Interleukin-17A Gene Expression in Morbidly Obese Women.

Fernando Zapata-Gonzalez,Gemma Aragonès,Alba Berlanga,Andreu Martí,Salomé Martinez,Joan Sirvent,Mercé Hernandez,Fátima Sabench,Carmen Aguilar,Daniel Del Castillo,Esther Guiu-Jurado,Teresa Auguet,Cristóbal Richart,Rosa Jorba

doi:10.3390/ijms160817469

Abstract

Data from recent studies conducted in rodent models and humans suggest that interleukin-17A (IL-17A) plays a role in the induction of inflammation in adipose tissue during obesity. The aim of this study was to assess the gene expression of IL-17A in adipose tissue of morbidly obese patients. We used RT-PCR to evaluate the expression of IL-17A and several adipo/cytokines in the visceral adipose tissue (VAT) and subcutaneous adipose tissue (SAT) of 10 normal-weight control women (BMI < 25 kg/m2) and 30 morbidly obese women (MO, BMI > 40 kg/m2). We measured serum levels of IL-17A and adipo/cytokines in MO and normal weight women. IL-17A expression was significantly higher in VAT than in SAT in MO patients (p = 0.0127). It was very low in normal-weight controls in both VAT and SAT tissues. We found positive correlations between IL-17A and IL-6, lipocalin-2 and resistin in VAT of MO patients. The circulating level of IL-17A was higher in the normal-weight group than the MO patients (p = 0.032), and it was significantly related to adiponectin and TNFRII levels. In conclusion, IL-17A expression in VAT is increased in morbidly obese women, which suggests a link between obesity and innate immunity in low-grade chronic inflammation in morbidly obese women.

Highlights

Nowadays, obesity is perceived as an a esthetic drawback, and as a serious, almost pandemic, health problem associated with an increased risk of developing such diseases as type 2 diabetes mellitus, metabolic syndrome, cardiovascular disease, cancer and autoimmune diseases [1].Nutrient excess and adiposity activate several metabolic pathways implicated in the development of insulin resistance, including inflammatory signaling, lipotoxicity, aberrant adipokine secretion, adipose tissue hypoxia, endoplasmic reticulum stress and mitochondrial dysfunction [2,3,4,5,6,7,8]
We classified the patients into two groups according to their body mass index (BMI): normal-weight patients (BMI < 25 kg/m2), who acted as controls and morbidly obese women (MO; BMI > 40 kg/m2)
We demonstrated that IL-17A mRNA expression was almost undetectable in normal-weight controls in both visceral adipose tissue (VAT) and subcutaneous adipose tissue (SAT) tissues

Summary

Introduction

Obesity is perceived as an a esthetic drawback, and as a serious, almost pandemic, health problem associated with an increased risk of developing such diseases as type 2 diabetes mellitus, metabolic syndrome, cardiovascular disease, cancer and autoimmune diseases [1].Nutrient excess and adiposity activate several metabolic pathways implicated in the development of insulin resistance, including inflammatory signaling, lipotoxicity, aberrant adipokine secretion, adipose tissue hypoxia, endoplasmic reticulum stress and mitochondrial dysfunction [2,3,4,5,6,7,8]. Subsequent studies have shown that changes in inflammatory signaling by adipocytes and infiltration of adipose tissue by immune cells are key features of obesity-induced insulin resistance and associated metabolic disease in animal models and humans [10,11,12]. In obese mice, both adipocytes and macrophages (and potentially other cell types) residing in adipose tissue secrete a number of cytokines, including TNFα, interleukin (IL)-6, IL-1β and migration inhibitory factor [11]. The precise point at which this infiltration occurs during disease progression and their pro-inflammatory cytokine production in the pathogenesis of metabolic dysfunction in obese people remains to be determined

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