No abstract

FXR activation prevents chemically induced intestinal inflammation, with improvement of colitis symptoms, inhibition of epithelial permeability, and reduced goblet cell loss. Furthermore, FXR activation inhibits proinflammatory cytokine production in vivo in the mouse colonic mucosa, and ex vivo in different immune cell populations. The findings provide a rationale to explore FXR agonists as a novel therapeutic strategy for IBD.

Pentraxins are a superfamily of conserved proteins involved in the acute-phase response and innate immunity. Pentraxin 3 (PTX3), a prototypical member of the long pentraxin subfamily, is a key component of the humoral arm of innate immunity that is essential for resistance to certain pathogens. A regulatory role for pentraxins in inflammation has long been recognized, but the underlying mechanisms remain unclear. Here we report that PTX3 bound P-selectin and attenuated neutrophil recruitment at sites of inflammation. PTX3 released from activated leukocytes functioned locally to dampen neutrophil recruitment and regulate inflammation. Antibodies have glycosylation-dependent regulatory effect on inflammation. Therefore, PTX3, which is an essential component of humoral innate immunity, and immunoglobulins share functional outputs, including complement activation, opsonization and, as shown here, glycosylation-dependent regulation of inflammation.

No abstract

Our study protocol was registered with PROSPERO (registration number: CRD42018112214). We followed a standardized methodology 7 and report findings according to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (ie, PRISMA) 8 and Meta-analyses of Observational Studies in Epidemiology (ie, MOOSE) 9 recommendations. Search Strategy We systematically searched PubMed, Embase, and Scopus from inception through September 28, 2018, to identify metaanalyses of studies assessing the association between environmental factors and IBD. Search terms included inflammatory bowel disease, Crohn's disease, or ulcerative colitis, combined with systematic review or meta-analysis. We excluded conference abstracts, letters, editorials, and articles published in languages other than English. The reference lists of the identified meta-analyses were screened for additional eligible articles. No other restrictions were imposed.