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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.

Delayed Clearance of Intraabdominal Abscesses Caused byCandida albicansin Tumor Necrosis Factor–α– and Lymphotoxin‐α–Deficient Mice