| First Author | Vonk AG | Year | 2002 |
| Journal | J Infect Dis | Volume | 186 |
| Issue | 12 | Pages | 1815-22 |
| PubMed ID | 12447768 | Mgi Jnum | J:80750 |
| Mgi Id | MGI:2447089 | Doi | 10.1086/345818 |
| Citation | Vonk AG, et al. (2002) Delayed clearance of intraabdominal abscesses caused by Candida albicans in tumor necrosis factor-alpha- and lymphotoxin-alpha-deficient mice. J Infect Dis 186(12):1815-22 |
| abstractText | The role of endogenous tumor necrosis factor-alpha (TNF) and lymphotoxin-alpha (LT) in a model of intraabdominal Candida sepsis and abscess formation was investigated. Significantly more abscesses were observed in TNF/LT double knockout (TNF(-/-)LT(-/-)) mice, compared with that in wild-type (TNF(+/+)LT(+/+)) mice. Outgrowth of Candida in abscesses of TNF(-/-)LT(-/-) mice was 10-fold increased on day 14 and 60-fold increased on day 21 of infection. The interleukin-10rcolon;interferon-gamma ratio, measured in supernatants of stimulated splenocytes, shifted from 131 for TNF(-/-)LT(-/-) mice and 13.9 for TNF(+/+)LT(+/+) mice on day 8 to 0.11 for TNF(-/-)LT(-/-) mice and 11.66 for TNF(+/+)LT(+/+) mice on day 14 of infection. The diminished host resistance is explained by an impaired extracellular killing capacity of granulocytes and a delayed development of a T helper 1 response in TNF(-/-)LT(-/-) mice. In conclusion, TNF and LT are critical to the stimulation of effector cells that leads to elimination of Candida from abscesses. |
