Literature DB >> 9260327

The immune system in inflammatory bowel disease.

C Fiocchi1.   

Abstract

During the last few decades it has become increasingly evident that inflammatory bowel disease (IBD) is associated with abnormalities of systemic and mucosal immunity. This association has slowly moved from the phenomenological to the mechanistic level, and today there is solid evidence that the immune system mediates inflammation and tissue damage in the gut of patients suffering from IBD. However, the exact mechanisms of injury and what triggers such mechanisms are yet to be understood in spite of expanding knowledge of the cellular and molecular events underlying gut inflammation. Phenomena detected in the peripheral blood of IBD patients reflect some, but not all, of the events occurring in the gut and have limited meaning. On the contrary, the investigation of phenomena occurring in the inflamed mucosa has yielded valuable information on which progress in the understanding of IBD pathogenesis and the development of new therapies are currently based. It seems that all immune and non-immune components of the mucosa are involved in IBD, either directly or indirectly, as shown by abnormalities of humoral and cell-mediated immunity, cytokine and growth factor, eicosanoids, neuropeptides, reactive oxygen and nitrogen metabolises, cell adhesion molecules, apoptosis, and non-immune cells. Because of the multiplicity and complexity of the interactions of all these elements it is presently impossible to discern between primary and secondary, and pathogenic and non-pathogenic phenomena. In spite of these difficulties, an impressive amount of information is being gathered which is translated, at times in a preliminary or empirical fashion, into novel immunopathology-based forms of treatment.

Entities:  

Mesh:

Substances:

Year:  1997        PMID: 9260327

Source DB:  PubMed          Journal:  Acta Gastroenterol Belg        ISSN: 1784-3227            Impact factor:   1.316


  6 in total

Review 1.  Anti-TNF antibody treatment of Crohn's disease.

Authors:  S J van Deventer
Journal:  Ann Rheum Dis       Date:  1999-11       Impact factor: 19.103

2.  Inflammatory bowel disease: definition, epidemiology, etiologic aspects, and immunogenetic studies.

Authors:  Bing Xia; JBA Crusius; SGM Meuwissen; AS Pe?a
Journal:  World J Gastroenterol       Date:  1998-10       Impact factor: 5.742

3.  Distal proctocolitis and n-3 polyunsaturated fatty acids (n-3 PUFAs): the mucosal effect in situ.

Authors:  Y Z Almallah; S W Ewen; A El-Tahir; N A Mowat; P W Brunt; T S Sinclair; S D Heys; O Eremin
Journal:  J Clin Immunol       Date:  2000-01       Impact factor: 8.317

4.  Inhibition of Pim-1 kinase ameliorates dextran sodium sulfate-induced colitis in mice.

Authors:  Yue-Ming Shen; Yan Zhao; Ya Zeng; Lu Yan; Bo-Lin Chen; Ai-Min Leng; Yi-Bin Mu; Gui-Ying Zhang
Journal:  Dig Dis Sci       Date:  2012-04-01       Impact factor: 3.199

5.  Pectolinarigenin Suppresses LPS-Induced Inflammatory Response in Macrophages and Attenuates DSS-Induced Colitis by Modulating the NF-κB/Nrf2 Signaling Pathway.

Authors:  Yuling Feng; Ramesh Bhandari; Imran Ibrahim Shaikh; Chunmeng Li; Pengfei Shu
Journal:  Inflammation       Date:  2022-08-06       Impact factor: 4.657

6.  Immunological alteration and changes of gut microbiota after dextran sulfate sodium (DSS) administration in mice.

Authors:  Å Håkansson; N Tormo-Badia; A Baridi; J Xu; G Molin; M-L Hagslätt; C Karlsson; B Jeppsson; C M Cilio; S Ahrné
Journal:  Clin Exp Med       Date:  2014-01-11       Impact factor: 3.984

  6 in total

北京卡尤迪生物科技股份有限公司 © 2022-2023.