Saito Maki, Nameda Sachiko, Miura Noriko N, Adachi Yoshiyuki, Ohno Naohito
Laboratory for Immunopharmacology of Microbial Products, School of Pharmacy, Tokyo University of Pharmacy and Life Science, 1432-1 Horinouchi, Hachioji, Tokyo 192-0392, Japan.
Microb Pathog. 2008 May;44(5):402-9. doi: 10.1016/j.micpath.2007.11.003. Epub 2007 Nov 22.
The administration of beta-glucan (sonifilan; SPG) in combination with a non-steroidal anti-inflammatory drug, indomethacin (IND), induced lethal septic shock in mice. To demonstrate the influence of bacterial lipopolysaccharide (LPS) in this lethal toxicity, LPS non-responder C3H/HeJ mice were used to compare features of sepsis and physicochemical parameters in the present study. The administration of SPG and IND induced the death of C3H/HeJ mice, lowering rectal temperature, reducing body weight, increasing serum tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6) levels, shortening the gastrointestinal tract, and increasing the GOT/GPT level. Microbial translocation to various organs was also significantly increased. These results strongly suggested that LPS-non-responding strain also induced septic shock in this experimental model, and other pathogen-associated molecular patterns (PAMPs) may significantly contribute to the septic shock.
将β-葡聚糖(小丝菌素;SPG)与非甾体抗炎药吲哚美辛(IND)联合使用会在小鼠中诱发致死性脓毒症休克。为了证明细菌脂多糖(LPS)对这种致死毒性的影响,在本研究中使用了LPS无反应性的C3H/HeJ小鼠来比较脓毒症的特征和理化参数。给予SPG和IND会导致C3H/HeJ小鼠死亡,降低直肠温度,减轻体重,增加血清肿瘤坏死因子-α(TNF-α)和白细胞介素-6(IL-6)水平,缩短胃肠道,并增加谷草转氨酶/谷丙转氨酶水平。微生物向各个器官的易位也显著增加。这些结果强烈表明,LPS无反应性菌株在该实验模型中也会诱发脓毒症休克,并且其他病原体相关分子模式(PAMPs)可能对脓毒症休克有显著影响。