Purified Shigella enterotoxin does not alter intestinal motility.
Journal: 1984/March - Infection and Immunity
ISSN: 0019-9567
PUBMED: 6363286
Abstract:
A purified Shigella enterotoxin (pST) and a cell-free lysate with pST removed (CFL-pST) from the whole-cell lysate of Shigella dysenteriae 60 R were used to study their effect on the myoelectric activity and mucosal integrity of rabbit ileal segments. We have previously defined two myoelectric patterns: the migrating action potential complex and repetitive bursts of action potentials that occur in response to certain bacteria and their enterotoxins. The in vivo model consisted of isolated ileal segments in male New Zealand White rabbits. The segments were infused with sterile saline (1 ml/h), pST (2.4-micrograms injection), or CFL-pST (1 ml/h). Myoelectric activity in the segments exposed to pST was similar to that with the saline infusion, but CFL-pST induced significant alterations in myoelectric activity in the form of repetitive bursts of action potentials. The mucosa of the segments exposed to pST showed only mild inflammatory changes. In contrast, CFL-pST caused moderate to severe inflammatory changes with enterocyte necrosis. These studies show that pST, a known enterotoxin, did not alter myoelectric activity and had no significant effect on the integrity of ileal mucosa, as determined by light microscopy. CFL-pST caused both inflammation and tissue necrosis with significant alterations in motor activity. These studies suggest that S. dysenteriae 60 R produces a substance or substances other than pST that cause florid in vivo cytotoxicity and alter myoelectric activity.
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Infect Immun 43(2): 477-481

Purified Shigella enterotoxin does not alter intestinal motility.

Abstract

A purified Shigella enterotoxin (pST) and a cell-free lysate with pST removed (CFL-pST) from the whole-cell lysate of Shigella dysenteriae 60 R were used to study their effect on the myoelectric activity and mucosal integrity of rabbit ileal segments. We have previously defined two myoelectric patterns: the migrating action potential complex and repetitive bursts of action potentials that occur in response to certain bacteria and their enterotoxins. The in vivo model consisted of isolated ileal segments in male New Zealand White rabbits. The segments were infused with sterile saline (1 ml/h), pST (2.4-micrograms injection), or CFL-pST (1 ml/h). Myoelectric activity in the segments exposed to pST was similar to that with the saline infusion, but CFL-pST induced significant alterations in myoelectric activity in the form of repetitive bursts of action potentials. The mucosa of the segments exposed to pST showed only mild inflammatory changes. In contrast, CFL-pST caused moderate to severe inflammatory changes with enterocyte necrosis. These studies show that pST, a known enterotoxin, did not alter myoelectric activity and had no significant effect on the integrity of ileal mucosa, as determined by light microscopy. CFL-pST caused both inflammation and tissue necrosis with significant alterations in motor activity. These studies suggest that S. dysenteriae 60 R produces a substance or substances other than pST that cause florid in vivo cytotoxicity and alter myoelectric activity.

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Selected References

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  • Burns TW, Mathias JR, Martin JL, Carlson GM, Shields RP. Alteration of myoelectric activity of small intestine by invasive Escherichia coli. Am J Physiol. 1980 Jan;238(1):G57–G62. [PubMed] [Google Scholar]
  • Cassuto J, Jodal M, Tuttle R, Lundgren O. On the role of intramural nerves in the pathogenesis of cholera toxin-induced intestinal secretion. Scand J Gastroenterol. 1981 Apr;16(3):377–384. [PubMed] [Google Scholar]
  • Cassuto J, Jodal M, Tuttle R, Lundgren O. 5-hydroxytryptamine and cholera secretion. Physiological and pharmacological studies in cats and rats. Scand J Gastroenterol. 1982 Aug;17(5):695–703. [PubMed] [Google Scholar]
  • Cuatrecasas P. Interaction of Vibrio cholerae enterotoxin with cell membranes. Biochemistry. 1973 Aug 28;12(18):3547–3558. [PubMed] [Google Scholar]
  • Finkelstein RA, Boesman M, Neoh SH, LaRue MK, Delaney R. Dissociation and recombination of the subunits of the cholera enterotoxin (choleragen). J Immunol. 1974 Jul;113(1):145–150. [PubMed] [Google Scholar]
  • Holmgren J, Lönnroth I, Svennerholm L. Fixation and inactivation of cholera toxin by GM1 ganglioside. Scand J Infect Dis. 1973;5(1):77–78. [PubMed] [Google Scholar]
  • Hubel KA. Intestinal ion transport: effect of norepinephrine, pilocarpine, and atropine. Am J Physiol. 1976 Jul;231(1):252–257. [PubMed] [Google Scholar]
  • Juorio AV, Gabella G. Noradrenaline in the guinea pig alimentary canal: regional distribution and sensitivity to denervation and reserpine. J Neurochem. 1974 May;22(5):851–858. [PubMed] [Google Scholar]
  • Justus PG, Martin JL, Goldberg DA, Taylor NS, Bartlett JG, Alexander RW, Mathias JR. Myoelectric effects of Clostridium difficile: motility-altering factors distinct from its cytotoxin and enterotoxin in rabbits. Gastroenterology. 1982 Oct;83(4):836–843. [PubMed] [Google Scholar]
  • Keusch GT, Grady GF, Mata LJ, McIver J. The pathogenesis of Shigella diarrhea. I. Enterotoxin production by Shigella dysenteriae I. J Clin Invest. 1972 May;51(5):1212–1218.[PMC free article] [PubMed] [Google Scholar]
  • Kimberg DV, Field M, Gershon E, Henderson A. Effects of prostaglandins and cholera enterotoxin on intestinal mucosal cyclic AMP accumulation. Evidence against an essential role for prostaglandins in the action of toxin. J Clin Invest. 1974 Mar;53(3):941–949.[PMC free article] [PubMed] [Google Scholar]
  • Koch KL, Martin JL, Mathias JR. Migrating action-potential complexes in vitro in cholera-exposed rabbit ileum. Am J Physiol. 1983 Mar;244(3):G291–G294. [PubMed] [Google Scholar]
  • Rifkind D, Frey JA, Petersen EA, Dinowitz M. Delayed hypersensitivity to fungal antigens in mice. II. Molecular classes in immunogenic RNA extracts that transfer delayed hypersensitivity. J Infect Dis. 1976 May;133(5):523–532. [PubMed] [Google Scholar]
  • Mathias JR, Carlson GM, DiMarino AJ, Bertiger G, Morton HE, Cohen S. Intestinal myoelectric activity in response to live Vibrio cholerae and cholera enterotoxin. J Clin Invest. 1976 Jul;58(1):91–96.[PMC free article] [PubMed] [Google Scholar]
  • Mathias JR, Carlson GM, Martin JL, Shields RP, Formal S. Shigella dysenteriae I enterotoxin: proposed role in pathogenesis of shigellosis. Am J Physiol. 1980 Nov;239(5):G382–G386. [PubMed] [Google Scholar]
  • Mathias JR, Martin JL, Burns TW, Carlson GM, Shields RP. Ricinoleic acid effect on the electrical activity of the small intestine in rabbits. J Clin Invest. 1978 Mar;61(3):640–644.[PMC free article] [PubMed] [Google Scholar]
  • McGowan K, Kane A, Asarkof N, Wicks J, Guerina V, Kellum J, Baron S, Gintzler AR, Donowitz M. Entamoeba histolytica causes intestinal secretion: role of serotonin. Science. 1983 Aug 19;221(4612):762–764. [PubMed] [Google Scholar]
  • O'Brien AD, LaVeck GD, Griffin DE, Thompson MR. Characterization of Shigella dysenteriae 1 (Shiga) toxin purified by anti-Shiga toxin affinity chromatography. Infect Immun. 1980 Oct;30(1):170–179.[PMC free article] [PubMed] [Google Scholar]
  • Sinar DR, Charles LG, Burns TW. Migrating action-potential complex activity in absence of fluid production is produced by B subunit of cholera enterotoxin. Am J Physiol. 1982 Jan;242(1):G47–G51. [PubMed] [Google Scholar]
  • Thompson MR, Steinberg MS, Gemski P, Formal SB, Doctor BP. Inhibition of in vitro protein synthesis by Shigella dysenteriae 1 toxin. Biochem Biophys Res Commun. 1976 Aug 9;71(3):783–788. [PubMed] [Google Scholar]
  • VICARI G, OLITZKI AL, OLITZKI Z. The action of the thermolabile toxin of Shigella dysenteriae on cells cultivated in vitro. Br J Exp Pathol. 1960 Apr;41:179–189.[PMC free article] [PubMed] [Google Scholar]
Abstract
A purified Shigella enterotoxin (pST) and a cell-free lysate with pST removed (CFL-pST) from the whole-cell lysate of Shigella dysenteriae 60 R were used to study their effect on the myoelectric activity and mucosal integrity of rabbit ileal segments. We have previously defined two myoelectric patterns: the migrating action potential complex and repetitive bursts of action potentials that occur in response to certain bacteria and their enterotoxins. The in vivo model consisted of isolated ileal segments in male New Zealand White rabbits. The segments were infused with sterile saline (1 ml/h), pST (2.4-micrograms injection), or CFL-pST (1 ml/h). Myoelectric activity in the segments exposed to pST was similar to that with the saline infusion, but CFL-pST induced significant alterations in myoelectric activity in the form of repetitive bursts of action potentials. The mucosa of the segments exposed to pST showed only mild inflammatory changes. In contrast, CFL-pST caused moderate to severe inflammatory changes with enterocyte necrosis. These studies show that pST, a known enterotoxin, did not alter myoelectric activity and had no significant effect on the integrity of ileal mucosa, as determined by light microscopy. CFL-pST caused both inflammation and tissue necrosis with significant alterations in motor activity. These studies suggest that S. dysenteriae 60 R produces a substance or substances other than pST that cause florid in vivo cytotoxicity and alter myoelectric activity.
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