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Published online before print September 12, 2003

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© by The Society for Leukocyte Biology
Journal of Leukocyte Biology, doi:10.1189/jlb.0603301

Received for publication June 30, 2003.
Revised August 1, 2003.
Accepted for publication August 4, 2003.

Article

Increased neutrophil influx but no impairment of protective immunity to tuberculosis in mice lacking the CD44 molecule

Andre Kipnis ^*@, Randall J. Basaraba ^*, Joanne Turner , and Ian M. Orme ^*

*Department of Microbiology, Immunology and Pathology, Colorado State University, Fort Collins; and Department of Internal Medicine, Center for Microbial Interface Biology, The Ohio State University, Columbus

^@ To whom correspondence should be addressed. E-mail: akipnis{at}lamar.colostate.edu.

	Abstract

Up-regulation of expression of the cell-surface marker CD44 is a major characteristic of T lymphocytes responding in the lungs of mice infected with Mycobacterium tuberculosis. These lymphocytes express an activated/memory phenotype as seen by their high expression of the CD44 molecule and low expression of CD62L and CD45RB cell-surface molecules. Based on increasing evidence that the CD44 molecule participates in several aspects of the inflammatory response, we evaluated its role in the response to infection with M. tuberculosis using gene-disrupted mice. In this report, we show that CD44 expression is not necessary for the proper trafficking of protective cells to the lungs of mice infected with M. tuberculosis or the direct expression of protective immunity leading to control and containment of the bacterial load in this organ. However, although there were no differences in the bacterial load or migration of activated T lymphocytes to the inflamed lung, the absence of the CD44 molecule resulted in a substantially increased accumulation of neutrophils in the lung. These data indicate that loss of CD44 expression does not alter expression of T helper cell type 1 immunity to tuberculosis in the lungs but has major effects on the overall cellular composition of the immunopathological response.

Key Words: mouse • tuberculosis infection • lung • cell recruitment • lung inflammation

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