Williams P, Ciurana B, Camprubi S, Tomas J M
Department of Pharmaceutical Sciences, University of Nottingham, University Park, U.K.
FEMS Microbiol Lett. 1990 Jun 1;57(3):305-9. doi: 10.1016/0378-1097(90)90085-5.
A series of isogenic mutants lacking either the O1 (O-:K66) or K66 (O1:K-) antigens or both (O-:K-), some of which had additional defects in their LPS core polysaccharide was used to examine the interaction between polymorphonuclear leucocytes (PMNLs) and K. pneumoniae serotype O1:K66. In the absence of serum complement, only a O-:K- strain with a deep rough LPS chemotype elicited a PMNL-dependent chemiluminescent (CL) response. However, following opsonization of the non-capsulated strains by complement, the largest CL response was to the O1:K- mutant. This mutant also activated and bound more complement C3 than any of the other encapsulated or non-capsulated strains examined. Despite the surface exposure of smooth and rough LPS in the encapsulated parent and mutant strains, the K66 antigen reduced the binding of C3 and prevented PMNL activation. Both anti-LPS and anti-K66 antibodies, however, stimulated a PMNL-dependent CL response to the K66 bearing strains.
使用一系列缺乏O1（O-:K66）或K66（O1:K-）抗原或两者（O-:K-）的同基因突变体，其中一些在其脂多糖核心多糖中还有其他缺陷，来研究多形核白细胞（PMNL）与肺炎克雷伯菌血清型O1:K66之间的相互作用。在没有血清补体的情况下，只有一种具有深粗糙脂多糖化学型的O-:K-菌株引发了依赖于PMNL的化学发光（CL）反应。然而，在用补体对非荚膜菌株进行调理后，最大的CL反应是针对O1:K-突变体。该突变体还比所检测的任何其他荚膜或非荚膜菌株激活并结合了更多的补体C3。尽管在荚膜亲本菌株和突变体菌株中光滑和粗糙脂多糖都暴露于表面，但K66抗原减少了C3的结合并阻止了PMNL的激活。然而，抗脂多糖和抗K66抗体均刺激了对携带K66菌株的依赖于PMNL的CL反应。
