Myeloid differentiation factor 88-dependent signalling controls bacterial growth during colonization and systemic pneumococcal disease in mice
Myeloid differentiation factor 88-dependent signalling controls bacterial growth during colonization and systemic pneumococcal disease in mice
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DOI：
10.1111/j.1462-5822.2005.00578.x
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发表时间：
2005-11-01
影响因子：
3.4
通讯作者：
Normark, BH
中科院分区：
文献类型：
--
作者：
Albiger, B;Sandgren, A;Normark, BH
Toll样受体（TLR）和髓样分化因子88（MyD88）是微生物感染期间激活先天免疫防御的关键参与者。使用不同的小鼠感染模型，我们表明，MyD88依赖的信号转导是至关重要的激活的先天免疫防御肺炎链球菌。我们的数据表明，局部和全身炎症反应的S。肺炎的发生依赖于MyD88的存在以清除上呼吸道的细菌定植并预防小鼠中的肺部和全身感染。最后，我们描述了MyD88缺陷小鼠血流中细菌生长增强与感染后血清铁浓度不能降低之间的强相关性。
The Toll-like receptors (TLRs) and the myeloid differentiation factor 88 (MyD88) are key players in the activation of the innate immune defence during microbial infections. Using different murine infection models, we show that MyD88-dependent signalling is crucial for the activation of the innate immune defence against Streptococcus pneumoniae. Our data demonstrate that both local and systemic inflammatory response to S. pneumoniae depends on the presence of MyD88 to clear bacterial colonization of the upper respiratory tract and to prevent pulmonary and systemic infection in mice. Finally, we described a strong correlation between enhanced bacterial growth in the bloodstream of MyD88-deficient mice and the inability to lower the serum iron concentration in response to infection.