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Prepublished online as a Blood First Edition Paper on October 31, 2002; DOI 10.1182/blood-2002-07-2319. This Article Full Text (PDF) All Versions of this Article: 2002-07-2319v1 101/6/2388    most recent Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Ganz, T. Articles by Cole, A. M Search for Related Content PubMed PubMed Citation Articles by Ganz, T. Articles by Cole, A. M Social Bookmarking                   What's this? Submitted August 1, 2002 Accepted October 28, 2002 Increased inflammation in lysozyme M-deficient mice in response to Micrococcus luteus and its peptidoglycan Tomas Ganz*, Victoria Gabayan, Hsiang-I Liao, Lide Liu, Ami Oren, Thomas Graf, and Alexander M Cole Department of Medicine, David Geffen School of Medicine at UCLA, Los Angeles, CA, USA Department of Pathology, David Geffen School of Medicine at UCLA, Los Angeles, CA, USA Albert Einstein School of Medicine, New York, NY, USA Department of Medicine, West Los Angeles Veterans Administration Hospital, Los Angeles, CA, USA * Corresponding author; email: tganz{at}mednet.ucla.edu. More than seventy years ago, Alexander Fleming discovered lysozyme and proposed that nonpathogenic bacteria fail to cause disease because they are very susceptible to destruction by lysozyme, an enzyme that is one of the principal proteins of phagocytes. Although much has been learned about the effects of lysozyme in vitro, its biological role in vivo has not been determined. We examined transgenic mice deficient in lysozyme M after challenge by the normally nonpathogenic and highly lysozyme-sensitive bacterium Micrococcus luteus. Despite partial compensation by newly expressed lysozyme P in macrophages, lysozyme M-deficient mice developed much more severe lesions than wild type mice. The tissue injury was due to the failure of lysozyme M-deficient mice to inactivate peptidoglycan, resulting in an intense and prolonged inflammatory response. Our data indicate that tissue injury is normally limited by prompt degradation of bacterial macromolecules that trigger innate immunity and inflammation. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: K. Ohmi, L. C. Kudo, S. Ryazantsev, H.-Z. Zhao, S. L. Karsten, and E. F. 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