Nameda Sachiko, Miura Noriko N, Adachi Yoshiyuki, Ohno Naohito
Laboratory for Immunopharmacology of Microbial Products, School of Pharmacy, Tokyo University of Pharmacy and Life Sciences, Hachioji, Yokyo, Japan.
Microbiol Immunol. 2007;51(9):851-9. doi: 10.1111/j.1348-0421.2007.tb03981.x.
We have developed an animal model of sepsis in mice by repeatedly administering beta-glucan, a biological response modifier, and indomethacin (IND), a nonsteroidal anti-inflammatory drug. The combination of these drugs induced bacteremia by translocation of the enterobacterial flora, resulting in increasing the number of activated leukocytes, and inducing hyper cytokinemia. In the present study, we examined the effect of antibiotics on beta-glucan and IND-induced septic shock. Treatment with antibiotics inhibited microbial translocation, inhibited contraction of the colon, reduced lipopolysaccharides (LPS)-elicited production of TNF-alpha and IL-6, and finally prolonged survival. However, the efficacy of antibiotics treatment was limited in mice administered IND orally. These findings strongly suggested that the antibiotics controlled the gut-associated action of IND and reduced various symptoms accompanying sepsis.
我们通过反复给予生物反应调节剂β-葡聚糖和非甾体抗炎药吲哚美辛(IND),建立了小鼠脓毒症动物模型。这些药物的组合通过肠道菌群易位诱导菌血症,导致活化白细胞数量增加,并诱导高细胞因子血症。在本研究中,我们研究了抗生素对β-葡聚糖和IND诱导的脓毒性休克的影响。抗生素治疗可抑制微生物易位,抑制结肠收缩,减少脂多糖(LPS)诱导的TNF-α和IL-6产生,并最终延长生存期。然而,抗生素治疗对口服IND的小鼠疗效有限。这些发现强烈表明,抗生素可控制IND的肠道相关作用,并减轻脓毒症伴随的各种症状。