Imbalance of prostacyclin and thromboxane synthesis in Crohn's disease.
Journal: 1983/November - Gut
ISSN: 0017-5749
PUBMED: 6578172
Abstract:
Synthesis of prostanoids in Crohn's disease was investigated using rectal biopsy specimens maintained in organ culture. As with ulcerative colitis increased synthesis of prostaglandin (PG)E2 was observed when the mucosa was inflamed, compared with uninflamed mucosa in Crohn's disease, and with control biopsy specimens. In contrast with ulcerative colitis differences from control specimens were observed even in the absence of inflammation. There was a raised synthesis of thromboxane (Tx)B2 (stable breakdown product of TxA2); concentrations of 6-keto PGF1 alpha (stable breakdown product of prostacyclin) were unchanged and hence the ratio of 6-keto PGF1 alpha/TxB2 was reduced. These changes might lead to an altered cytoprotective capacity or reduced suppressor cell activity, such as has previously been reported in intestinal lymphocytes in Crohn's disease.
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Gut 24(10): 881-885

Imbalance of prostacyclin and thromboxane synthesis in Crohn's disease.

Abstract

Synthesis of prostanoids in Crohn's disease was investigated using rectal biopsy specimens maintained in organ culture. As with ulcerative colitis increased synthesis of prostaglandin (PG)E2 was observed when the mucosa was inflamed, compared with uninflamed mucosa in Crohn's disease, and with control biopsy specimens. In contrast with ulcerative colitis differences from control specimens were observed even in the absence of inflammation. There was a raised synthesis of thromboxane (Tx)B2 (stable breakdown product of TxA2); concentrations of 6-keto PGF1 alpha (stable breakdown product of prostacyclin) were unchanged and hence the ratio of 6-keto PGF1 alpha/TxB2 was reduced. These changes might lead to an altered cytoprotective capacity or reduced suppressor cell activity, such as has previously been reported in intestinal lymphocytes in Crohn's disease.

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Selected References

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  • Gould SR. Assay of prostaglandin-like substances in faeces and their measurement in ulcerative colitis. Prostaglandins. 1976 Mar;11(3):489–497. [PubMed] [Google Scholar]
  • Sharon P, Ligumsky M, Rachmilewitz D, Zor U. Role of prostaglandins in ulcerative colitis. Enhanced production during active disease and inhibition by sulfasalazine. Gastroenterology. 1978 Oct;75(4):638–640. [PubMed] [Google Scholar]
  • Hawkey CJ, Truelove SC. Effect of prednisolone on prostaglandin synthesis by rectal mucosa in ulcerative colitis: investigation by laminar flow bioassay and radioimmunoassay. Gut. 1981 Mar;22(3):190–193.[PMC free article] [PubMed] [Google Scholar]
  • Ligumsky M, Karmeli F, Sharon P, Zor U, Cohen F, Rachmilewitz D. Enhanced thromboxane A2 and prostacyclin production by cultured rectal mucosa in ulcerative colitis and its inhibition by steroids and sulfasalazine. Gastroenterology. 1981 Sep;81(3):444–449. [PubMed] [Google Scholar]
  • Moncada S, Vane JR. Pharmacology and endogenous roles of prostaglandin endoperoxides, thromboxane A2, and prostacyclin. Pharmacol Rev. 1978 Sep;30(3):293–331. [PubMed] [Google Scholar]
  • Rachmilewitz D, Ligumsky M, Haimovitz A, Treves AJ. Prostanoid synthesis by cultured peripheral blood mononuclear cells in inflammatory diseases of the bowel. Gastroenterology. 1982 Apr;82(4):673–679. [PubMed] [Google Scholar]
  • Smith PR, Dawson DJ, Swan CH. Prostaglandin synthetase activity in acute ulcerative colitis: effects of treatment with sulphasalazine, codeine phosphate and prednisolone. Gut. 1979 Sep;20(9):802–805.[PMC free article] [PubMed] [Google Scholar]
  • Hoult JR, Page H. 5-Aminosalicylic acid, a co-factor for colonic prostacyclin synthesis? Lancet. 1981 Aug 1;2(8240):255–255. [PubMed] [Google Scholar]
  • Hoult JR, Moore PK. Sulphasalazine is a potent inhibitor of prostaglandin 15-hydroxydehydrogenase: possible basis for therapeutic action in ulcerative colitis. Br J Pharmacol. 1978 Sep;64(1):6–8.[PMC free article] [PubMed] [Google Scholar]
  • Morley J, Bray MA, Jones RW, Nugteren DH, van Dorp DA. Prostaglandin and thromboxane production by human and guinea-pig macrophages and leucocytes. Prostaglandins. 1979 May;17(5):729–746. [PubMed] [Google Scholar]
  • Kelly JP, Johnson MC, Parker CW. Effect of inhibitors of arachidonic acid metabolism on mitogenesis in human lymphocytes: possible role of thromboxanes and products of the lipoxygenase pathway. J Immunol. 1979 Apr;122(4):1563–1571. [PubMed] [Google Scholar]
  • Goodacre RL, Bienenstock J. Reduced suppressor cell activity in intestinal lymphocytes from patients with Crohn's disease. Gastroenterology. 1982 Apr;82(4):653–658. [PubMed] [Google Scholar]
  • Gordon D, Bray MA, Morley J. Control of lymphokine secretion by prostaglandins. Nature. 1976 Jul 29;262(5567):401–402. [PubMed] [Google Scholar]
  • Bland PW, Richens ER, Britton DC, Lloyd JV. Isolation and purification of human large bowel mucosal lymphoid cells: effect of separation technique on functional characteristics. Gut. 1979 Dec;20(12):1037–1046.[PMC free article] [PubMed] [Google Scholar]
  • Robert A. Cytoprotection by prostaglandins. Gastroenterology. 1979 Oct;77(4 Pt 1):761–767. [PubMed] [Google Scholar]
  • Whittle BJ, Kauffman GL, Moncada S. Vasoconstriction with thromboxane A2 induces ulceration of the gastric mucosa. Nature. 1981 Jul 30;292(5822):472–474. [PubMed] [Google Scholar]
Abstract
Synthesis of prostanoids in Crohn's disease was investigated using rectal biopsy specimens maintained in organ culture. As with ulcerative colitis increased synthesis of prostaglandin (PG)E2 was observed when the mucosa was inflamed, compared with uninflamed mucosa in Crohn's disease, and with control biopsy specimens. In contrast with ulcerative colitis differences from control specimens were observed even in the absence of inflammation. There was a raised synthesis of thromboxane (Tx)B2 (stable breakdown product of TxA2); concentrations of 6-keto PGF1 alpha (stable breakdown product of prostacyclin) were unchanged and hence the ratio of 6-keto PGF1 alpha/TxB2 was reduced. These changes might lead to an altered cytoprotective capacity or reduced suppressor cell activity, such as has previously been reported in intestinal lymphocytes in Crohn's disease.
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