The Relationship between Interleukin-18 Polymorphisms and Allergic Disease: A Meta-Analysis

Cheng, Da‐Chuan; Hao, Ying; Zhou, Wenling; Ma, Yanhong

doi:10.1155/2014/290687

Cited by 23 publications

(24 citation statements)

References 50 publications

(66 reference statements)

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“…While originally characterized for its role with IL-12 in stimulating Th1 cell differentiation, IL-18 is also known to influence type 2 inflammation as polymorphisms in IL-18 are protective for some atopic conditions and IL-18 promotes allergic inflammation in some animal models [135, 136]. Recently, a role for IL-18 in the pathogenesis of EoE has also been postulated.…”

Section: Cytokines Chemokines and Other Moleculesmentioning

confidence: 99%

The Immunologic Mechanisms of Eosinophilic Esophagitis

Hill

Spergel

2016

Curr Allergy Asthma Rep

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Eosinophilic esophagitis (EoE) is a chronic allergic inflammatory disease that is triggered by food and/or environmental allergens and is characterized by a clinical and pathologic phenotype of progressive esophageal dysfunction due to tissue inflammation and fibrosis. EoE is suspected in patients with painful swallowing, among other symptoms, and is diagnosed by the presence of 15 or more eosinophils per high-power field in one or more of at least four esophageal biopsy specimens. The prevalence of EoE is increasing and has now reached rates similar to those of other chronic gastrointestinal disorders such as Crohn’s disease. In recent years, our understanding of the immunologic mechanisms underlying this condition has grown considerably. Thanks to new genetic, molecular, cellular, animal, and translational studies, we can now postulate a detailed pathway by which exposure to allergens results in a complex and coordinated type 2 inflammatory cascade that, if not intervened upon, can result in pain on swallowing, esophageal strictures, and food impaction. Here, we review the most recent research in this field to synthesize and summarize our current understanding of this complex and important disease.

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Section: Cytokines Chemokines and Other Moleculesmentioning

confidence: 99%

The Immunologic Mechanisms of Eosinophilic Esophagitis

Hill

Spergel

2016

Curr Allergy Asthma Rep

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“…The IL-18 promoter polymorphisms 137G/C and 607C/A that decrease IL-18 transcription have been linked to a decreased risk of allergic dermatitis in a meta-analysis [131]. IL-18 was first implicated in allergic dermatitis when transgenic mice for caspase-1 developed dermatitis with spontaneous apoptosis, and high levels of IL-18 were found in the skin [132].…”

Section: Il-18-induced Allergic Diseasesmentioning

confidence: 99%

“…The 137G allele in the IL-18 gene was identified as a risk factor for atopic asthma [136], and the previously mentioned Cheng et al meta-analysis found a significantly decreased risk of allergic asthma in certain polymorphisms [131]. In one study, the combination of IL-18 an IL-12 decreased airway hyper-responsiveness, airway eosinophilia, and serum IgE [66].…”

Section: Il-18-induced Allergic Diseasesmentioning

confidence: 99%

Role of interleukin-18 in the pathophysiology of allergic diseases

Sanders

Mishra

2016

Cytokine & Growth Factor Reviews

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Interleukin (IL)-18 is an IL-1 family cytokine expressed by macrophages, dendritic cells, epithelial cells, and keratinocytes and is implicated in various aspects of both the innate and adaptive immune systems. IL-18 signals similar to IL-1β intracellularly to activate gene transcription. Since its discovery, IL-18 has been demonstrated to play a key role in pathogen defense from helminths and some bacteria. Recently however, evidence has accumulated that IL-18 expression is increased in many presentations of allergic disease. A pathologic role for IL-18 includes stimulating mast cell and basophil degranulation, recruiting granulocytes to sites of inflammation, increasing cytotoxic activity of natural killer (NK) and NK-T cells, inducing Immunoglobulin (Ig)E production and isotype switching, and affecting a broad range of T cells to promote a type II helper T cell (Th2) response. Evidence and importance of these effects are presented, including novel results from our lab implicating IL-18 in the direct expansion of mast cells, basophils, and other myeloid-lineage cells from bone-marrow precursors. The development of urticaria, asthma, dermatitis, rhinitis, and eosinophilic disorders all have demonstrated correlations to increased IL-18 levels either in the tissue or systemically. IL-18 represents a novel site of immune regulation in not only allergic conditions, but also autoimmune diseases and other instances of aberrant immune functioning. Diagrammatic summarized abstract for readers convinanceis presented in figure 1.

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“…A meta-analysis by Cheng et al aimed to clarify whether the -607C/A and -137G/C polymorphisms in the gene encoding for interleukin (IL)-18 (IL18) were associated with the risk of allergic disease. 7 The pooled results demonstrated no significant association between IL-18 polymorphisms and allergic disease. However, the subgroup analysis indicated that the IL-18 -137G/C polymorphism may be a protective factor for the risk of development of AE.…”

Section: Epidemiology Risk Factorsmentioning

confidence: 86%

“…A meta‐analysis by Cheng et al . aimed to clarify whether the ‐607C/A and ‐137G/C polymorphisms in the gene encoding for interleukin (IL)‐18 ( IL18 ) were associated with the risk of allergic disease …”

Section: Epidemiologymentioning

confidence: 99%

What's new in atopic eczema? An analysis of systematic reviews published in 2014. Part 1. Epidemiology, risk factors and outcomes

et al. 2016

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SummaryThis review summarizes key findings from nine systematic reviews on atopic eczema (AE) published or first indexed in 2014. It focuses on epidemiology, disease processes and methodological issues. There is reasonable evidence to conclude that high birth weight (> 4000 g) is a risk factor for the development of AE. A lower socioeconomic position is associated with lower prevalence of AE. The effect of exposure to traffic-related air pollution in childhood on the development of AE is uncertain. CD14 polymorphisms do not appear to have an effect in AE. There may be a role for interleukin-18 in AE development. Patients with AE are at decreased risk of brain tumours, but at increased risk of developing attention deficit hyperactivity disorder. Evidence supports the view that normal-appearing skin in AE is in fact structurally abnormal. Lower success rates at inducing remission in AE are associated with increased risk of relapse during long-term follow-up. The Eczema Area Severity Index (EASI) has been agreed as the preferred core instrument to measure clinical signs in future research. There remains a lack of consensus on the definition of an AE flare.

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The Relationship between Interleukin-18 Polymorphisms and Allergic Disease: A Meta-Analysis

Cited by 23 publications

References 50 publications

The Immunologic Mechanisms of Eosinophilic Esophagitis

The Immunologic Mechanisms of Eosinophilic Esophagitis

Role of interleukin-18 in the pathophysiology of allergic diseases

What's new in atopic eczema? An analysis of systematic reviews published in 2014. Part 1. Epidemiology, risk factors and outcomes

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