Mechanisms of diarrhea in collagenous colitis

Buergel, N.S.; Bojarski, Christian; Mankertz, Joachim; Stockmann, Martin; Amasheh, Salah; Fromm, Michael; Schulzke, Joerg D.

doi:10.1016/s0016-5085(01)80195-5

Cited by 26 publications

(45 citation statements)

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“…Distinct Expression Patterns of Claudin-7, -8, -12, -13, and -15 mRNAs Along the Mouse Intestinal Tract Because claudins 1 to 5 are known to be expressed in the intestine (Rahner et al 2001;Bü rgel et al 2002;Tamagawa et al 2003), we first determined, by RT-PCR analysis, mRNA levels of other claudins throughout the mouse intestinal tract. For these experiments, gene expression of claudins in the kidney, testis, bladder, or stomach was analyzed as a positive control (Gow et al 1999;Niimi et al 2001;Kiuchi-Saishin et al 2002;Acharya et al 2004;Luk et al 2004).…”

Section: Resultsmentioning

confidence: 99%

“…Furthermore, we have revealed that claudin-13 and -15 exhibit gradients along the crypt-surface axis of the colon, and that claudin-7 is very weakly expressed in Brunner's glands of the duodenum compared with the villous epithelium. Taken together with the expression profile of claudins 1 to 5 in the intestine (Rahner et al 2001;Bü rgel et al 2002;Tamagawa et al 2003), the heterogeneity in expression of claudin-7, -8, -12, -13, and -15 might determine differences in paracellular permeable properties such as ion selectivity in each segment of the intestinal tract. Our findings are of great interest for studying the contributions of claudins to gastrointestinal diseases, including IBD and colorectal cancers.…”

Section: Discussionmentioning

confidence: 99%

“…Among claudin family members, claudins 2 to 5 and 2 to 4 are reported to be expressed in the rat and mouse intestine, respectively (Rahner et al 2001;Tamagawa et al 2003), and expression of claudin-1, -3, -4, and -5 is observed in the human intestine (Bü rgel et al 2002). There are also variations in the expression levels and subcellular localization of these claudins throughout the segments of the intestinal tract and/or along the crypt-to-villus axis (Rahner et al 2001;Tamagawa et al 2003).…”

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confidence: 99%

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Differential Expression and Subcellular Localization of Claudin-7, −8, −12, −13, and −15 Along the Mouse Intestine

Fujita

Chiba

Yokozaki

et al. 2006

J Histochem Cytochem.

215

172

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(HY) S U M M A R Y Among tight-junction proteins, claudins, which play a key role in paracellular transport across epithelia, claudins 1 to 5 are expressed in the intestine, and changes in their abundance and/or distribution are considered to contribute to various gastrointestinal diseases. We investigated, by reverse transcription-PCR, immunoblot, and immunofluorescence analyses, which other claudin species were expressed in the mouse intestine, and whether they showed unique expression profiles. Rabbit polyclonal antibodies against mouse claudin-8, claudin-12, and claudin-15 were generated, and their specificity was verified by immunoblotting using COS-7 cells transfected with individual claudin cDNAs. Claudin-7, -8, -12, -13, and -15 appeared to be expressed in the duodenum, jejunum, ileum, and/or colon with remarkable variations in the expression levels along the intestinal tract, and had distinct subcellular localization in the intestinal epithelium. In addition, claudin-13 and -15 exhibited gradients along the crypt-surface axis of the colon. By contrast,

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Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

See 1 more Smart Citation

Differential Expression and Subcellular Localization of Claudin-7, −8, −12, −13, and −15 Along the Mouse Intestine

Fujita

Chiba

Yokozaki

et al. 2006

J Histochem Cytochem.

215

172

View full text Add to dashboard Cite

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“…In contrast to ulcerative colitis and CD, the apoptotic rate was not elevated in collagenous colitis. 3 In order to investigate which size of molecule becomes permeant after apoptosis induction, epithelial apoptosis was upregulated by the topoisomerase-1 inhibitor, camptothecin. The increase in overall conductivity was caused by increases in the number as well as the mean conductance associated with single apoptoses.…”

Section: Discussionmentioning

confidence: 99%

Disrupted Barrier Function through Epithelial Cell Apoptosis

Schulzke

Bojarski

Zeißig

et al. 2006

Annals of the New York Academy of Sciences

164

106

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Epithelial barrier function is determined by trans- and paracellular permeabilities, the latter of which is mainly influenced by tight junctions (TJs) and apoptotic leaks within the epithelium. The present article aims to present experimental evidence for a functional role of epithelial apoptoses by means of cell culture models as well as in tissues from patients with inflammatory bowel disease. It is shown that epithelial apoptoses are sites of elevated conductance within the intestinal epithelium and that proinflammatory cytokines like TNF-alpha upregulate both the apoptotic rate and single apoptotic conductivity, making cytokine-induced apoptosis functionally far more relevant than is spontaneous apoptosis. In ulcerative colitis and Crohn's disease (CD), but not in collagenous colitis, apoptotic rates are increased to about 5%, in mild-to-moderately inflamed colon specimens, where as the control apoptotic rate is about 2%. Thus, epithelial apoptoses lead to a loss of ions and water into the intestinal lumen, causing leak flux diarrhea and enabling small antigens of <4,000 Da in the intestinal lumen to enter the intestinal mucosa, thereby perpetuating inflammatory responses. In addition to TNF-alpha, interleukin (IL)-13 is an important inductor of epithelial apoptosis in Th2 immune responses. Therapeutically,TNF-alpha-antibodies (infliximab) can restore barrier function in Crohn's disease by downregulating epithelial apoptoses, while epithelial TJs are unaffected.

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“…[52][53][54] The role of proinflammatory cytokines was first demonstrated in the setting of inflammatory bowel disorders (IBDs). 36 A major clinical manifestation of IBDs is chronic and relapsing diarrhoea, 55 however more importantly, IBDs are characterized by elevated proinflammatory cytokines and poor tight junction integrity. 36 Intestinal sections are characterized by reduced tight junction strand formation, strand breaks and altered to tight junction protein expression and distribution.…”

Section: Chemotherapy Disrupts Mucosal Barrier Function and Intestinamentioning

confidence: 99%

TLR4/PKC‐mediated tight junction modulation: A clinical marker of chemotherapy‐induced gut toxicity?

Wardill

Gibson

Logan

et al. 2014

Intl Journal of Cancer

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Chemotherapy‐induced gut toxicity is a major clinical and economic burden to oncology practice. The mechanisms responsible for its development are ill defined, hampering the development of therapeutic interventions. In light of newly published research foci and clinical practice guidelines in supportive care in cancer, there has been renewed interest in the role tight junctions play in the pathobiology of chemotherapy‐induced gut toxicity. Several preclinical studies have identified molecular defects in intestinal tight junctions following chemotherapy. Despite these findings, the mechanisms responsible for chemotherapy‐induced tight junction disruption remain unclear. Recent research has highlighted roles for toll‐like receptor 4 and protein kinase C signalling in the regulation of tight junctions. This critical review therefore aims to provide evidence linking toll‐like receptor 4 expression, protein kinase C activation and tight junction disruption and their relationship to clinical toxicity.

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Mechanisms of diarrhea in collagenous colitis

Cited by 26 publications

References 0 publications

Differential Expression and Subcellular Localization of Claudin-7, −8, −12, −13, and −15 Along the Mouse Intestine

Differential Expression and Subcellular Localization of Claudin-7, −8, −12, −13, and −15 Along the Mouse Intestine

Disrupted Barrier Function through Epithelial Cell Apoptosis

TLR4/PKC‐mediated tight junction modulation: A clinical marker of chemotherapy‐induced gut toxicity?

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