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Prepublished online as a Blood First Edition Paper on October 31, 2002; DOI 10.1182/blood-2002-07-2319.
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Blood, 15 March 2003, Vol. 101, No. 6, pp. 2388-2392
PHAGOCYTES
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
From the Departments of Medicine and Pathology, David
Geffen School of Medicine, Los Angeles, CA; the West Los Angeles
Veterans Administration Hospital, University of California, Los
Angeles, Los Angeles, CA; and the Albert Einstein School of Medicine,
Bronx, NY.
More than 70 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.
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