Resolution of Crohn's disease

Abstract

Crohn's disease (CD) is characterized by chronic inflammation of the gastrointestinal tract and represents one of the main inflammatory bowel disease (IBD) forms. The infiltration of immune cells into the mucosa and uncontrolled production of pro-inflammatory cytokines and other mediators trigger the chronic inflammatory reaction in the intestine [1]. The inflammatory setting consists of subsequent events that comprise an induction phase, the peak of inflammation which is subsequently followed by the resolution phase. The induction phase, which represents the first phase of inflammation, is important for the rapid and efficient activation of the immune system for sufficient host defense. The permanent sensing of exogenous or endogenous danger signals enables the fast initiation of the inflammatory reaction. The immune cell infiltrate initiates an inflammatory cascade where released lipid and protein mediators play an indispensable role [2, 3]. The last decades of research strongly suggest that resolution of inflammation is similarly a tightly coordinated and active process. The basic concept that resolution of inflammation has to be regarded as an active process has been thoroughly described by others [4-6]. The following review focuses on mechanisms, pathways, and specific mediators that are actively involved in the resolution of inflammation in CD.

Keywords: Anti-TNF therapy; Apoptosis; Crohn’s disease; IL23; Intestine; Resolution of inflammation.