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Research Article Free access | 10.1172/JCI107201
Department of Gastroenterology, Walter Reed Army Institute of Research, Washington, D. C. 20012
Department of Applied Immunology, Walter Reed Army Institute of Research, Washington, D. C. 20012
Department of Pathology, Harvard Medical School and Peter Bent Brigham Hospital, Boston, Massachusetts 02115
Find articles by Giannella, R. in: JCI | PubMed | Google Scholar
Department of Gastroenterology, Walter Reed Army Institute of Research, Washington, D. C. 20012
Department of Applied Immunology, Walter Reed Army Institute of Research, Washington, D. C. 20012
Department of Pathology, Harvard Medical School and Peter Bent Brigham Hospital, Boston, Massachusetts 02115
Find articles by Formal, S. in: JCI | PubMed | Google Scholar
Department of Gastroenterology, Walter Reed Army Institute of Research, Washington, D. C. 20012
Department of Applied Immunology, Walter Reed Army Institute of Research, Washington, D. C. 20012
Department of Pathology, Harvard Medical School and Peter Bent Brigham Hospital, Boston, Massachusetts 02115
Find articles by Dammin, G. in: JCI | PubMed | Google Scholar
Department of Gastroenterology, Walter Reed Army Institute of Research, Washington, D. C. 20012
Department of Applied Immunology, Walter Reed Army Institute of Research, Washington, D. C. 20012
Department of Pathology, Harvard Medical School and Peter Bent Brigham Hospital, Boston, Massachusetts 02115
Find articles by Collins, H. in: JCI | PubMed | Google Scholar
Published February 1, 1973 - More info
Strains of Salmonella typhimurium were studied in the ligated rabbit ileal loop model to gain insight into the mechanisms whereby bacteria which invade the gastrointestinal mucosa evoke fluid exsorption. The organisms employed differed in various biologic attributes including the ability to invade the ileal epithelium, multiply within the mucosa, elicit an acute inflammatory reaction, and disseminate across the intestinal wall. Some strains provoked small intestinal fluid exsorption although these did not elaborate enterotoxin. Only those strains which invaded the mucosa were accompanied by either mucosal inflammation or fluid exsorption. Noninvasive strains produced neither histologic abnormalities nor fluid secretion. While strains which invaded the mucosa caused an acute inflammatory reaction, not all such strains evoked fluid secretion. Furthermore, there was no correlation in ability of invasive organisms to evoke fluid secretion or in the intensity of mucosal inflammation, number of intramucosal salmonellae, or in ability to disseminate from the rabbit ileum.
These observations suggest that, as is the case in shigellosis, mucosal invasion may be a necessary factor for the intestinal fluid loss in salmonellosis. A bacterial property or factor, in addition to invasion of the gastrointestinal mucosa, seems to be responsible for fluid exsorptin. However, it is unlikely that a salmonella enterotoxin comparable to that elaborated by Vibrio cholerae, toxigenic Escherichia coli, or Shigella dysenteriae 1 is related to fluid secretion in salmonellosis.
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