The Role of Long-Chain Fatty Acids in Inflammatory Bowel Disease.

Reshma Vasu,Hu Zhang,Chunxiang Ma

doi:10.1155/2019/8495913

Abstract

Inflammatory bowel disease (IBD) is a complicated disease involving multiple pathogenic factors. The complex relationships between long-chain fatty acids (LCFAs) and the morbidity of IBD drive numerous studies to unravel the underlying mechanisms. A better understanding of the role of LCFAs in IBD will substitute or boost the current IBD therapies, thereby obtaining mucosal healing. In this review, we focused on the roles of LCFAs on the important links of inflammatory regulation in IBD, including in the pathogen recognition phase and in the inflammatory resolving phase, and the effects of LCFAs on immune cells in IBD.

Highlights

Inflammatory bowel disease (IBD), comprising Crohn’s disease (CD) and ulcerative colitis (UC), is a chronic, remitted, and disabled inflammatory condition
Regarding the effectiveness of long-chain fatty acids (LCFAs) in regulating Peroxisome proliferator-activated receptor- (PPAR-)γ expression, Marion-Letellier et al [41] investigated that docosahexaenoic acid (DHA) and Eicosapentaenoic acid (EPA) could even attain the similar role of troglitazone on PPARγ in Caco-2 cells. These findings show that the induction and activation of Conjugated linoleic acid (CLA), DHA and EPA, which act as PPAR-γ agonists, contribute to the abrogation of intestinal inflammation in IBD
The mechanisms comprise the fact that LCFAs protect or dampen intestinal barriers, promote or inhibit toll-like receptors (TLRs)/nucleotide-binding oligomerisation domain (NOD) signaling pathways, and influence the balance between proinflammatory transcription factor NF-κB and anti-inflammatory transcription factor PPAR-γ

Summary

Introduction

Inflammatory bowel disease (IBD), comprising Crohn’s disease (CD) and ulcerative colitis (UC), is a chronic, remitted, and disabled inflammatory condition. Using anti-inflammatory treatments to counteract the overproduction of intestinal proinflammatory cytokines represents the primary therapeutic approaches to control IBD aggravation. Aside from the expensive medical expenditure, the side effects carried by these drugs motivate doctors to develop other cheaper and more available therapeutic approaches. These emerging treatments are expected to substitute or boost the current IBD therapies. The wealth of evidence supports that various LCFAs have complex effects on intestinal inflammation and IBD. We will provide a comprehensive insight into the mechanisms, by which LCFAs have an important role in regulating intestinal inflammation, especially in IBD, aimed at holding potential as targets for novel curative treatment

LCFA Derivatives

Regulation of LCFAs in the Inflammatory Process

Fatty Acid Receptors as Drug Targets for IBD

Findings

Conclusion