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Biomedical subjects

C C Carpenter

Publications and source records attributed to C C Carpenter.

At least 73 records · Page 4Linked to original sources

Secretory IgA against enterotoxins in breast-milk.

A pool of colostrum from Guatemalan mothers (Guatemalan colostrum)) obtained 2-4 days post partum inhibited the induced fluid accumulation in rabbit ileal loops when incubated with Vibrio cholerae or Escherichia coli enterotoxin. There was a linear relationship between the quantity of colostrum used and the protection achieved. Pools of Guatemalan breast-milk obtained 15-30 days post partum and North American breast-milk had the same effect when tested with E. coli and V. cholerae enterotoxins, respectively. The antitoxic activity of a given pool correlated with its IgA content but not with the concentration of IgG or IgM. Guatemalan colostrum globulins were precipitated by ammonium sulphate. The globulins were filtered through a 'Biogel A5' column and fractions obtained. When tested in rabbit ileal loops the antienterotoxin activity in these fractions closely paralleled their IgA but not their detectable IgG or IgM content. We hypothesise that IgA antibody to enterotoxin, present in breast-milk of normal mothers, is probably a manifestation of natural immunity. The passive transfer of these antibodies to the infant may explain why breast-milk prevents E. coli diarrhoea in the neonate.

Animals↗

Diarrheagenic effect of volume expansion: intestinal fluid secretion without mucosal adenyl cyclase stimulation.

Rapid intravenous saline infusion causes secretion of isotonic fluid by the canine duodenum. The duodenal fluid secretion is not accompanied either by increased adenyl cyclase activity in the mucosal epithelial cells or by widening of the "tight junctions" between epithelial cells. These data clearly indicate that the diarrheagenic effect of volume expansion is not mediated by the adenyl cyclase system. Furthermore, these data provide support for the concept that, when increased mucosal adenyl cyclase activity is associated with gut fluid secretion, the adenyl cyclase stimulation is a primary event, and is not secondary to the transmucosal isotonic fluid movement.

Adenylyl Cyclases↗

Cholera.

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Acute Disease↗

Effect of Escherichia coli on fluid transport across canine small bowel. Mechanism and time-course with enterotoxin and whole bacterial cells.

An Escherichia coli strain isolated from a patient with severe cholera-like diarrhea elaborates a partly heat-labile enterotoxin shown to cause prompt adenyl cyclase stimulation and isotonic fluid secretion by canine jejunum. Both responses disappear upon removal of the enterotoxin. The duration of action of a submaximal dose of this E. coli enterotoxin was brief, despite sustained exposure to the jejunum, suggesting inactivation of the enterotoxin by its interaction with the mucosa. Inoculation of whole bacterial cultures of this E. coli strain into canine duodenum was followed by bacterial survival and induction of net secretion after 4-7 h. The onset of fluid production was associated with increasing gut mucosal adenyl cyclase activity. Washed bacterial cells could also produce fluid secretion. In vivo multiplication of this enterotoxin-producing E. coli was demonstrated 6-12 h after intraduodenal inoculation of approximately 10(6) organisms. This was associated with fluid secretion. Intestinal fluid production occurred without microscopic pathology in the mucosa.

Adenylyl Cyclases↗