Resistance of Streptococcus gordonii to polymorphonuclear leukocyte killing is a potential virulence determinant of infective endocarditis
Resistance of Streptococcus gordonii to polymorphonuclear leukocyte killing is a potential virulence determinant of infective endocarditis
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DOI：
10.1128/iai.00087-06
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发表时间：
2006-06-01
影响因子：
3.1
通讯作者：
Sandberg, Ann L.
中科院分区：
文献类型：
--
作者：
Lee, Si Young;Cisar, John O.;Sandberg, Ann L.
用大鼠感染性心内膜炎模型观察到7株具有代表性的戈登链球菌的毒力有显著差异。包括S.gordonii DL1在内的五个菌株引起了严重的疾病，而包括S.gordonii SK12在内的另外两个菌株引起的疾病很少或没有。毒力的差异很明显，因为在接受单独菌株攻击的插管大鼠的主动脉瓣上存在明显的链球菌，而且从同时感染这两种细菌的动物的心脏中，对利福平耐药的戈登链球菌DL1的恢复要比对链霉素耐药的戈登链球菌SK12大得多。通过刺激中性粒细胞(PMN)产生超氧阴离子，每株戈登葡萄球菌都与人血小板聚集，并与PMN结合。用唾液酸酶处理血小板或中性粒细胞可以减少或消除这些相互作用，这表明细菌对宿主唾液酸受体有识别作用。粘附素介导的每个戈登链球菌菌株与中性粒细胞的结合也触发了吞噬作用。然而，随后对这七个菌株的PMN依赖的杀伤力有很大的不同。这5株毒力菌株包括3株未被杀死的菌株和2株数量减少了约50%的菌株。相比之下，在相同的条件下，每个无毒菌株的杀灭水平明显更高，接近添加的细菌的90%。用大鼠中性粒细胞进行的平行研究表明，具有代表性的强毒株和无毒株在耐药性或敏感性方面存在类似的差异。因此，戈登葡萄球菌在粘附素介导的吞噬作用后在中性粒细胞中存活的能力可能是感染性心内膜炎的一个重要毒力决定因素。
Significant differences in virulence among seven representative Streptococcus gordonii strains were observed by using the rat model of infective endocarditis. Five strains, including S. gordonii DL1, caused severe disease, while the other two strains, including S. gordonii SK12, caused minimal or no disease. The differences in virulence were evident from the visible presence of streptococci in the vegetations present on the aortic valves of catheterized rats that were challenged with individual strains and also from the much greater recovery of rifampin-resistant S. gordonii DL1 than of streptomycin-resistant S. gordonii SK12 from the hearts of animals coinfected with both organisms. Each S. gordonii strain aggregated with human platelets and bound to polymorphonuclear leukocytes (PMNs), as shown by the stimulation of PMN superoxide anion production. These interactions were reduced or abolished by pretreatment of the platelets or PMNs with sialidase, indicating that there was bacterial recognition of host sialic acid-containing receptors. Adhesin-mediated binding of each S. gordonii strain to PMNs also triggered phagocytosis. However, the subsequent PMN-dependent killing differed significantly for the seven strains. The five virulent strains included three strains that were not killed and two strains whose numbers were reduced by approximately 50%. In contrast, the level of killing of each avirulent strain under the same conditions was significantly greater and approached 90% of the bacteria added. Parallel studies performed with rat PMNs revealed comparable differences in the resistance or susceptibility of representative virulent and avirulent strains. Thus, the ability of S. gordonii to survive in PMNs following adhesin-mediated phagocytosis may be an important virulence determinant of infective endocarditis.