Enhanced vulnerability for Streptococcus pneumoniae sepsis during asplenia is determined by the bacterial capsule
Enhanced vulnerability for Streptococcus pneumoniae sepsis during asplenia is determined by the bacterial capsule
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DOI：
10.1016/j.imbio.2011.02.004
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发表时间：
2011-08-01
期刊：
影响因子：
2.8
通讯作者：
van der Poll, Tom
中科院分区：
文献类型：
--
作者：
Lammers, Adriana J.;de Porto, Alexander P.;van der Poll, Tom
没有脾脏的患者很容易患上肺炎链球菌引起的严重败血症。我们研究了肺炎球菌荚膜在脾切除后宿主防御降低中的相对贡献。假手术或脾切除的小鼠接种了血清型2或4肺炎链球菌（039，TIGR4）或同基因非包膜突变体（D39 Delta cps，TIGR4 Delta cps）。脾切除后，鼻内感染 039 导致死亡率增加、细菌传播增加并加剧全身炎症，而不是改变肺部炎症。静脉感染还导致脾切除后死亡率、细菌生长和全身炎症增加。相比之下，在 D39 Delta cps 感染期间，脾脏对宿主防御没有贡献。对 TIGR4 也进行了类似的观察：静脉注射野生型细菌后，细菌生长和炎症增加，但脾切除小鼠中的非包膜细菌则不然。这些结果表明，肺炎链球菌的包膜确实导致无脾小鼠对侵袭性肺炎球菌疾病的脆弱性增加。 (C) 2011 爱思唯尔有限公司。版权所有。
Patients without a spleen are susceptible for overwhelming sepsis with Streptococcus pneumoniae. We investigated the relative contribution of the pneumococcal capsule in the reduced host defense after splenectomy.Sham-operated or splenectomized mice were inoculated with serotype 2 or 4 S. pneumoniae (039, TIGR4) or the isogenic nonencapsulated mutants (D39 Delta cps, TIGR4 Delta cps). After splenectomy, intranasal infection with 039 resulted in increased mortality, increased bacterial dissemination and exaggerated systemic inflammation rather then altering inflammation in the lungs. Intravenous infection also resulted in enhanced mortality, bacterial growth and systemic inflammation after splenectomy. In contrast, the spleen did not contribute to host defense during infection with D39 Delta cps. Similar observations were made for TIGR4: increased bacterial growth and inflammation after intravenous infection with wild-type, but not nonencapsulated bacteria in splenectomized mice.These results indicate that the capsule of S. pneumoniae is indeed responsible for increased vulnerability of asplenic mice to invasive pneumococcal disease. (C) 2011 Elsevier GmbH. All rights reserved.