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From the Departments of Bacteriology, Immunology, and Gastroenterology, Walter Reed Army Institute of Research, Washington, D. C. 20012, the Department of Immunology, Naval Medical Research Institute, Bethesda, Maryland 20014, and the Departments of Medicine and Microbiology, Uniformed Services University of the Health Sciences, Bethesda, Maryland 20014
Abstract
CBA/N mice have an X-linked immune defect that is associated with the absence of a subpopulation of mature or late developing B lymphocytes. The effect of this B cell defect on susceptibility of mice to Salmonella typhimurium was investigated. The 50% lethal dose (LD50) of S. typhimurium for CBA/N mice was 1000-fold less than for the immunologically normal, histocompatible CBA/CaHN strain. Genetic analysis revealed that the susceptibility of the CBA/N strain to S. typhimurium, like the immune defect, was X-linked since immune-defective F1 male mice derived from crosses between CBA/N and immunologically normal strains were susceptible to S. typhimurium (LD50 
20), whereas immunologically normal F1 males and females derived from these matings were resistant (LD50 
5 x 103). By contrast, both immune-defective and normal F1 mice were resistant to another facultative intracellular parasite, Listeria monocytogenes. Deaths among the immune-defective mice occurred primarily late in the course of infection (>10 days) whereas deaths of immunologically normal, S. typhimurium-susceptible strains (e.g., C57BL/6 and BALB/c) occurred early in the infectious process. To determine if the increased susceptibility of B cell-defective mice to S. typhimurium and the expression of the X-linked immune-deficiency gene (xid) were actually linked, F2 and backcross mice were phenotyped for the immune defect by measuring serum IgM levels and then challenged with the organism. Although no formal linkage was established, there was a close correlation between low serum IgM levels and susceptibility, since 93% of such mice succumbed to infection. These studies suggest that B cells play an important role in those events that govern the development of resistance to S. typhimurium late in the course of infection.
Footnotes
1 This work was supported by the Uniformed Services University of the Health Sciences Protocol No. R07306, and the Naval Medical Research and Development Command, Work Unit No. M0095-PN.001-1030. The opinions and assertations contained herein are the private ones of the authors and are not to be construed as official or reflecting the views of the Navy Department or the naval service at large. The experiments reported herein were conducted according to the principles set forth in the "Guide for the Care and Use of Laboratory Animals," Institute of Laboratory Resources, National Research Council, DHEW, Pub. No. (NIH) 78-23.
2 Send reprint requests to: Dr. A. O'Brien: Department of Microbiology, Uniformed Services University of the Health Sciences Bethesda, Maryland 20014. Part of this work was performed while A. D. O'Brien held a National Research Council Research Associationship at the Walter Reed Army Institute of Research, Washington, D. C.
3 Current Address: Malaria Research Program, University of New Mexico, Albuquerque, New Mexico 87131.
4 Current Address: Division of Gastroenterology, Washington University Medical School, St. Louis, Missouri 63110.
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