Sulphomucin Expression in Ileal Pouches: Emerging Differences Between Ulcerative Colitis and Familial Adenomatous Polyposis Pouches

Bambury, Niamh; Coffey, J. Calvin; Burke, John P.; Redmond, H. P.; Kirwan, W. O.

doi:10.1007/s10350-008-9200-0

Cited by 20 publications

(25 citation statements)

References 30 publications

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“…The released sulfate may then be utilized by D. desulfuricans indicating that SRB may be dependent on other intestinal bacteria to cleave and release sulfate, necessary as a metabolite 74 . Within the setting of UC an increased presence of SRB has been identified by several groups, 31 , 32 , 90 with an association between D. desulfuricans and active inflammation being demonstrated by Rowen et al 32 SRB have also been found to be exclusive to ileal pouches fashioned for UC, 91 , 92 with their presence corresponding to the expression of sulfated mucins 92 . Further studies focusing on the co-colonization rates of MDB and SRB during both active and quiescent disease are necessary in order to fully elucidate the role SRB may play in the pathogenesis of UC.…”

Section: Mucin Degrading Bacteria: Syntrophic and Antagonisticmentioning

confidence: 98%

Influences of the colonic microbiome on the mucous gel layer in ulcerative colitis

et al. 2014

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The colonic mucus gel layer (MGL) is a critical component of the innate immune system acting as a physical barrier to microbes, luminal insults, and toxins. Mucins are the major component of the MGL. Selected microbes have the potential to interact with, bind to, and metabolize mucins. The tolerance of the host to the presence of these microbes is critical to maintaining MGL homeostasis. In disease states such as ulcerative colitis (UC), both the mucosa associated microbes and the constituent MGL mucins have been shown to be altered. Evidence is accumulating that implicates the potential for mucin degrading bacteria to negatively impact the MGL and its stasis. These effects appear more pronounced in UC. This review is focused on the host-microbiome interactions within the setting of the MGL. Special focus is given to the mucolytic potential of microbes and their interactions in the setting of the colitic colon.

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Section: Mucin Degrading Bacteria: Syntrophic and Antagonisticmentioning

confidence: 98%

Influences of the colonic microbiome on the mucous gel layer in ulcerative colitis

et al. 2014

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“…10 Increased sulphomucin production has also been described in the ulcerative colitis pouch, which is more characteristic of the colon, while FAP pouches retain a more sialomucin predominant mucus layer. 11 …”

Section: Introductionmentioning

confidence: 99%

Early Transcriptomic Changes in the Ileal Pouch Provide Insight into the Molecular Pathogenesis of Pouchitis and Ulcerative Colitis

Huang

Dalal

Antonopoulos

et al. 2017

Inflammatory Bowel Diseases

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Background Ulcerative colitis (UC) only involves the colonic mucosa. Yet, nearly 50% of UC patients who undergo total proctocolectomy with ileal pouch anal anastomosis (IPAA) develop UC-like inflammation of the ileal pouch (pouchitis). In contrast, patients with familial adenomatous polyposis (FAP) with IPAA develop pouchitis far less frequently. We hypothesized that pathogenic events associated with the development of UC are recapitulated by colonic-metaplastic transcriptomic reprogramming of the UC pouch. Methods We prospectively sampled pouch and pre-pouch ileum mucosal biopsies in UC patients with IPAA 4, 8, and 12 months after their pouch was in continuity. Mucosal samples were also obtained from FAP patients. Transcriptional profiles of the UC and FAP pouch and pre-pouch ileum were investigated via RNA sequencing and compared to data from a previously published microarray study. Results Unlike FAP patients, UC subjects exhibited a large set of differentially expressed genes (DEGs) between the pouch and pre-pouch ileum as early as 4 months after pouch functionalization. Functional pathway analysis of DEGs in the UC pouch revealed an enhanced state of immune/inflammatory response and extra cellular matrix remodeling. Moreover, >70% of DEGs mapped to published IBD microarray datasets displayed directional changes consistent with active UC, but not Crohn’s disease. Conclusions The UC pouch, well before histologic inflammation, already displays a systems-level gain of colon-associated and loss of ileum-associated genes. UC patients exhibit a unique transcriptomic response to ileal pouch creation that can be observed well before disease and may in part explain their susceptibility to the development of pouchitis.

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“…79,82,86 These data suggest that the microenvironment of the ileal pouch in UC patients predisposes individuals to colonisation by specific bacterial populations, such as SRB, which can then increase the likelihood for developing pouchitis. 87 During a pouchitis episode, reduced bacterial diversity of the ileal pouch has been described, 81,82,86 that includes a reduction of the anaerobic to aerobic ratio, seen in both mucosal biopsies 81,88,89 and faecal samples. 13,82,90 In particular, an increase in the abundance of Enterobacteriaceae 81, 82 and reduced abundance of Bacteroides 82, 86 and F. prausnitzii 82 have been described.…”

Section: Dysbiosis Of Pouch Microbiotamentioning

confidence: 99%

Review article: the pathogenesis of pouchitis

Schieffer

Williams

Yochum

et al. 2016

Aliment Pharmacol Ther

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SUMMARY Background A total proctocolectomy followed by ileal pouch-anal anastomosis (IPAA) is a potentially curative surgery for ulcerative colitis (UC) or familial adenomatous polyposis (FAP). About 5-35% of UC patients and 0-11% of FAP patients develop subsequent inflammation of the ileal pouch termed pouchitis. Aim The aim of this review was to provide a comprehensive analysis of the research studying the possible pathogenesis of pouchitis. The goals were to identify promising areas of investigation, to help focus clinicians, researchers, and patients on how to better understand and then potentially manage ileal pouchitis, and to provide avenues for future research investigations. Methods This review examined manuscripts from 1981 through 2015 that discussed and/or proposed hypotheses with supportive evidence for the potential underlying pathogenic mechanism for pouchitis. Results The pathogenesis of pouchitis is not definitively understood, but various hypotheses have been proposed, including: 1) recurrence of UC, 2) dysbiosis of the ileal pouch microbiota, 3) deprivation of nutritional short chain fatty acids, 4) mucosal ischemia and oxygen free radical injury, 5) host genetic susceptibility, and 6) immune dysregulation. However, none of these alone are able to fully explain pouchitis pathogenesis. Conclusions Pouchitis, similar to IBD, is a complex disorder that is not caused by any one single factor. More likely, pouchitis occurs through a combination of both dysregulated host inflammatory mechanisms and interaction with luminal microbiota.

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Sulphomucin Expression in Ileal Pouches: Emerging Differences Between Ulcerative Colitis and Familial Adenomatous Polyposis Pouches

Abstract: Sulphomucin expression is increased in the mucous gel layer of the ulcerative colitis pouch compared with that of the familial adenomatous polyposis pouch. Sulphomucin expression is associated with colonization by sulphate-reducing bacteria and increased chronic inflammation.

Cited by 20 publications

References 30 publications

Influences of the colonic microbiome on the mucous gel layer in ulcerative colitis

Influences of the colonic microbiome on the mucous gel layer in ulcerative colitis

Early Transcriptomic Changes in the Ileal Pouch Provide Insight into the Molecular Pathogenesis of Pouchitis and Ulcerative Colitis

Review article: the pathogenesis of pouchitis

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