Skurnik M, Venho R, Bengoechea J A, Moriyón I
Department of Medical Biochemistry, University of Turku, Finland.
Mol Microbiol. 1999 Mar;31(5):1443-62. doi: 10.1046/j.1365-2958.1999.01285.x.
Lipopolysaccharide (LPS) of Yersinia enterocolitica O:3 has an inner core linked to both the O-antigen and to an outer core hexasaccharide that forms a branch. The biological role of the outer core was studied using polar and non-polar mutants of the outer core biosynthetic operon. Analysis of O-antigen- and outer core-deficient strains suggested a critical role for the outer core in outer membrane properties relevant in resistance to antimicrobial peptides and permeability to hydrophobic agents, and indirectly relevant in resistance to killing by normal serum. Wild-type bacteria but not outer core mutants killed intragastrically infected mice, and the intravenous lethal dose was approximately 10(4)-fold higher for outer core mutants. After intragastric infection, outer core mutants colonized Peyer's patches and invaded mesenteric lymph nodes, spleen and liver, and induced protective immunity against wild-type bacteria. In mice co-infected intragastrically with an outer core mutant-wild type mixture, both strains colonized Peyer's patches similarly during the first 2 days, but the mutant was much less efficient in colonizing deeper organs and was cleared faster from Peyer's patches. The results demonstrate that outer core is required for Y. enterocolitica O:3 full virulence, and strongly suggest that it provides resistance against defence mechanisms (most probably those involving bactericidal peptides).
小肠结肠炎耶尔森菌O:3的脂多糖(LPS)具有一个与O抗原以及一个形成分支的外核六糖相连的内核。利用外核生物合成操纵子的极性和非极性突变体研究了外核的生物学作用。对缺乏O抗原和外核的菌株的分析表明,外核在与抗微生物肽抗性和对疏水剂的通透性相关的外膜特性中起关键作用,并且与对正常血清杀伤的抗性间接相关。野生型细菌而非外核突变体可杀死经胃内感染的小鼠,外核突变体的静脉内致死剂量约高10^4倍。经胃内感染后,外核突变体定殖于派尔集合淋巴结,并侵入肠系膜淋巴结、脾脏和肝脏,并诱导针对野生型细菌的保护性免疫。在经胃内共同感染外核突变体-野生型混合物的小鼠中,两种菌株在最初2天内同样定殖于派尔集合淋巴结,但突变体在定殖于更深层器官方面效率低得多,并且从派尔集合淋巴结清除得更快。结果表明,外核是小肠结肠炎耶尔森菌O:3完全毒力所必需的,并且强烈提示它提供对防御机制(很可能是那些涉及杀菌肽的机制)的抗性。