Abstract
Inflammatory bowel disease (IBD), comprised of Crohn’s disease (CD) and ulcerative colitis (UC), is a group of chronic inflammatory disorders. IBD is regarded as a severe healthcare problem worldwide, with high morbidity and lethality. So far, despite of numerous studies on this issue, the specific mechanisms of IBD still remain unclarified and ideal treatments are not available for IBD. The intestinal mucosal barrier is vital for maintaining the function of the intestinal self-defensive system. Among all of the components, macrophage is an important one in the intestinal self-defensive system, normally protecting the gut against exotic invasion. However, the over-activation of macrophages in pathological conditions leads to the overwhelming induction of intestinal inflammatory and immune reaction, thus damaging the intestinal functions. Autophagy is an important catabolic mechanism. It has been proven to participate the regulation of various kinds of inflammation- and immune-related disorders via the regulation of inflammation in related cells. Here in this paper, we will review the role and mechanism of intestinal macrophage autophagy in IBD. In addition, several well-studied kinds of agents taking advantage of intestinal macrophage autophagy for the treatment of IBD will also be discussed. We aim to bring novel insights in the development of therapeutic strategies against IBD.
Highlights
Inflammatory bowel disease (IBD), including Crohn’s disease (CD) and ulcerative colitis (UC), is referred to as a group of idiopathic inflammation-related bowel diseases, which mainly affects the ileum, rectum and colon (Dun et al, 2021; Gallagher et al, 2021; Mazur et al, 2021)
In another colitis model induced by trinitro-benzene-sulfonic acid (TNBS), interleukin-33 (IL-33), a well-known anti-inflammatory cytokine, was reported to ameliorate colitis through the enhancement of intestinal macrophage autophagy in the inflammatory gut tissue via regulation of TLR4 signaling pathway (Wang et al, 2019)
A previous study revealed that the administration of PNU282987, a selective α7nAChR agonist, protected against dextran sulphate sodium (DSS)-induced colitis via the induction of AMPK-mTOR-p70S6K signaling-mediated autophagy in intestinal macrophages (Shao et al, 2019a)
Summary
Inflammatory bowel disease (IBD), including Crohn’s disease (CD) and ulcerative colitis (UC), is referred to as a group of idiopathic inflammation-related bowel diseases, which mainly affects the ileum, rectum and colon (Dun et al, 2021; Gallagher et al, 2021; Mazur et al, 2021). Intestinal macrophages have been revealed to play a vital role in the protection of the gut against exotic invasion and damage via the engulfment and presentation of invading antigens to other immune cells for clearance and killing (Vannella and Wynn, 2017; Muller et al, 2020; Viola and Boeckxstaens, 2020). The overwhelming activation of such self-protective immune and inflammatory responses induced by macrophages may lead to the disturbance of gut functions and intestinal microbiota homeostasis, resulting in certain gut diseases such as IBD (Baumgart and Carding, 2007; Wallace et al, 2014; Fan et al, 2017). As a result, uncovering the role and underlying mechanisms of autophagy in inflammation-related disorders is necessary and vital for the development of effective therapeutic strategies. We hope to provide insights in the development of new strategies against IBD
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