Cytokines in Crohn's colitis

Sher, Marc E.; D’Angelo, Anthony J.; Stein, Theodore A.; Bailey, Beverly; Burns, Gerard P.; Wise, Leslie

doi:10.1016/s0002-9610(99)80121-4

Cited by 35 publications

(19 citation statements)

References 19 publications

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“…15,34 These studies were recently con rmed by Patel et al and Sher et al, who also reported elevated levels of IL-8 in non-in amed tissue from ileoanal pouches and CD. 14,30 The role of IL-1 and TNFa in regulating IL-8 in colitis was demonstrated by Cominelli's group in the study referred to above. 16 They found that an inhibitor of the synthesis of IL-1 and TNFa (CGP 47969A) reduced the severity of damage in a rabbit model of colitis and this reduction of damage was associated with decreased colonic IL-1 and IL-8 levels.…”

Section: Pro-in¯ammatory Cytokinesmentioning

confidence: 93%

“…29 Previous studies noted elevations of IL-6 in both CD and UC and more recently in pouchitis. 3,14,15,30 Serum levels of IL-6 and soluble IL-6 receptor as well as tissue levels of IL-6 appear to correlate well with disease activity in both CD and UC. 31,32 Recently, a group from Belgium found that serum IL-6 levels in patients with inactive CD, followed for one year, correctly predicted whether a patient would relapse in 29 of 32 cases.…”

Section: Pro-in¯ammatory Cytokinesmentioning

confidence: 98%

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Cytokines in inflammatory bowel disease

Beck

Wallace

1997

Mediators of Inflammation

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Over the past decade, much has been learned regarding the role of various cytokines in the pathogenesis of inflammatory bowel disease. Several cytokine ‘knockout’ models in mice have been shown to develop colitis, while alterations in the production of various cytokines has been documented in human Crohn's disease and ulcerative colitis. In recent years, attempts have been made to treat these diseases through modulation of cytokine production or action. This review focuses on the cytokines that have been implicated in the pathogenesis of inflammatory bowel disease. The evidence for and against a role for particular cytokines in intestinal inflammation is reviewed, as is the experimental and clinical data suggesting that cytokines are rational targets for the development of new therapies.

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Section: Pro-in¯ammatory Cytokinesmentioning

confidence: 93%

Section: Pro-in¯ammatory Cytokinesmentioning

confidence: 98%

Cytokines in inflammatory bowel disease

Beck

Wallace

1997

Mediators of Inflammation

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“…Although there are plenty of causes for diarrhea in IBD (such as malabsorption, infections, or iatrogenic), the effects of inflammation on ion intestinal transport and smooth muscle tone are the most important ones (142). The effectors are endogenous inflammatory mediators found in high concentrations in CD and/or UC, such as TNF-␣, IL-1␤, IL-6, IFN-␥, monochloramine (NH 2 Cl), and nitric oxide (NO), and also pathogen-associated molecular patterns from gut microbiota (12,19,26,32,104,124). Thus a comprehensive understanding of the epithelial hydroelectrolytic disequilibrium is of utmost relevance to develop better treatments.…”

mentioning

confidence: 99%

Role of epithelial ion transports in inflammatory bowel disease

Magalhães

Cabral

Soares‐da‐Silva

et al. 2016

American Journal of Physiology-Gastrointestinal and Liver Physi

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Inflammatory bowel disease (IBD) is a chronic inflammatory disorder with a complex pathogenesis. Diarrhea is a highly prevalent and often debilitating symptom of IBD patients that results, at least in part, from an intestinal hydroelectrolytic imbalance. Evidence suggests that reduced electrolyte absorption is more relevant than increased secretion to this disequilibrium. This systematic review analyses and integrates the current evidence on the roles of epithelial Na+-K+-ATPase (NKA), Na+/H+ exchangers (NHEs), epithelial Na+ channels (ENaC), and K+ channels (KC) in IBD-associated diarrhea. NKA is the key driving force of the transepithelial ionic transport and its activity is decreased in IBD. In addition, the downregulation of apical NHE and ENaC and the upregulation of apical large-conductance KC all contribute to the IBD-associated diarrhea by lowering sodium absorption and/or increasing potassium secretion.

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“…Immunological studies are dominated by cytokines, chemokines and other soluble factors, and have shown how different anti-infl ammatory and pro-infl ammatory mediators are improperly regulated and how immune imbalance can be restored. In Crohn's disease, pro-infl ammatory cytokines and chemokines such as IL-1beta and IL-8 are to some degree up-regulated even in clinically uninvolved segments (Sher et al, 1995;Daig et al, 1996). Immunological abnormalities may also be involved in the upper gastrointestinal lesions of Crohn's disease.…”

Section: Mucosal Proinfl Ammatory Cytokine and Chemokine Expression Imentioning

confidence: 99%

Abnormalities in the upper gastrointestinal tract in inflammatory bowel disease

et al. 2007

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The predominant histopathologic feature of inflammatory bowel disease is the infiltration of acute and chronic inflammatory cells, including polymorphonuclear neutrophils, macrophages and lymphocytes, in the affected intestine. Helicobacter pylori is recognized as the most common cause of upper gastrointestinal lesions, and Helicobacter pylori-associated gastritis is characterized by increased numbers of acute and chronic inflammatory cells. The pathogenesis of inflammatory bowel disease or Helicobacter pylori-associated gastritis involves immunological abnormalities, including the deficient or excessive expression of cytokines. The chronic inflammatory process in patients with Crohn's disease may affect any part of the gastrointestinal tract, whereas ulcerative colitis affects mainly the colon and rectum. Here, we discuss abnormalities in the upper gastrointestinal tract in inflammatory bowel disease. Although the prevalence rate of Helicobacter pylori infection is low in Crohn's disease, these patients often have abnormalities in the upper gastrointestinal tract.

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Cytokines in Crohn's colitis

Cited by 35 publications

References 19 publications

Cytokines in inflammatory bowel disease

Cytokines in inflammatory bowel disease

Role of epithelial ion transports in inflammatory bowel disease

Abnormalities in the upper gastrointestinal tract in inflammatory bowel disease

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