Association between human IL-10 gene polymorphisms and serum IL-10 level in patients with food allergy

Chen, Tuo Kang; Lee, Jyh‐Hong; Yu, Hsin-Hui; Yang, Yunan; Wang, Li‐Chieh; Lin, Yu-Tsan; Chiang, Bor‐Luen

doi:10.1016/j.jfma.2011.11.027

Cited by 22 publications

(19 citation statements)

References 30 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…The IL-10 SNP rs3024496 is shown to be related to inflammatory response with increased levels of IgE to dust mite[38], or decreased production of IL-10 by peripheral blood leukocytes[39], and with prostate[40] and colorectal[41] cancer, but has not been shown to be associated with IBD. The IL-10 rs1800872 is associated with IBD[37] and also with increased serum IL-10 levels in CD[42,43], as well as with irritable bowel syndrome[44] and cancer susceptibility[42,43,45,46]. In this study, we found that IL-10 rs3024496 is associated with pediatric IBD, and rs1800872, although by itself is not associated with pediatric IBD, appears to contribute to pediatric IBD via epistatic interaction with rs3024496.…”

Section: Discussionmentioning

confidence: 99%

Genetic association and epistatic interaction of the interleukin-10 signaling pathway in pediatric inflammatory bowel disease

Lin

Wang

Hegarty

et al. 2017

WJG

View full text Add to dashboard Cite

AIMTo study the genetic association and epistatic interaction of the interleukin (IL)-10 and IL-10/STAT3 pathways in pediatric inflammatory bowel disease (IBD).METHODSA total of 159 pediatric inflammatory IBD patients (Crohn’s disease, n = 136; ulcerative colitis, n = 23) and 129 matched controls were studied for genetic association of selected single nucleotide polymorphisms (SNPs) of the IL-10 gene and the genes IL10RA, IL10RB, STAT3, and HO1, from the IL-10/STAT3 signaling pathway. As interactions between SNPs from different loci may significantly affect the associated risk for disease, additive (a) and dominant (d) modeling of SNP interactions was also performed to examine high-order epistasis between combinations of the individual SNPs.RESULTSThe results showed that IL-10 rs304496 was associated with pediatric IBD (P = 0.022), but no association was found for two other IL-10 SNPs, rs1800872 and rs2034498, or for SNPs in genes IL10RA, IL10RB, STAT3, and HO1. However, analysis of epistatic interaction among these genes showed significant interactions: (1) between two IL-10 SNPs rs1800872 and rs3024496 (additive-additive P = 0.00015, Bonferroni P value (Bp) = 0.003); (2) between IL-10RB rs2834167 and HO1 rs2071746 (dominant-additive, P = 0.0018, Bp = 0.039); and (3) among IL-10 rs1800872, IL10RB rs2834167, and HO1 rs2071746 (additive-dominant-additive, P = 0.00015, Bp = 0.005), as well as weak interactions among IL-10 rs1800872, IL-10 rs3024496, and IL-10RA (additive-additive-additive, P = 0.003; Bp = 0.099), and among IL10RA, IL10RB, and HO1 genes (additive-dominant-additive, P = 0.008, Bp = 0.287).CONCLUSIONThese results indicate that both the IL-10 gene itself, and through epistatic interaction with genes within the IL-10/STAT3 signaling pathway, contribute to the risk of pediatric IBD.

show abstract

Section: Discussionmentioning

confidence: 99%

Genetic association and epistatic interaction of the interleukin-10 signaling pathway in pediatric inflammatory bowel disease

Lin

Wang

Hegarty

et al. 2017

WJG

View full text Add to dashboard Cite

show abstract

“…Thus far, multiple genes and their variants have been interrogated for their association with FA. Since FA, like AD, was primarily thought to be a disease of the immune system, all of the genes investigated and found to be associated with FA, aside from FLG , were immune-related and included the major histocompatibility complex cluster, CD14, FOXP3, STAT6, SPINK5, TNF, GSTP1, IL13, IL10 , 111–113 and IL4RA . 114 In general, these were small-scale, candidate-gene studies that lacked replication, and the findings were frequently inconsistent among studies.…”

Section: Gene-environment Interactions In Atopic Disordersmentioning

confidence: 99%

Resolving the etiology of atopic disorders by using genetic analysis of racial ancestry

Gupta

Johansson

Bernstein

et al. 2016

Journal of Allergy and Clinical Immunology

View full text Add to dashboard Cite

Atopic dermatitis (AD), food allergy (FA), allergic rhinitis (AR) and asthma are common atopic disorders of complex etiology. The frequently observed “atopic march” from early AD to asthma and/or AR later in life as well as the extensive comorbidity of atopic disorders, suggests common causal mechanisms in addition to distinct ones. Indeed, both disease-specific and shared genomic regions exist for atopic disorders. Their prevalence also varies among races; for example, AD and asthma have a higher prevalence in African-Americans when compared to European-Americans. Whether this disparity stems from true genetic or race-specific environmental risk factors or both is unknown. Thus far, the majority of the genetic studies on atopic diseases have utilized populations of European ancestry, limiting their generalizability. Large cohort initiatives and new analytic methods such as admixture mapping are currently being employed to address this knowledge gap. Here we discuss the unique and shared genetic risk factors for atopic disorders in the context of ancestry variations, and the promise of high-throughput “-omics” based systems biology approach in providing greater insight to deconstruct into their genetic and non-genetic etiologies. Future research will also focus on deep phenotyping and genotyping of diverse racial ancestry, gene-environment, and gene-gene interactions.

show abstract

“…Our previous work also found that IL-10-producing B cells were less in the intestine of mice with food allergy [19, 20]. Clinical study indicates that IL-10 gene polymorphism is associated with food allergy and lower serum IL-10 levels [21]. Others also found that the myeloid-derived monocytes express IL-10, which suppresses most immune effector cells [22].…”

Section: Discussionmentioning

confidence: 88%

Galectin-1 inhibits oral-intestinal allergy syndrome

Xie

Yang

et al. 2017

Oncotarget

View full text Add to dashboard Cite

Background and aimsThe pathogenesis of oral-intestinal allergy syndrome (OIAS) has not been well understood. Published data indicate that galectin (Gal) 1 has immune regulatory functions. This study tests a hypothesis that Gal1 inhibits oral-intestinal allergy syndrome.MethodsMice were sensitized to peanut extracts (PE) via the buccal mucosa with or without using Gal1 together.ResultsUpon re-exposure to specific antigen, the OIAS mice showed the systemic allergic response, the oral allergic reactions, and intestinal allergic inflammation, including increases in serum histamine, drop of the core temperature, higher levels of PE-specific IgE and interleukin (IL)-4. Increases in mast cell and eosinophil in the oral mucosa and intestinal mucosa were also observed. The OIAS was inhibited by co-administration with Gal1 via a mechanism of suppressing micro RNA (miR)-98 and reversing the expression of IL-10 in CD14+ cells in the intestine.ConclusionsThe OIAS can be induced by applying specific antigens to the oral mucosa, which can be inhibited by co-administration with Gal1.

show abstract

Association between human IL-10 gene polymorphisms and serum IL-10 level in patients with food allergy

Cited by 22 publications

References 30 publications

Genetic association and epistatic interaction of the interleukin-10 signaling pathway in pediatric inflammatory bowel disease

Genetic association and epistatic interaction of the interleukin-10 signaling pathway in pediatric inflammatory bowel disease

Resolving the etiology of atopic disorders by using genetic analysis of racial ancestry

Galectin-1 inhibits oral-intestinal allergy syndrome

Contact Info

Product

Resources

About