Tateda K, Goto S, Hirakata Y, Yamaguchi K, Matsumoto T, Furuya N, Shimoguchi K, Irifune K, Kaku M, Kohno S
Department of Microbiology, Toho University School of Medicine.
Kansenshogaku Zasshi. 1992 Aug;66(8):1053-61. doi: 10.11150/kansenshogakuzasshi1970.66.1053.
In this study, role of capsular polysaccharide (CPS) and lipopolysaccharide (LPS) of Klebsiella pneumoniae was investigated in experimental mice pneumonia model. Inoculation with K. pneumoniae mucoid strain DT-S into mice lung induced expansive, voluminous lethal pneumonia characterized with thickening of the alveolar septa caused by infiltration of inflammatory cell and packing of bacteria within alveolar spaces. On the other hand, mice lung inoculated with K. pneumoniae DT-X, which was non-mucoid mutant isolated from DT-S during natural passage, showed infiltration of inflammatory cell into alveolar spaces but there was no death of mice during the course of this pneumonia. Inoculation of CPS 100 micrograms of DT-S strain into mice lung induced lesser extent of accumulation of inflammatory cell than that of LPS 4 micrograms of this strain. Stimulation of alveolar and peritoneal macrophage with CPS, even at a concentration of 100 micrograms/ml, induced weaker Interleukin-1 (IL-1) activity than stimulation with LPS 4 micrograms/ml. These results suggest that since CPS of K. pneumoniae DT-S encapsulate bacteria including LPS, CPS may inhibit chemotaxis of inflammatory cell and IL-1 production of macrophage to be induced by LPS during course of pneumonia. It is speculated that existence of CPS have important role in modulating host response to bacterial LPS, and this effect of CPS may be related with difference of pathological findings of lung and lethality between K. pneumoniae DT-S and DT-X.
在本研究中,对肺炎克雷伯菌的荚膜多糖(CPS)和脂多糖(LPS)在实验性小鼠肺炎模型中的作用进行了研究。将肺炎克雷伯菌黏液型菌株DT-S接种到小鼠肺部,可诱发广泛性、大量致死性肺炎,其特征为肺泡间隔增厚,这是由炎症细胞浸润和肺泡腔内细菌堆积所致。另一方面,接种从DT-S自然传代过程中分离出的非黏液型突变体肺炎克雷伯菌DT-X的小鼠肺部,可见炎症细胞浸润至肺泡腔,但在该肺炎病程中无小鼠死亡。将100微克DT-S菌株的CPS接种到小鼠肺部,诱导的炎症细胞聚集程度低于4微克该菌株的LPS。用CPS刺激肺泡巨噬细胞和腹腔巨噬细胞,即使浓度为100微克/毫升,诱导的白细胞介素-1(IL-1)活性也低于用4微克/毫升LPS刺激的情况。这些结果表明,由于肺炎克雷伯菌DT-S的CPS包裹包括LPS在内的细菌,CPS可能在肺炎病程中抑制LPS诱导的炎症细胞趋化作用和巨噬细胞IL-1的产生。据推测,CPS的存在在调节宿主对细菌LPS的反应中具有重要作用,而CPS的这种作用可能与肺炎克雷伯菌DT-S和DT-X之间肺部病理表现和致死率的差异有关。