1,721,737 research outputs found
Inflammation and the mucosal microcirculation in inflammatory bowel disease: the ebb and flow
No full textPurpose of review Inflammatory bowel disease pathogenesis involves the interplay of multiple biological factors among which nonimmune cells, including the endothelium represent a crucial component of disease pathogenesis. Recent findings Endothelial cells play a key role in chronic inflammation through multiple and disparate activities. The mucosal microvasculature in inflammatory bowel disease is dysfunctional, overexpresses inflammatory molecules and undergoes intense angiogenesis, failing to exert its physiological antiinflammatory and anticoagulant activities. Summary The mucosal microcirculation is abnormal in inflammatory bowel disease and represents a novel component of disease pathogenesis, targeting the various abnormalities of the inflammatory bowel disease microcirculation may lead to new forms of therapeutic intervention
Mechanisms of action of infliximab in inflammatory bowel disease: an anti-inflammatory multitasker
No full textNegative regulators of angiogenesis in inflammatory bowel disease: Thrombospondin in the spotlight
No full textAngiogenesis is the growth of new blood vessels. In the two major forms of inflammatory bowel disease (IBD), Crohn's disease and ulcerative colitis, robust angiogenesis exists, and its blockade may have therapeutic potential, as shown in animal models of experimental intestinal inflammation. While abundant literature is available on the positive regulators of intestinal pathological angiogenesis, e. g. VEGF, bFGF, IL-8, CD40 and CD40L, almost no data exist on negative regulators. Thrombospondin-1 is a negative regulator of angiogenesis, and it plays a new role in IBD-associated angiogenesis. In addition, recombinant thrombospondin-1 may inhibit pathological angiogenesis and may offer a new therapeutic approach to intestinal inflammation. Copyright (c) 2008 S. Karger AG, Base
Nonimmune cells in inflammatory bowel disease: from victim to villain
No full textNonimmune cells have traditionally been viewed as target cells of the aberrant inflammatory process present in chronic immune-mediated conditions such as inflammatory bowel disease (IBD). However, the discovery that many of the functions traditionally attributed to immune cells are also performed by nonimmune cells has caused a shift to a multidirectional hypothesis in which nonimmune cells and acellular elements play active roles. Many types of interactions occur within this multidirectional system, and the difficulties associated with modeling these complex interactions currently limit our understanding of the cellular network that occurs in IBD. I describe the current knowledge of the roles played by nonimmune cells in the pathogenesis of IBD, as they emerge as crucial alternative targets for therapeutic intervention
Editorial [Hot Topic: Ulcerative Colitis: A Cinderella Story (Guest Editor: Silvio Danese)]
No full textOf mice and men—shedding new light on IL-13 activity in IBD
No full textA recent study in a mouse model of colitis has demonstrated that interleukin (IL)-13, through inhibition of the mixed type 1 and type 17 T-helper cell inflammatory response, has a protective effect. the decoy receptor Il-13R alpha 2 inhibits this protective effect, suggesting blockade of IL-13R alpha 2 as a potential therapy for patients with IBD
Immune and nonimmune components orchestrate the pathogenesis of inflammatory bowel disease
No full textInflammatory bowel disease (IBD) pathogenesis is driven by the interactions between the innate and the adaptive immune system. Both systems are actually expressed not only by immune cells, but also by essentially all types of nonimmune cells. Nonimmune cells have classically been considered as simple targets of the aberrant inflammatory process occurring in IBD. However, the discovery that many of the functions traditionally attributed to immune cells are also performed by nonimmune cells has caused a shift to a multidirectional hypothesis in which nonimmune cells and even acellular elements are considered active players of IBD pathogenesis. The aim of this review is to summarize the current role played by each cell type in IBD pathogenesis.</jats:p
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