Intestinal fibrosis in IBD-a dynamic, multifactorial process

被引:280
作者
Rieder, Florian [1 ]
Fiocchi, Claudio [1 ]
机构
[1] Cleveland Clin Fdn, Lerner Res Inst, Dept Pathobiol, Cleveland, OH 44195 USA
基金
美国国家卫生研究院;
关键词
INFLAMMATORY-BOWEL-DISEASE; HUMAN COLONIC MYOFIBROBLASTS; GROWTH-FACTOR-BETA; NF-KAPPA-B; CROHNS-DISEASE; MESENCHYMAL TRANSITION; CIRCULATING FIBROCYTES; MOLECULAR-MECHANISMS; EXPERIMENTAL COLITIS; IMMUNE-RESPONSES;
D O I
10.1038/nrgastro.2009.31
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
Intestinal fibrosis is a common and potentially serious complication of IBD that results from the reaction of intestinal tissue to the damage inflicted by chronic inflammation. The traditional view that fibrosis is inevitable or irreversible in patients with IBD is progressively changing in light of improved understanding of the cellular and molecular mechanisms that underlie the pathogenesis of fibrosis in general, and, in particular, intestinal fibrosis. These mechanisms are complex and dynamic, and involve multiple cell types, interconnected cellular events and a large number of soluble factors. in addition, owing to a breakdown of the epithelial barrier during inflammation of the gut, luminal bacterial products induce an innate immune response, which is triggered by activation of immune and nonimmune cells alike. Comprehension of the mechanisms of intestinal fibrosis will create a conceptual and practical framework that could achieve the specific blockade of fibrogenic pathways, allow for the estimation of risk of fibrotic complications, permit the detection of early fibrotic changes and, eventually, enable the development of treatments customized to the type and stage of each patient's IBD.
引用
收藏
页码:228 / 235
页数:8
相关论文
共 79 条
[1]   Mutations in NOD2 are associated with fibrostenosing disease in patients with Crohn's disease [J].
Abreu, MT ;
Taylor, KD ;
Lin, YC ;
Hang, T ;
Gaiennie, J ;
Landers, CJ ;
Vasiliauskas, EA ;
Kam, LY ;
Rojany, M ;
Papadakis, KA ;
Rotter, JI ;
Targan, SR ;
Yang, HY .
GASTROENTEROLOGY, 2002, 123 (03) :679-688
[2]  
Aiba S, 1997, J CUTAN PATHOL, V24, P65
[3]  
ALON R, 1994, J IMMUNOL, V152, P1304
[4]   Pancreatic stellate cells are activated by proinflammatory cytokines: implications for pancreatic fibrogenesis [J].
Apte, MV ;
Haber, PS ;
Darby, SJ ;
Rodgers, SC ;
McCaughan, GW ;
Korsten, MA ;
Pirola, RC ;
Wilson, JS .
GUT, 1999, 44 (04) :534-541
[5]   Expression of transforming growth factors alpha and beta in colonic mucosa in inflammatory bowel disease [J].
Babyatsky, MW ;
Rossiter, G ;
Podolsky, DK .
GASTROENTEROLOGY, 1996, 110 (04) :975-984
[6]   Bone marrow transplantation ameliorates pathology in interleukin-10 knockout colitic mice [J].
Bamba, S. ;
Lee, C-Y ;
Brittan, M. ;
Preston, S. L. ;
Direkze, N. C. ;
Poulsom, R. ;
Alison, M. R. ;
Wright, N. A. .
JOURNAL OF PATHOLOGY, 2006, 209 (02) :265-273
[7]   Proinflammatory effects of TH2 cytokines in a murine model of chronic small intestinal inflammation [J].
Bamias, G ;
Martin, C ;
Mishina, M ;
Ross, WG ;
Rivera-Nieves, J ;
Marini, M ;
Cominelli, F .
GASTROENTEROLOGY, 2005, 128 (03) :654-666
[8]   CD34+fibrocytes in neoplastic and inflammatory pancreatic lesions [J].
Barth, PJ ;
Ebrahimsade, S ;
Hellinger, A ;
Moll, R ;
Ramaswamy, A .
VIRCHOWS ARCHIV, 2002, 440 (02) :128-133
[9]  
BATAILLE F, 2008, INFLAMM BOWEL DIS, V7, P226
[10]   The role of the fibrocyte, a bone marrow-derived mesenchymal progenitor, in reactive and reparative fibroses [J].
Bellini, Alberto ;
Mattoli, Sabrina .
LABORATORY INVESTIGATION, 2007, 87 (09) :858-870