HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) 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 Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Beamer, G. L. Articles by Turner, J. Search for Related Content PubMed PubMed Citation Articles by Beamer, G. L. Articles by Turner, J.

Interleukin-10 Promotes Mycobacterium tuberculosis Disease Progression in CBA/J Mice¹

Gillian L. Beamer^*,, David K. Flaherty, Barnabe D. Assogba^*, Paul Stromberg, Mercedes Gonzalez-Juarrero^¶, Rene de Waal Malefyt^||, Bridget Vesosky^* and Joanne Turner^2,*,

^* Center for Microbial Interface Biology, Department of Veterinary Biosciences and Department of Internal Medicine, Division of Infectious Diseases, The Ohio State University, Columbus, OH 43210; Vanderbilt University Medical Center, Nashville, TN 37212; ^¶ Department of Microbiology, Immunology and Pathology, Colorado State University, Fort Collins, CO 80523; and ^|| Department of Immunology, Schering-Plough Biopharma (formerly DNAX), Palo Alto, CA 94304

IL-10 is a potent immunomodulatory cytokine that affects innate and acquired immune responses. The immunological consequences of IL-10 production during pulmonary tuberculosis (TB) are currently unknown, although IL-10 has been implicated in reactivation TB in humans and with TB disease in mice. Using Mycobacterium tuberculosis-susceptible CBA/J mice, we show that blocking the action of IL-10 in vivo during chronic infection stabilized the pulmonary bacterial load and improved survival. Furthermore, this beneficial outcome was highly associated with the recruitment of T cells to the lungs and enhanced T cell IFN- production. Our results indicate that IL-10 promotes TB disease progression. These findings have important diagnostic and/or therapeutic implications for the prevention of reactivation TB in humans.

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 Support was provided by the American Lung Association (CI-8609-N) and National Institutes of Health Grants R01 (AI-064522) and T32 (RR007073). Contents of this paper are the authors’ responsibility and do not necessarily represent views of the National Center for Research Resources or the National Institutes of Health. Schering-Plough Biopharma is supported by the Schering Plough Corporation.

² Address correspondence and reprint requests to Dr. Joanne Turner, 1010 Biomedical Research Tower, 460 West 12th Avenue, Columbus, OH 43210. E-mail: joanne. turner{at}osumc.edu

³ Abbreviations used in this paper: TB, tuberculosis; M.tb, Mycobacterium tuberculosis.