Skip to main content
Gut logoLink to Gut
. 1985 May;26(5):466–469. doi: 10.1136/gut.26.5.466

Faecal sulphatase in health and in inflammatory bowel disease.

J M Rhodes, R Gallimore, E Elias, J F Kennedy
PMCID: PMC1432666  PMID: 3996936

Abstract

Histochemical studies have shown a relative depletion of colonic sulphated mucins (sulphomucins) in active ulcerative colitis. One possible explanation for this could be desulphation by bacterial sulphatases. Studies have therefore been done to determine whether normal faeces contain sulphatase and if so to determine whether this activity is increased in ulcerative colitis. Using a fluorimetric assay considerable sulphatase activity (greater than 0.3 IU/g pellet weight) was found in bacteria free filtrates of the homogenates of nine of 17 faecal samples from healthy controls. This sulphatase activity had an alkaline pH optimum (pH 8.5-9.5). A similar range of faecal sulphatase activity with a similar pH optimum was found in samples from patients with ulcerative colitis (n = 39) and Crohn's disease (n = 17) and there was no correlation with disease activity in either disease. This faecal sulphatase activity may be involved in the degradation of colonic mucus and merits further study but these findings do not explain the relative depletion of colonic mucosal sulphomucins in ulcerative colitis.

Full text

PDF
468

Selected References

These references are in PubMed. This may not be the complete list of references from this article.

  1. Cowen A. E., Korman M. G., Hofmann A. F., Cass O. W. Metabolism of lethocholate in healthy man. I. Biotransformation and biliary excretion of intravenously administered lithocholate, lithocholylglycine, and their sulfates. Gastroenterology. 1975 Jul;69(1):59–66. [PubMed] [Google Scholar]
  2. De Dombal F. T., Burton I., Goligher J. C. The early and late results of surgical treatment for Crohn's disease. Br J Surg. 1971 Nov;58(11):805–816. doi: 10.1002/bjs.1800581102. [DOI] [PubMed] [Google Scholar]
  3. Ehsanullah M., Filipe M. I., Gazzard B. Mucin secretion in inflammatory bowel disease: correlation with disease activity and dysplasia. Gut. 1982 Jun;23(6):485–489. doi: 10.1136/gut.23.6.485. [DOI] [PMC free article] [PubMed] [Google Scholar]
  4. Farooqui A. A. Sulfatases, sulfate esters and their metabolic disorders. Clin Chim Acta. 1980 Jan 31;100(3):285–299. doi: 10.1016/0009-8981(80)90278-8. [DOI] [PubMed] [Google Scholar]
  5. Filipe M. I. Mucins in the human gastrointestinal epithelium: a review. Invest Cell Pathol. 1979 Jul-Sep;2(3):195–216. [PubMed] [Google Scholar]
  6. Hoskins L. C., Boulding E. T. Mucin degradation in human colon ecosystems. Evidence for the existence and role of bacterial subpopulations producing glycosidases as extracellular enzymes. J Clin Invest. 1981 Jan;67(1):163–172. doi: 10.1172/JCI110009. [DOI] [PMC free article] [PubMed] [Google Scholar]
  7. Jordan T. W., Heiss F., Monk B., Nicholls J. The 4-methylumbelliferone sulphate sulphatases of human tears. J Inherit Metab Dis. 1980;3(2):55–60. doi: 10.1007/BF02312523. [DOI] [PubMed] [Google Scholar]
  8. Lloyd A. G. The metabolism of exogenous N-acetyl-d-glucosamine 6-O[S]-sulphate in the normal rat. Biochem J. 1961 Sep;80(3):572–578. doi: 10.1042/bj0800572. [DOI] [PMC free article] [PubMed] [Google Scholar]
  9. Mian N., Anderson C. E., Kent P. W. Neuraminidase inhibition by chemically sulphated glycopeptides. Biochem J. 1979 Aug 1;181(2):377–385. doi: 10.1042/bj1810377. [DOI] [PMC free article] [PubMed] [Google Scholar]
  10. Scott T. W., Ward P. F., Dawson R. M. The formation and metabolism of phenyl-substituted fatty acids in the ruminant. Biochem J. 1964 Jan;90(1):12–24. doi: 10.1042/bj0900012. [DOI] [PMC free article] [PubMed] [Google Scholar]
  11. TRUELOVE S. C., WITTS L. J. Cortisone in ulcerative colitis; final report on a therapeutic trial. Br Med J. 1955 Oct 29;2(4947):1041–1048. doi: 10.1136/bmj.2.4947.1041. [DOI] [PMC free article] [PubMed] [Google Scholar]

Articles from Gut are provided here courtesy of BMJ Publishing Group

RESOURCES