Tissue cytokine and chemokine expression in inflammatory bowel disease

McCormack, G; Moriarty, D. C.; O’Donoghue, D.; McCormick, PA; Sheahan, Kieran; Baird, Alan W.

doi:10.1007/pl00000223

Cited by 161 publications

(121 citation statements)

References 30 publications

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“…Impairment of epithelial barrier function is a typical phenomenon observed in the intestinal mucosa of inflammatory bowel disease (IBD) patients. An accumulation of polymorphic mononuclear cells at sites of inflammation, changes in cytokine levels (Andus et al, 1991;McCormack et al, 2001;Nikolaus et al, 1998) and increased rates of epithelial apoptosis (Anderson, 2000;Iwamoto et al, 1996;Levine, 2000;Sträter et al, 1997) were found to be associated with an increased permeability of the intestinal barrier. In human HT-29/B6 cells, increased cytokine levels resulted in a decrease in the transepithelial resistance and altered tight junction strand formation (Schmitz et al, 1999a).…”

Section: Discussionmentioning

confidence: 99%

The specific fates of tight junction proteins in apoptotic epithelial cells

Bojarski

Weiske

Schöneberg³

et al. 2004

Journal of Cell Science

153

129

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The polarized morphology of epithelial cells depends on the establishment and maintenance of characteristic intercellular junctions. The dramatic morphological changes observed in apoptotic epithelial cells were ascribed at least in part to the specific fragmentation of components of adherens junctions and desmosomes. Little, however, is known about tight junctions during apoptosis. We have found that after induction of apoptosis in epithelial cells, tight junction proteins undergo proteolytic cleavage in a distinctive manner correlated with a disruption of tight junctions. The transmembrane protein occludin and, likewise, the cytoplasmic adaptor proteins ZO-1 and ZO-2 are fragmented by caspase cleavage. In addition, occludin is cleaved at an extracellular site by a metalloproteinase. The caspase cleavage site in occludin was mapped C-terminally to Asp320 within the C-terminal cytoplasmic domain. Mutagenesis of this site efficiently blocked fragmentation. In the presence of caspase and/or metalloproteinase inhibitors, fragmentation of occludin, ZO-1 and ZO-2 was blocked and cellular morphology was almost fully preserved. Interestingly, two members of the claudin family of transmembrane tight junction proteins exhibited a different behavior. While the amount of claudin-2 protein was reduced similarly to occludin, ZO-1 and ZO-2, claudin-1 was either fully preserved or was even increased in apoptotic cells.

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Section: Discussionmentioning

confidence: 99%

The specific fates of tight junction proteins in apoptotic epithelial cells

Bojarski

Weiske

Schöneberg³

et al. 2004

Journal of Cell Science

153

129

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“…Humans with Crohn's disease and inflammatory bowel disease have been shown to express CCL5 in intestinal lesions and in homogenates from surgical specimens [28,29]. CCL5 also is reported to play a role in the induction of oral tolerance [30,31], suggesting a possible regulatory role during inflammation under normal conditions.…”

Section: Discussionmentioning

confidence: 99%

Selective upregulation of immune regulatory and effector cytokine synthesis by intestinal intraepithelial lymphocytes following CD43 costimulation

Montufar-Solis¹,

Garza²,

Klein³

2005

Biochemical and Biophysical Research Communications

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The involvement of the CD43 molecule in the activation of mouse small intestinal intraepithelial lymphocytes (IELs) has been studied using a panel of twenty-two regulatory and effector immune response analytes. In the absence of stimulation in vitro, IELs produced low levels of CCL5 only. Upon CD3 stimulation, the activity of seven of twenty-two analytes were elevated relative to unstimulated cultures, including several proinflammatory cytokines and chemokines. Notably, CD3 stimulation in the presence of CD43 costimulation resulted in elevated levels of five analytes (interleukin-2, interferon-γ, CCL5, granulocyte colony-stimulating factor, and granulocytemonocyte colony stimulating factor) above that produced by CD3 stimulation alone. That CD43 costimulation was responsible for elevated cytokine/chemokine activity was confirmed at the transcriptional level by real-time PCR for IFN-γ and CCL5, and by ELISA assay for IFN-γ. These findings open the way to a better understanding of the process by which T cells are activated in the intestinal epithelium.

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“…Total colonic mucosa of patients with UC (13,14) and a lower plasma concentration of the RANTES chemokine following 5-ASA medication in patients with IBD suggests that this chemokine may play a significant role in the pathogenesis of IBD (15).…”

Section: Rantes Genotype N or (95% Ci) Or (95% Ci) -----------------mentioning

confidence: 99%

“…Previous studies have reported that the expression of RANTES is enhanced in the colonic mucosa of patients with UC (13,14). In addition, it was reported that treatment with 5-aminosalicylic acid (ASA) medication in IBD patients resulted in a lower plasma concentration of RANTES, indicating that this is a beneficial product of 5-ASA treatment (15 (19,20).…”

Section: Introductionmentioning

confidence: 99%

Effect of RANTES gene promoter genotypes in patients with ulcerative colitis

et al. 2014

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Abstract.A complex interaction of genetic and environmental factors is closely associated with the development of inflammatory bowel disease. Previous studies reported that the expression of the regulated upon activation, normal T-cell expressed and secreted (RANTES) gene is enhanced in the colonic mucosa of ulcerative colitis (UC). Quantitative differences in RANTES gene expression among numerous promoter genotypes have also been reported. The aim of the present study was to clarify the effect of RANTES promoter polymorphism on the risk of UC, including its clinical phenotypes. A total of 150 UC patients and 372 healthy control (HC) subjects participated in the study. The UC patients were classified by disease behavior, severity and extent of disease. Restriction fragment length polymorphism analysis was performed for polymorphisms at -28 C/G in the RANTES gene promoter region. Although no significant difference of the RANTES promoter genotype distribution was observed between the HC and UC groups, the G/G genotype was significantly higher among female (OR=3.95, 95% CI=1.22-12.82, P=0.03), non-steroid dependent (OR=3.37, 95% CI=1.16-9.85, P= 0.03) and non-refractory (OR=3.76, 95% CI=1.29-10.98, P=0.02) UC patients. The G carrier was also found to be associated with an increased risk of rectal colitis (OR=2.21, 95% CI=1.12-4.39, P= 0.03). The data indicate that the polymorphism of the RANTES promoter is not directly associated with the susceptibility to UC, but the -28 G allele is associated with female UC patients and mild clinical phenotypes of UC, including non-steroid dependency, non-refractory and rectal colitis.

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Tissue cytokine and chemokine expression in inflammatory bowel disease

Abstract: Chemokines, together with key cytokines that promote their release are elevated in mucosal tissues from patients with IBD. It is likely that these chemokines play an important role in the perpetuation of tissue destructive inflammatory processes.

Cited by 161 publications

References 30 publications

The specific fates of tight junction proteins in apoptotic epithelial cells

The specific fates of tight junction proteins in apoptotic epithelial cells

Selective upregulation of immune regulatory and effector cytokine synthesis by intestinal intraepithelial lymphocytes following CD43 costimulation

Effect of RANTES gene promoter genotypes in patients with ulcerative colitis

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