Role of the endothelium in inflammatory bowel diseases

Abstract

Inflammatory bowel diseases (IBD) are a complex group of diseases involving alterations in mucosal immunity and gastrointestinal physiology during both initiation and progressive phases of the disease. At the core of these alterations are endothelial cells, whose continual adjustments in structure and function coordinate vascular supply, immune cell emigration, and regulation of the tissue environment. Expansion of the endothelium in IBD (angiogenesis), mediated by inflammatory growth factors, cytokines and chemokines, is a hallmark of active gut disease and is closely related to disease severity. The endothelium in newly formed or inflamed vessels differs from that in normal vessels in the production of and response to inflammatory cytokines, growth factors, and adhesion molecules, altering coagulant capacity, barrier function and blood cell recruitment in injury. This review examines the roles of the endothelium in the initiation and propagation of IBD pathology and distinctive features of the intestinal endothelium contributing to these conditions.

Differences in the expression of hepatocyte growth factor in acute and chronic bowel inflammation—Implications for diagnosis?

“…Chronic inflammation is characterised by a shift in the type of cells present at the site of inflammation, such as a predomination of lymphocytes and macrophages [6]. Chronic inflammation may ultimately lead to tissue destruction and cancer [7].…”

Update on the mechanisms of action of anti‑TNF-α antibodies and their clinical implications in inflammatory bowel disease

“…5 Several studies have also detected the alterations in serum levels of angiogenesis-regulating peptides following anti-TNF-α therapy. [48][49][50] Moreover, we have demonstrated that initial serum levels of vascular endothelial growth factor (VEGF) in patients with CD may be of predictive value for response to anti-TNF-α treatment. 50 In this respect, Rutella et al 51 have analyzed the release of VEGF by cultured mucosal extracts obtained from patients with CD before and after IFX administration, as well as by cultured human intestinal fibroblasts stimulated with TNF-α in the presence or absence of IFX.…”

“…In this review, we have highlighted some recruitment of proinflammatory cells from bloodstream to the site of disease. 48 Moreover, vascular endothelial cells (ECs) serve as a potent source of cytokines engaged in a complex crosstalk between innate and adaptive immunity in the intestines. 48,49 It has been shown that anti-TNF-α agents have a significant impact on these processes.…”

“…48 Moreover, vascular endothelial cells (ECs) serve as a potent source of cytokines engaged in a complex crosstalk between innate and adaptive immunity in the intestines. 48,49 It has been shown that anti-TNF-α agents have a significant impact on these processes. It has been observed that an early decrease in lymphocyte infiltration after administration of TNF-α blockers in patients with rheumatoid arthritis and psoriasis is related to downregulation of adhesion molecules on ECs and immune cells rather than to an increase in lymphocyte clearance via apoptosis.…”

A szabadidős mozgás kardiovaszkuláris és vastagbélgyulladást csökkentő hatása patkányban: a hem-oxigenáz és a nitrogénmonoxid-szintáz enzimek szerepe

“…Ezek az enzimek által termelt NO gyulladáscsökkentő hatást fejt ki, ugyanis gátolja a leukociták kitapadását az endotélhez, értágító hatású és szabályozza az endotél permeabilitását. Paradox módon a leukocitákban található iNOS a gyulladásos reakciókhoz járul hozzá, míg az endotél sejtekben lévő NOS feltehetően gyulladáscsökkentő (Cromer, Mathis et al 2011, Danese 2011) (3.ábra).…”