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This Article Full Text Full Text (PDF) All Versions of this Article: jimmunol.0900772v1 183/2/1263    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Google Scholar Articles by Griffin, A. Articles by McSorley, S. J. PubMed PubMed Citation Articles by Griffin, A. Articles by McSorley, S. J.

Successful Treatment of Bacterial Infection Hinders Development of Acquired Immunity¹

Center for Infectious Diseases and Microbiology Translational Research, Department of Medicine, Division of Gastroenterology, Hepatology, and Nutrition, McGuire Translational Research Facility, University of Minnesota Medical School, Minneapolis, MN 55455

Antibiotics are routinely used to control bacterial infection, but the acquisition of acquired immunity following successful treatment has rarely been examined. We developed a model that allows visualization of acquired immunity during and following antibiotic treatment of typhoid. Pathogen-specific humoral and cellular immune responses were activated rapidly in antibiotic-treated mice, but were not sustained after successful antibiotic treatment and did not confer protection to secondary infection. In marked contrast, pathogen-specific Th1 and Ab responses matured over several weeks following immunization with a live vaccine strain. The deficiency in protective immunity following antibiotic treatment could be overcome by administering flagellin during antibiotic therapy. Thus, development of protective immunity is hindered by rapid therapeutic elimination of bacteria, but can be overcome by providing additional inflammatory and/or antigenic stimuli.

The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ This work was supported by National Institutes of Health Grants AI055743 and AI073672.

² Address correspondence and reprint requests to Dr. Stephen J. McSorley, Center for Infectious Diseases and Microbiology Translational Research, Department of Medicine, Division of Gastroenterology, Hepatology, and Nutrition, McGuire Translational Research Facility, University of Minnesota Medical School, 2001 6th Street SE, Minneapolis, MN 55455. E-mail address: mcsor002{at}umn.edu

³ Abbreviations used in this paper: LVS, live vaccine strain; EHAA, Eagle’s Hanks amino acids; MLN, mesenteric lymph node; PAMP, pathogen-associated molecular pattern; Wt, wild type.