Perinodal adipose tissue and mesenteric lymph node activation during reactivated TNBS-colitis in rats

Colitis induced by trinitrobenzene sulfonic acid (TNBS) with reactivation is a good experimental model for studying inflammatory bowel disease pathogenesis and appropriate therapeutics. This experimental model allows the induction of colitis relapse and remission periods and the establishment of chronic disease features, such as the mesenteric adipose tissue alterations observed in Crohn's disease. Lymph node activation and the role of perinodal adipose tissue (PAT) have been poorly studied in this model. Thus, a study of the interactions of lymph nodes and PAT could help to elucidate the mechanisms behind IBD pathogenesis.

The purpose of this study was to examine lymph nodes and PAT alterations during reactivated TNBS-colitis in Wistar rats.

In this study, the alterations of PAT and lymph node cells during experimental colitis, induced by repeated intracolonic TNBS instillations, were evaluated, focusing on fatty acid and adipocytokine profile analysis and cytokines production, respectively.

Fatty acid analysis of PAT reveals an increase of ω-6 polyunsaturated fatty acids during colits, such as linoleic acid, gamma-linolenic acid and arachidonic acid. ω-6 arachidonic acid was not increased in lymph node cells or serum. PAT also produces elevated levels of pro- and anti-inflammatory adipokines during colitis. Lymph node cells release high levels of IFN-γ and TNF-α but not IL-10, characterizing the predominant Th-1 response associated with this disease. Nevertheless, T cells from animals with colitis demonstrated increased IFN-γ production via a COX-2-dependent mechanism after supplementation with ω-6 arachidonic acid, suggesting that PAT modification could contribute to the lymph node cell activation observed during colitis.