Secretion of RANTES (CCL5) and interleukin‐10 from mesenteric adipose tissue and from creeping fat in Crohn’s disease: Regulation by steroid treatment

Abstract

Both RANTES and IL-10 secretion can be detected from mesenteric adipose tissue and from creeping fat. The elevated RANTES and IL-10 secretion from creeping fat in CD is not due to a CD-specific effect but caused by steroid treatment.

Perinodal Adipose Tissue and Mesenteric Lymph Node Activation During Reactivated TNBS-Colitis in Rats

“…However, the overexpression of leptin, adiponectin and resistin in mesenteric adipose tissue and significant alterations in the circulating serum levels of these adipokines have been described in with Crohn's disease [32]. Additionally, PAT also produces higher levels of TNF-a, IL-10 and other cytokines during human intestinal inflammation [33,34]. We showed that PAT from rats with TNBS-reactivated colitis produced higher levels of leptin, adiponectin, TNF-a and IL-10 compared to control rats, confirming that inflammation alters adipose tissue production of pro-and anti-inflammatory mediators.…”

The role of resistin as a regulator of inflammation: Implications for various human pathologies

“…Immune cells infiltrating fat create a milieu that perpetuates inflammation within the adipose tissue and stimulates the adipocytes themselves to produce inflammatory mediators, including adipokines, completing a vicious circle of inflammation related to obesity [65][66][67][68].…”

Adipose tissue as an immunological organ: Toll-like receptors, C1q/TNFs and CTRPs

“…The phenomenon of creeping fat (proliferation and hypertrophy of local adipose tissue enveloping the gut) in Crohn's disease (a chronic inflammatory bowel disease) and the macrophage infiltration of the omentum (abdominal adipose tissue) during abdominal infection (e.g. in diverticulitis or peritoneal fluid infection) are clinical examples that are potentially caused by these mechanisms [30][31][32][33]. Moreover, metabolic alterations, such as hyperglycemia, insulin resistance and elevated levels of free fatty acids, observed commonly during infection might be caused by the activation of TLRs expressed on adipocytes and preadipocytes.…”