title: Expression of inflammation-related genes is altered in gastric tissue of patients with advanced stages of NAFLD.
abstract: Obesity is associated with chronic low-grade inflammation perpetuated by visceral adipose. Other organs, particularly stomach and intestine, may also overproduce proinflammatory molecules. We examined the gene expression patterns in gastric tissue of morbidly obese patients with nonalcoholic fatty liver disease (NAFLD) and compared the changes in gene expression in different histological forms of NAFLD. Stomach tissue samples from 20 morbidly obese NAFLD patients who were undergoing sleeve gastrectomy were profiled using qPCR for 84 genes encoding inflammatory cytokines, chemokines, their receptors, and other components of inflammatory cascades. Interleukin 8 receptor-beta (IL8RB) gene overexpression in gastric tissue was correlated with the presence of hepatic steatosis, hepatic fibrosis, and histologic diagnosis of nonalcoholic steatohepatitis (NASH). Expression levels of soluble interleukin 1 receptor antagonist (IL1RN) were correlated with the presence of NASH and hepatic fibrosis. mRNA levels of interleukin 8 (IL8), chemokine (C-C motif) ligand 4 (CCL4), and its receptor chemokine (C-C motif) receptor type 5 (CCR5) showed a significant increase in patients with advanced hepatic inflammation and were correlated with the severity of the hepatic inflammation. The results of our study suggest that changes in expression patterns for inflammatory molecule encoding genes within gastric tissue may contribute to the pathogenesis of obesity-related NAFLD.
authors: Betty and Guy Beatty Obesity and Liver Program, Inova Health System, Falls Church, VA 22042, USA.
authors: Rohini
authors: R
authors: Mehta
authors: Aybike
authors: A
authors: Birerdinc
authors: Arpan
authors: A
authors: Neupane
authors: Amirhossein
authors: A
authors: Shamsaddini
authors: Arian
authors: A
authors: Afendy
authors: Hazem
authors: H
authors: Elariny
authors: Vikas
authors: V
authors: Chandhoke
authors: Ancha
authors: A
authors: Baranova
authors: Zobair M
authors: ZM
authors: Younossi
mesh_terms: D000328:Adult; D054407:Chemokine CCL4 / Q000235:genetics; D018925:Chemokines / Q000378:metabolism; D016207:Cytokines / Q000378:metabolism; D005234:Fatty Liver / Q000276:immunology* / Q000378:metabolism*; D005260:Female; D005753:Gastric Mucosa / Q000378:metabolism*; D006801:Humans; D007249:Inflammation / Q000378:metabolism*; D053590:Interleukin 1 Receptor Antagonist Protein / Q000378:metabolism; D016209:Interleukin-8 / Q000235:genetics; D008099:Liver / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D008103:Liver Cirrhosis / Q000276:immunology / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D065626:Non-alcoholic Fatty Liver Disease; D019713:Receptors, CCR5 / Q000235:genetics; D023063:Receptors, Interleukin-8B / Q000378:metabolism; D013270:Stomach / Q000276:immunology*
chemical_list: D054407:Chemokine CCL4; D018925:Chemokines; D016207:Cytokines; C507763:IL1RN protein, human; D053590:Interleukin 1 Receptor Antagonist Protein; D016209:Interleukin-8; D019713:Receptors, CCR5; D023063:Receptors, Interleukin-8B
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