| First Author | Cogen AL | Year | 2009 |
| Journal | Infect Immun | Volume | 77 |
| Issue | 1 | Pages | 360-6 |
| PubMed ID | 18981251 | Mgi Jnum | J:143765 |
| Mgi Id | MGI:3828914 | Doi | 10.1128/IAI.00909-08 |
| Citation | Cogen AL, et al. (2009) Beta2-microglobulin-dependent bacterial clearance and survival during murine Klebsiella pneumoniae bacteremia. Infect Immun 77(1):360-6 |
| abstractText | 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 alpha281 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. |
