Toll-like receptor 4, F4/80 and pro-inflammatory cytokines in intestinal and mesenteric fat tissue of Crohn’s disease

International Journal of Clinical and Experimental Medicine

Luiza M F Oliveira¹  João J Fagundes¹  Viviane S Rodrigues¹  Lício A Velloso¹  Mariana Portovedo¹  Andressa Coope¹  Maria de Lourdes S Ayrizono¹  Cláudio S R Coy¹  Raquel F Leal¹  Marciane Milanski¹ 

关键词: Crohn’s disease;    inflammatory bowel disease;    innate immunity;    cytokines;   

DOI  :  

学科分类：医学（综合）

来源: e-Century Publishing Corporation

【 摘 要 】

Introduction: Crohn’s disease (CD) is a chronic intestinal ailment with a multifactorial etiology, whose incidence has increased during the last three decades. Recently, a role for mesenteric fat has been proposed in CD pathophysiology, since fat hypertrophy is detected nearby the affected intestinal area; however, there are few studies on this aspect. Aim: To evaluate inflammatory activity in intestinal mucosa and mesenteric fat tissue of patients with CD and controls. Materials and Methods: Ten patients with ileocecal CD and 16 patients with non-inflammatory disease (control groups) were studied. The specimens were snap-frozen and the expression of TLR-4, F4/80, IL1-β and IL-6 were determined by immunoblot of protein extracts. TLR4 RNA level were measured using RT-PCR. The t Test was applied (p<0.05). The local ethical committee approved the study. Results: The intestinal mucosa of CD group had significantly higher protein levels of TLR-4, F4/80, IL-1β and IL-6 than the controls. The gene expression of TLR4 was lower in the intestinal mucosa of CD compared to the control group. Regard the mesenteric fat tissue, there was no statistical difference related to TLR-4, F4/80, IL-1β and IL-6 proteins expression. Conclusions: These findings may result from an up-regulation of macrophage activation and intracellular pathways activated by bacterial antigens, which are more important in intestinal mucosa than fat tissue in CD patients. This may represent an anomalous regulation of innate immunity and could contribute to the production of proinflammatory mediators and disease development.

【 授权许可】

Unknown