Akademik Veri Yönetim Sistemi
Mediterranean journal of infection, microbes & antimicrobials, cilt.12, ss.30-35, 2023 (ESCI)
Introduction: An irregular systemic inflammatory response in sepsis can induce acute lung injury (ALI), which is characterized by the exaggerated
inflammation of the lung tissue. Colchicine inhibits several inflammatory pathways which may prevent sepsis-induced secondary lung injury. We
aimed to examine the histopathological effects of colchicine on lung tissue in a lipopolysaccharide (LPS)-induced sepsis model in rats.
Materials and Methods: Twenty-eight rats were randomly divided into the following four groups: “sham” (n=6), “colchicine only” (n=6), “sepsis
only” (n=8) and “sepsis+colchicine” (n=8). In the “sham” group, 0.9% NaCl was administered intraperitoneally (IP) and intragastrically (IG). In
the “Colchicine only” group, 0.9% NaCl was administered IP and colchicine was administered IG. Sepsis was induced in the “sepsis only” and
“sepsis+colchicine” groups by administering of 1 mg/kg of LPS IP at the 0-time point. In the “sepsis+colchicine” group, colchicine was also
administered IG at the 90th minute. An observational sepsis scoring system was used to evaluate the signs of sepsis. Subsequently, the rats were
sacrificed at the 24th hour. The lung tissues were examined according to the American Thorax Association’s assessment report on ALI in animals.
Results: The histopathological lung injury score in the “sepsis+colchicine” group was significantly higher than in the “sham” group (0.23±0.18
vs. 0±0; p<0.05) and was significantly lower than in the “sepsis” only group (0.23±0.18 vs. 0.57±0.14; p<0.001). Evaluation of the lung damage
score revealed that colchicine suppressed the increase in alveolar and interstitial neutrophil counts and limited the increase in hyaline membrane
neutrophil counts and alveolar wall thickness in the “sepsis+colchicine” group when compared with the “sepsis only” group.
Conclusion: In our experimental sepsis rat model, administration of colchicine for sepsis limited the secondary lung damage.