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Cholera toxin-induced fluid secretion in rat gut ligated loops: influence of bile from normal or cholera
P G Pierre1, P Solbreux, J P Vaerman
1Catholic University of Louvain, International Institute of Cellular and Molecular Pathology, Brussels, Belgium.
Fresh normal rat bile premixed with cholera toxin (CT) did not significantly affect the CT-induced fluid accumulation in rat jejunal ligated loops. Bile from rats intrajejunally (i.j.) immunized three times with CT definitely inhibited CT-induced fluid secretion. Bile duct ligature (BDL) for 1-4 days in unimmunized rats, in contrast with mice, did not significantly affect subsequent CT-elicited fluid secretion in their ligated loops. BDL for 4 days in rats i.j. immunized with CT, only slightly decreased the CT-neutralizing ability of their gut loops. Passive transfer during 24 hr of bile from i.j.-immunized rats, but not from normal rats, into gut of normal recipient rats with BDL, significantly protected loops made in such recipients. The affinity-purified antibodies of immune bile, mixed with CT, neutralized its effect. Our data show that, unlike mice, rat bile acids are not required for expression of the CT effect in gut loops. In addition, bile from i.j.-immunized rats contains enough anti-CT antibodies to be protective on its own, but is not necessary for substantial gut protection against CT in i.j.-immunized BDL rats. Our results confirm a major and complementary role of both biliary and intestinal secretory IgA antibodies in protection of the rat gut mucosa against CT-induced fluid secretion.
Fresh normal rat bile premixed with cholera toxin (CT) did not significantly affect the CT-induced fluid accumulation in rat jejunal ligated loops. Bile from rats intrajejunally (i.j.) immunized three times with CT definitely inhibited CT-induced fluid secretion. Bile duct ligature (BDL) for 1-4 days in unimmunized rats, in contrast with mice, did not significantly affect subsequent CT-elicited fluid secretion in their ligated loops. BDL for 4 days in rats i.j. immunized with CT, only slightly decreased the CT-neutralizing ability of their gut loops. Passive transfer during 24 hr of bile from i.j.-immunized rats, but not from normal rats, into gut of normal recipient rats with BDL, significantly protected loops made in such recipients. The affinity-purified antibodies of immune bile, mixed with CT, neutralized its effect. Our data show that, unlike mice, rat bile acids are not required for expression of the CT effect in gut loops. In addition, bile from i.j.-immunized rats contains enough anti-CT antibodies to be protective on its own, but is not necessary for substantial gut protection against CT in i.j.-immunized BDL rats. Our results confirm a major and complementary role of both biliary and intestinal secretory IgA antibodies in protection of the rat gut mucosa against CT-induced fluid secretion.
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