Figure 3
Figure 3. COX inhibition enhances bacteria killing in rodents. Mice were given dual (indomethacin/aspirin), COX1 (SC-560) or COX2 (NS-398) selective inhibitors orally either (A) 1 hour before or (B) therapeutically 1 hour after intraperitoneal inoculation of GBS. To exclude dampened bacterial translocation as a potential explanation for reduced plasma GBS titres after COX inhibition, peritoneal exudate levels of (C) GBS were measured 3 hours after inoculation. GBS was also injected intraperitoneally to (D) COX1 knockout mice with plasma taken 3 hours later for overnight cfu culture number determination as well as (E) incubated in culture media only with NSAIDs in the absence of leukocytes. Data were analyzed by one-way ANOVA and Dunnett multiple comparison test or by unpaired Student t test. Values are expressed as the mean ± SEM of 5-12 mice/group. * P < .05 and ** P < .01.

COX inhibition enhances bacteria killing in rodents. Mice were given dual (indomethacin/aspirin), COX1 (SC-560) or COX2 (NS-398) selective inhibitors orally either (A) 1 hour before or (B) therapeutically 1 hour after intraperitoneal inoculation of GBS. To exclude dampened bacterial translocation as a potential explanation for reduced plasma GBS titres after COX inhibition, peritoneal exudate levels of (C) GBS were measured 3 hours after inoculation. GBS was also injected intraperitoneally to (D) COX1 knockout mice with plasma taken 3 hours later for overnight cfu culture number determination as well as (E) incubated in culture media only with NSAIDs in the absence of leukocytes. Data were analyzed by one-way ANOVA and Dunnett multiple comparison test or by unpaired Student t test. Values are expressed as the mean ± SEM of 5-12 mice/group. * P < .05 and ** P < .01.

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