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The Journal of Immunology, 1974, 113: 740-749.
Copyright © 1974 by The American Association of Immunologists, Inc.

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Pathophysiologic Effects of Lethal and Immunoregulatory Doses of Cholera Enterotoxin in the Mouse

Francis V. Chisari1 and Robert S. Northrup2

From the Laboratories of Pathology and Bacterial Products, Division of Biologics Standards, National Institutes of Health, Bethesda, Maryland 20014

Abstract

Cholera enterotoxin (CE) can kill mice, produce severe thymic cortical atrophy and depletion of lymphoid cells from splenic red pulp. Furthermore, lethal doses can decrease the viability of spleen cells and thymocytes in vitro and produce severe hypercalcemia which probably is responsible for the lethal effect. However, a sublethal dose known to have the capacity to modulate the immune response exerts a distinct stimulatory effect on cells in the splenic red pulp whereas cortical thymocytes are destroyed even at this lower dose. A lesser degree of serum calcium elevation is also produced. The differential susceptibility of thymus and bone marrow-derived cells to CE and the role which the adenyl cyclase-cyclic AMP system plays in these effects is discussed.

Footnotes

1 Current address: Department of Molecular Immunology, Scripps Clinic and Research Foundation, La Jolla, California 92037.

2 Current address: University of Hawaii Postgraduate Medical Education Program for Okinawa, Okinawa Central Hospital, Gushikawa City, Okinawa, Japan.




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