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Infection and Immunity, January 2009, p. 360-366, Vol. 77, No. 1
0019-9567/09/$08.00+0 doi:10.1128/IAI.00909-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

Department of Internal Medicine, Division of Pulmonary and Critical Care Medicine, University of Michigan Medical Center, Ann Arbor, Michigan
Received 23 July 2008/ Returned for modification 18 September 2008/ Accepted 24 October 2008
Klebsiella pneumoniae is a leading cause of both community-acquired and nosocomial gram-negative bacterial pneumonia. A significant clinical complication of Klebsiella pulmonary infections is peripheral blood dissemination, resulting in a systemic infection concurrent with the localized pulmonary infection. We report here on the critical importance of β2-microglobulin expression during murine K. pneumoniae bacteremia. β2-Microglobulin knockout mice displayed significantly increased mortality upon intravenous inoculation that correlated with increased bacterial burden in the blood, liver, and spleen. As β2-microglobulin knockout mice lack both CD8+ T cells and invariant NK T cells, mouse models specifically deficient in either cell population were examined to see if this would account for the increased mortality noted in β2-microglobulin knockout mice. Surprisingly, neither CD8 T-cell-deficient (TAP-1 knockout; in vivo anti-CD8 antibody treatment) nor invariant NK (iNK) T-cell-deficient (CD1d knockout, J
281 knockout) mice were more susceptible to K. pneumoniae bacteremia. Combined, these studies clearly indicate the importance of a β2-microglobulin-dependent but CD8 T-cell- and iNK T-cell-independent mechanism critical for survival during K. pneumoniae bacteremia.
Published ahead of print on 3 November 2008.
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