20170307
DCOM- 20170317
LR  - 20170317
IS  - 1744-313X (Electronic)
IS  - 1744-3121 (Linking)
VI  - 44
IP  - 2
DP  - 2017 Apr
TI  - IL33 and IL1RL1 variants are associated with asthma and atopy in a Brazilian
      population.
PG  - 51-61
LID - 10.1111/iji.12306 [doi]
AB  - Atopic asthma is a chronic inflammatory disease in airways resulting from genetic
      and environmental factors, characterized by production of the Th2 cytokines
      interleukin-4 (IL-4), interleukin-5 (IL-5) and interleukin-13 (IL-13).
      Interleukin-33 (IL-33) appears to be a potent inducer of Th2 immune response.
      This occurs when IL-33 binds and activates its receptor, the membrane ST2 (ST2L) 
      in mast cells, dendritic cells, basophils, eosinophils, innate lymphoids and Th2 
      cells, leading to the release of these cytokines and intensifying allergic
      inflammation. Polymorphisms in the IL33 and IL1RL1 can act as protective or risk 
      factors for asthma and/or allergy in humans. No study was conducted to replicate 
      such findings in a European and African descendent mixed population. DNA was
      extracted from peripheral blood from 1223 subjects, and the samples were
      genotyped using Illumina 2.5 Human Omni Beadchip. We tested for possible
      associations between SNPs in the IL33 and ST2 with asthma and allergy markers
      such as specific IgE (sIgE), IL-5 and IL-13 production and skin prick test (SPT).
      Logistics regressions were performed using PLINK software 1.07. The analyses were
      adjusted for sex, age, helminth infection and ancestry markers. The G allele of
      IL33 SNP rs12551256 was negatively associated with asthma (OR 0.71, 95% CI:
      0.53-0.94, P = 0.017). In contrast, the A allele of IL1RL1 rs1041973 was
      positively associated with IL-5 production (OR 1.36, 95% CI: 1.09-1.84, P =
      0.044), sIgE levels (OR 1.40, 95% CI: 1.07-1.84, P = 0.013) and positive SPT (OR 
      1.48, 95% CI: 1.08-2.03, P = 0.014), for Blomia tropicalis mite. The same allele,
      in atopic subjects, was associated with decreased production of soluble ST2
      (sST2) (P &lt; 0.05). Moreover, expression quantitative trait loci (eQTL) analysis
      suggests that rs1041973 and rs873022 regulate the expression of IL1RL1 gene. This
      latest SNP, rs873022, the T allele, was also associated with a lower production
      of sST2 in plasma of Brazilians. The genetic risk score for rs1041973 and
      rs16924161 demonstrated a higher risk for SPT positivity against B. tropicalis,
      the greater the number of risk alleles for both SNPs. Our findings demonstrate a 
      robust association of genetic variants in IL1RL1 and IL33 SNPs with allergy
      markers and asthma.
CI  - (c) 2017 John Wiley &amp; Sons Ltd.
FAU - Queiroz, G A
AU  - Queiroz GA
AD  - Laboratory of Immunopharmacology and Molecular Biology, Federal University of
      Bahia, Salvador, Brazil.
FAU - Costa, R S
AU  - Costa RS
AD  - Laboratory of Immunopharmacology and Molecular Biology, Federal University of
      Bahia, Salvador, Brazil.
FAU - Alcantara-Neves, N M
AU  - Alcantara-Neves NM
AD  - Laboratory of Allergy and Acarology, Federal University of Bahia, Salvador,
      Brazil.
FAU - Nunes de Oliveira Costa, G
AU  - Nunes de Oliveira Costa G
AD  - Laboratory of Immunopharmacology and Molecular Biology, Federal University of
      Bahia, Salvador, Brazil.
FAU - Barreto, M L
AU  - Barreto ML
AD  - Department of Epidemiology, Oswaldo Cruz Fundation, Salvador, Brazil.
FAU - Carneiro, V L
AU  - Carneiro VL
AD  - Laboratory of Immunopharmacology and Molecular Biology, Federal University of
      Bahia, Salvador, Brazil.
FAU - Figueiredo, C A
AU  - Figueiredo CA
AD  - Laboratory of Immunopharmacology and Molecular Biology, Federal University of
      Bahia, Salvador, Brazil.
LA  - eng
PT  - Journal Article
PL  - England
TA  - Int J Immunogenet
JT  - International journal of immunogenetics
JID - 101232337
RN  - 0 (IL1RL1 protein, human)
RN  - 0 (IL33 protein, human)
RN  - 0 (IL5 protein, human)
RN  - 0 (Interleukin-1 Receptor-Like 1 Protein)
RN  - 0 (Interleukin-33)
RN  - 0 (Interleukin-5)
RN  - 37341-29-0 (Immunoglobulin E)
SB  - IM
MH  - Animals
MH  - Asthma/blood/*genetics/microbiology/pathology
MH  - Brazil
MH  - Child
MH  - Child, Preschool
MH  - Female
MH  - *Genetic Association Studies
MH  - Genetic Predisposition to Disease
MH  - Genotype
MH  - Humans
MH  - Hypersensitivity/*genetics/immunology/microbiology
MH  - Hypersensitivity, Immediate/genetics
MH  - Immunoglobulin E/blood
MH  - Interleukin-1 Receptor-Like 1 Protein/*genetics
MH  - Interleukin-33/*genetics
MH  - Interleukin-5/genetics
MH  - Male
MH  - Mites/immunology/pathogenicity
MH  - Polymorphism, Single Nucleotide
MH  - Skin/immunology/microbiology
MH  - Th2 Cells
EDAT- 2017/03/08 06:00
MHDA- 2017/03/18 06:00
CRDT- 2017/03/08 06:00
PHST- 2016/07/22 [received]
PHST- 2016/12/05 [revised]
PHST- 2017/01/14 [accepted]
AID - 10.1111/iji.12306 [doi]
PST - ppublish
SO  - Int J Immunogenet. 2017 Apr;44(2):51-61. doi: 10.1111/iji.12306.

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