Journal
INFECTION AND IMMUNITY
Volume 77, Issue 1, Pages 360-366Publisher
AMER SOC MICROBIOLOGY
DOI: 10.1128/IAI.00909-08
Keywords
-
Categories
Funding
- National Institutes of Health [AI49448]
- American Lung Association
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [R01AI049448] Funding Source: NIH RePORTER
Ask authors/readers for more resources
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 beta(2)-microglobulin expression during murine K. pneumoniae bacteremia. beta(2)-Microglobulin knockout mice displayed significantly increased mortality upon intravenous inoculation that correlated with increased bacterial burden in the blood, liver, and spleen. As beta(2)-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 beta(2)-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 alpha 281 knockout) mice were more susceptible to K. pneumoniae bacteremia. Combined, these studies clearly indicate the importance of a beta(2)-microglobulin-dependent but CD8 T-cell-and iNK T-cell-independent mechanism critical for survival during K. pneumoniae bacteremia.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available