Streptococcus pneumoniae-associated human macrophage apoptosis after bacterial internalization via complement and Fcγ receptors correlates with intracellular bacterial load
Streptococcus pneumoniae-associated human macrophage apoptosis after bacterial internalization via complement and Fcγ receptors correlates with intracellular bacterial load
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DOI：
10.1086/378675
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发表时间：
2003-10-15
影响因子：
6.4
通讯作者：
Dockrell, DH
中科院分区：
文献类型：
--
作者：
Ali, F;Lee, ME;Dockrell, DH
调理作用可增强肺炎链球菌诱导的人单核细胞源性巨噬细胞 (MDM) 凋亡。调理血清中补体和免疫球蛋白的消耗以及巨噬细胞 CR1、CR3、FcgammaRII 和 FcgammaRIII 的阻断均部分减少了肺炎链球菌吞噬后 MDM 细胞凋亡，这些效应与内化细菌数量减少相关。氯霉素对调理后的肺炎链球菌蛋白质合成的抑制作用下调了随后的 MDM 细胞凋亡。肺炎链球菌未包膜突变体的吞噬作用导致 MDM 细胞凋亡增加，并与内化增强相关。半胱天冬酶抑制与细菌杀灭率降低有关。调理后的肺炎链球菌对细胞凋亡的诱导增强是细菌细胞内负荷增加的结果，而不是补体受体或 FcgammaR 的特定参与模式的结果。活细胞内细菌与宿主细胞之间的动态相互作用对于诱导 MDM 细胞凋亡是必要的，并且细胞凋亡的诱导有助于宿主针对肺炎链球菌的防御。
Opsonization enhances Streptococcus pneumoniae-induced human monocyte-derived macrophage (MDM) apoptosis. Both depletion of complement and immunoglobulin from opsonizing serum and blockade of the macrophages CR1, CR3, FcgammaRII, and FcgammaRIII partially decreased MDM apoptosis after S. pneumoniae phagocytosis, and these effects correlated with reduced numbers of internalized bacteria. Chloramphenicol inhibition of protein synthesis by opsonized S. pneumoniae down-regulated subsequent MDM apoptosis. Phagocytosis of an unencapsulated mutant of S. pneumoniae resulted in increased MDM apoptosis, in association with enhanced internalization. Caspase inhibition was associated with decreased killing of bacteria. Enhanced induction of apoptosis by opsonized S. pneumoniae is the result of increased intracellular burden of bacteria, rather than of a specific pattern of engagement of complement receptor or FcgammaR. A dynamic interaction between live intracellular bacteria and the host cell is necessary for induction of apoptosis in MDMs, and induction of apoptosis contributes to the host defense against S. pneumoniae.