Associations of functional NLRP3 polymorphisms with susceptibility to food-induced anaphylaxis and aspirin-induced asthma

Hitomi, Yuki; Ebisawa, Motohiro; Tomikawa, Morimitsu; Imai, Takanori; Komata, Takatsugu; Hirota, Tomomitsu; Harada, Michishige; Sakashita, Masafumi; Suzuki, Yôichi; Shimojo, Naoki; Kohno, Yoichi; Fujita, Kimie; Miyatake, Akihiko; Doi, Satoru; Enomoto, Tadao; Taniguchi, Masami; Higashi, Noritaka; Nakamura, Yusuke; Tamari, Mayumi

doi:10.1016/j.jaci.2009.07.044

Cited by 174 publications

(171 citation statements)

References 35 publications

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“…Subsequently, 124 articles were excluded, and16 articles were examined closely for qualitative analysis. This resulted in elimination of 3 studies that had insufficient information; finally, 13 casecontrol studies were incorporated into this meta-analysis that contained a total of 7719 patients diagnosed with diverse diseases and 7094 healthy controls (Hitomi et al, 2009;Villani et al, 2009a,b;Roberts et al, 2010;Roberts et al, 2011;Ben Hamad et al, 2012;Carlstrom, 2012;Pontillo et al, 2012a,b;Ungerback, 2012;Kastbom et al, 2013;Pontillo et al, 2013;Varghese et al, 2013). The various diseases in the included studies were myocardial infarction, Alzheimer's disease, leprosy, ankylosing spondylitis, colorectal cancer (CRC), HIV-1 infection, systemic lupus erythematosus, malignant mesothelioma, rheumatoid arthritis (RA), abdominal aortic aneurysms (AAA), inflammatory bowel disease (IBD), ulcerative colitis (UC), Crohn's disease (CD), type 1 diabetes, celiac disease, and atopic dermatitis.…”

Section: Description Of Included Studiesmentioning

confidence: 99%

“…The pathogenic mechanism involving NLRP3 rs35829419 SNP is dramatically similar in the diverse disease settings discussed above (Roberts et al, 2010;Ben Hamad et al, 2012), and accumulated evidence suggests that the Q705K polymorphism promotes a disease state by causing a hyper-sensitive response to pathogen-associated molecular patterns and sustained activation of inflammation (Villani et al, 2009b;Kastbom et al, 2013). However, in direct contrast, other studies have shown a protective role for the NLRP3 polymorphism Q705K; therefore, the clinical relevance of this polymorphism remains uncertain (Hitomi et al, 2009;Ben Hamad et al, 2012). In order to address this issue, we performed a comprehensive meta-analysis to evaluate the association of the NLRP3 Q705K gene polymorphism with the progression of a variety of human diseases of high clinical value.…”

Section: Introductionmentioning

confidence: 99%

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NLRP3 rs35829419 polymorphism is associated with increased susceptibility to multiple diseases in humans

Zhang¹,

Fan²,

Zhang³

et al. 2015

Genet. Mol. Res.

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ABSTRACT. Using a meta-analysis framework, we investigated the association between the NLRP3 rs35829419 polymorphism and increased susceptibility to diverse diseases in humans. Relevant published studies were identified through a comprehensive and systematic electronic search, using the following scientific literature databases: Science Citation Index, the Cochrane Library, PubMed, Embase, CINAHL, Current Contents Index, Chinese Biomedical, the Chinese Journal Full-Text, and the Weipu Journal. Statistical analysis of data extracted from the selected high quality studies was performed using the Version 12.0 STATA software. A total of 13 case-control studies met our stringent inclusion and exclusion criteria for the present meta-analysis. These 13 high quality studies contained relevant information on 7719 patients with various diseases and 7094 healthy controls. Our meta-analysis results showed that the NLRP3 gene rs35829419 C>A polymorphism was associated with a significantly increased risk of developing multiple diseases in humans under 5 genetic models (all P < 0.05). Data stratification and subgroup analysis based on the disease type revealed that rs35829419 C>A carriers displayed a markedly increase susceptibility to leprosy, colorectal cancer, HIV-1 infection, 13969 NLRP3 rs35829419 SNP and human disease ©FUNPEC-RP www.funpecrp.com.br Genetics and Molecular Research 14 (4): 13968-13980 (2015) rheumatoid arthritis, abdominal aortic aneurysms, inflammatory bowel disease, ulcerative colitis, and atopic dermatitis. In summary, our metaanalysis results revealed the first identified strong correlation between the NLRP3 rs35829419 polymorphism and increased susceptibility to various diseases in humans.

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Section: Description Of Included Studiesmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

NLRP3 rs35829419 polymorphism is associated with increased susceptibility to multiple diseases in humans

Zhang¹,

Fan²,

Zhang³

et al. 2015

Genet. Mol. Res.

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“…Clinical data demonstrating elevated concentrations of IL-1b in status asthmaticus and neutrophilic asthma further support the contributions of IL-1R to asthma severity (2,30,31). Although data are limited regarding the role of Nlrp3 and caspase-1 in human asthma (32), gene analysis studies have linked nucleotide-binding oligomerization (NOD)-like receptors, including Nlrp3, to asthma and asthma subtypes (33,34). Given IL-1R's regulation of Th17 development, these data suggest a role for the Nlrp3-IL-1R axis in Th17-dependent allergic airway disease, and identify IL-1R as a potential pharmacologic target in severe asthma (35).…”

Section: T Cell Receptor (Tcr)bmentioning

confidence: 99%

Interleukin-1 Receptor and Caspase-1 Are Required for the Th17 Response in Nitrogen Dioxide–Promoted Allergic Airway Disease

Martin¹,

Ather²,

Lundblad³

et al. 2013

Am J Respir Cell Mol Biol

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“…123,124 Urticarial reactions are recurrent clinical manifestations in the continuum of CAPS, and skin disorders are a phenotypic feature of knock-in mice carrying NLRP3 hypermutations. 77 Moreover, mast cells from CAPS patients Genetics of the inflammasomes in human pathologies C Conforti-Andreoni et al 141 express NLRP3 and constitutively secrete IL-1b.…”

Section: Adaptive Immunity-mediated Diseasesmentioning

confidence: 99%

The inflammasomes in health and disease: from genetics to molecular mechanisms of autoinflammation and beyond

2011

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Nucleotide-binding oligomerization domain (NOD)-containing protein-like receptors (NLRs) are a recently discovered class of innate immune receptors that play a crucial role in initiating the inflammatory response following pathogen recognition. Some NLRs form the framework for cytosolic platforms called inflammasomes, which orchestrate the early inflammatory process via IL-1b activation. Mutations and polymorphisms in NLR-coding genes or in genetic loci encoding inflammasome-related proteins correlate with a variety of autoinflammatory diseases. Moreover, the activity of certain inflammasomes is associated with susceptibility to infections as well as autoimmunity and tumorigenesis. In this review, we will discuss how identifying the genetic characteristics of inflammasomes is assisting our understanding of both autoinflammatory diseases as well as other immune system-driven disorders.

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Associations of functional NLRP3 polymorphisms with susceptibility to food-induced anaphylaxis and aspirin-induced asthma

Cited by 174 publications

References 35 publications

NLRP3 rs35829419 polymorphism is associated with increased susceptibility to multiple diseases in humans

NLRP3 rs35829419 polymorphism is associated with increased susceptibility to multiple diseases in humans

Interleukin-1 Receptor and Caspase-1 Are Required for the Th17 Response in Nitrogen Dioxide–Promoted Allergic Airway Disease

The inflammasomes in health and disease: from genetics to molecular mechanisms of autoinflammation and beyond

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