Antibiotic-induced release of inflammatory mediators from bacteria in experimental Klebsiella pneumoniae-induced sepsis.
In a fibrin-clot model of sepsis, developed in mice, treatment with the antibiotics ceftazidime (Cfz) and ofloxacin (Ofl) caused significant (p < 0.01) release of endotoxin and TNF-alpha after 4.5 h when compared with control (untreated) and amikacin (Ami) treated group. Except for control group, the level of bacteremia declined in all three antibiotic-treated groups. The results suggest that antibiotic therapy, irrespective of the agent used, results in an increase in endotoxin levels in vivo. The amount of endotoxin liberated by Ami was much smaller than with Cfz and Ofl therapy, which makes it an appropriate agent for the treatment of sepsis. An increase in the level of TNF-alpha along with endotoxin is suggestive of increased inflammatory response.
Toky
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Department of Microbiology, Panjab University, 160 014 Chandigarh, India. kltoky@yahoo.com
Sharma
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Bramhne
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Chhibber
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D000583:Amikacin / Q000494:pharmacology / Q000627:therapeutic use; D000818:Animals; D000900:Anti-Bacterial Agents / Q000494:pharmacology* / Q000627:therapeutic use*; D002442:Ceftazidime / Q000494:pharmacology / Q000627:therapeutic use; D004195:Disease Models, Animal; D004731:Endotoxins / Q000378:metabolism*; D006801:Humans; D007249:Inflammation; D007710:Klebsiella Infections / Q000150:complications / Q000188:drug therapy / Q000382:microbiology; D007711:Klebsiella pneumoniae / Q000187:drug effects / Q000472:pathogenicity*; D051379:Mice; D015242:Ofloxacin / Q000494:pharmacology / Q000627:therapeutic use; D018805:Sepsis / Q000188:drug therapy* / Q000382:microbiology / Q000401:mortality; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism*
D000900:Anti-Bacterial Agents; D004731:Endotoxins; D014409:Tumor Necrosis Factor-alpha; D000583:Amikacin; D002442:Ceftazidime; D015242:Ofloxacin