Inflammation, Allergy and Asthma, Complex Immune Origin Diseases: Mechanisms and Therapeutic Agents

Naik, Suresh R.; Wala, Santosh M.

doi:10.2174/1872213x11307010062

Cited by 17 publications

(11 citation statements)

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“…IL-18 is mainly generated by macrophages, dendritic cells, keratinocytes, osteoblasts, intestinal epithelial cells, and so on and is capable of increasing the IFN-g production by Th1 cells together with IL-12 (Enoksson et al, 2011;Smith, 2011;Naik and Wala, 2013). Furthermore, IL-18 is also responsible for stimulating the expression of TNF-a and IL-1b, promoting the differentiation of T cells to the proinflammatory Th1 phenotype and impairing the synthesis of the anti-inflammatory cytokine IL-10 (Saito et al, 2010;Veenbergen et al, 2010).…”

Section: Introductionmentioning

confidence: 99%

Genetic Polymorphisms in the IL-18 Gene and Ulcerative Colitis Risk: A Meta-Analysis

Wang

Tong

Chang

et al. 2014

DNA and Cell Biology

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This meta-analysis was performed to evaluate the relationships between genetic polymorphisms in the IL-18 gene and ulcerative colitis (UC) risk. The PubMed, CISCOM, CINAHL, Web of Science, Google Scholar, EBSCO, Cochrane Library, and CBM databases were searched for relevant articles published before November 1st, 2013 without any language restrictions. Meta-analysis was conducted using the STATA 12.0 software. Crude odds ratios (ORs) with their 95% confidence intervals (95% CI) were calculated. Eight case-control studies with a total of 1000 UC cases and 1392 healthy subjects met the inclusion criteria. Six common polymorphisms in the IL-18 gene were evaluated, including rs1946518 A>C, rs187238 G>C, rs917997 G>A, Codon35, rs1946519 C>A, and rs360718 A>C. The results of our meta-analysis suggest that the IL-18 rs1946518 (allele model: OR=1.22, 95% CI: 1.01-1.48, p=0.039; dominant model: OR=1.44, 95% CI: 1.01-2.06, p=0.045; respectively), rs187238 (allele model: OR=1.38, 95% CI: 1.19-1.61, p<0.001; dominant model: OR=1.50, 95% CI: 1.03-2.19, p=0.034; respectively), and rs360718 (allele model: OR=2.18, 95% CI: 1.22-3.90, p=0.008) polymorphisms might be strongly correlated with an increased risk of UC. A subgroup analysis was conducted to investigate the effect of ethnicity on an individual's risk of UC. Our results revealed positive significant correlations between IL-18 genetic polymorphisms and an increased risk of UC among Asians (allele model: OR=1.36, 95% CI: 1.16-1.60, p<0.001; dominant model: OR=1.50, 95% CI: 1.14-1.98, p=0.004; respectively) and Africans (allele model: OR=1.45, 95% CI: 1.03-2.05, p=0.034), but not among Caucasians (all p>0.05). Our findings provide convincing evidence that IL-18 genetic polymorphisms may contribute to susceptibility to UC, especially the rs1946518, rs187238, and rs360718 polymorphisms among Asians and Africans.

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Section: Introductionmentioning

confidence: 99%

Genetic Polymorphisms in the IL-18 Gene and Ulcerative Colitis Risk: A Meta-Analysis

Wang

Tong

Chang

et al. 2014

DNA and Cell Biology

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“…VEGF expression is significantly elevated in mice with allergic inflammation and in humans with asthma or AR. 18 VEGF increases inflammatory response through the expression of ICAM-1 19,20 and regulates vascular permeability and the inflammatory response in the rat. 20 Expression of VEGF also induced a high inflammatory response through an increase in vascular permeability.…”

Section: Discussionmentioning

confidence: 97%

Protective Effects of Rutin through Regulation of Vascular Endothelial Growth Factor in Allergic Rhinitis

Kim

Nam

Hong

et al. 2015

Am J Rhinol�Allergy

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“…Immunopathology of allergic rhinitis is also similar with a predominance of T-helper type 2 inflammation and tissue eosinophilia [42]. Allergy and asthma trigger the various associated biological, cellular, and molecular events with inflammation, such as increased vascular permeability, vasodilatation, cellular migration, increased mucus secretion, bronchoconstriction, structural changes of airway architecture, decline in pulmonary functions, release of intracellular mediators, increased formation of reactive oxygen species, cartilage degradation, and loss of function [43].…”

Section: The Role Of Allergy Related To Orthodontically Induced Root mentioning

confidence: 99%

Effect of Allergy on Root Resorption Induced by Orthodontic Tooth Movement

Ioi¹,

Kido²,

Murata³

et al. 2015

Issues in Contemporary Orthodontics

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Inflammation, Allergy and Asthma, Complex Immune Origin Diseases: Mechanisms and Therapeutic Agents

Cited by 17 publications

References 0 publications

Genetic Polymorphisms in the IL-18 Gene and Ulcerative Colitis Risk: A Meta-Analysis

Genetic Polymorphisms in the IL-18 Gene and Ulcerative Colitis Risk: A Meta-Analysis

Protective Effects of Rutin through Regulation of Vascular Endothelial Growth Factor in Allergic Rhinitis

Effect of Allergy on Root Resorption Induced by Orthodontic Tooth Movement

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