rTMD1 reduces K pneumonae–induced inflammatory response and lethality, and enhances bacterial clearance. (A,B) rTMD1 was administered before injection of K pneumoniae (5 × 10² CFU/mouse) to mice. Sera were collected 12 hours after administration of K pneumoniae for assay of (A) TNF-α and (B) NO production. Values are the mean plus or minus SD (n = 10). **P < .01 and ***P < .001 compared with the K pneumoniae–treated group; ^###P < .001 compared with the PBS-treated group. (C) rTMD1 (10 mg/kg) was administered before injection of K pneumoniae (5 × 10³ CFU/mouse) to mice. Survival was determined. For each experimental group, n = 20. ***P < .001 compared with the K pneumoniae–treated group. These graphs represent the results from 3 independent experiments. (D) rTMD1 enhanced K pneumoniae clearance in circulation. FVB mice were intraperitoneally injected with K pneumoniae (5 × 10² CFU/mouse) without or with rTMD1 (10 mg/kg; intravenously). The blood samples from each group were collected at various time intervals and assayed for viable bacterial CFU counts. Values are the mean plus or minus SD. For each time interval group, n = 5; *P < .05 compared with the K pneumoniae–treated mice. (E,F) rTMD1 (10 mg/kg) was administered immediately, 30, or 60 minutes after injection of K pneumoniae (5 × 10² CFU/mouse) to mice. The serum levels of TNF-α (E) and K pneumoniae clearance (F) were determined. Values are the mean plus or minus SD. For each time interval group, n = 8-10; *P < .05 and ***P < .001 compared with the K pneumoniae–treated mice on each time interval group; ^###P < .001 compared with the PBS-treated group. Similar results were obtained in 2 independent experiments.