The Gram-negative bacterium Klebsiella pneumoniae is an opportunistic pathogen, which can cause life-threatening infections such as sepsis. Worldwide, emerging multidrug resistant K. pneumoniae infections are challenging to treat, hence leading to increased mortality. Therefore, understanding the interactions between K. pneumoniae and the immune system is important to develop new treatment options. We characterized ten clinical K. pneumoniae isolates obtained from blood of bacteremia patients. The interaction of the isolates with human serum was investigated to elucidate how K. pneumoniae escapes the host immune system, and how complement activation by K. pneumoniae changed the capsule structure. All K. pneumoniae isolates activated the alternative complement pathway despite serum resistance of seven isolates. One serum sensitive isolate activated two or all three pathways, and this isolate was lysed and had numerous membrane attack complexes in the outer membrane. However, we also found deposition of complement components in the capsule of serum resistant isolates resulting in morphological capsule changes and capsule shedding. These bacteria did not lyse, and no membrane attack complex was observed despite deposition of C5b-9 within the capsule, indicating that the capsule of serum resistant K. pneumoniae isolates is a defense mechanism against complement-mediated lysis.

中文翻译：

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补体介导的肺炎克雷伯菌胶囊改变。

革兰氏阴性细菌肺炎克雷伯菌是一种机会病原体，可引起危及生命的感染，如败血症。在世界范围内，新兴的耐多药肺炎克雷伯菌感染难以治疗，因此导致死亡率增加。因此，了解肺炎克雷伯菌和免疫系统之间的相互作用对于开发新的治疗方案很重要。我们表征了从菌血症患者血液中获得的十种临床肺炎克雷伯菌分离株。研究了分离物与人血清的相互作用，以阐明肺炎克雷伯菌如何逃逸宿主免疫系统，以及肺炎克雷伯菌的补体激活如何改变胶囊结构。尽管有七个分离株具有血清抗性，但所有肺炎克雷伯菌分离株均激活了补体途径。一种血清敏感性分离物激活了两个或所有三个途径，并且该分离物被裂解并且在外膜中具有许多膜攻击复合物。但是，我们还发现补体成分在抗血清分离株的胶囊中沉积，导致胶囊形态改变和胶囊脱落。这些细菌没有裂解，尽管在胶囊中有C5b-9沉积，也没有观察到膜攻击复合物，表明血清抗性肺炎克雷伯菌分离物的胶囊是针对补体介导的裂解的防御机制。