Cutting Edge: Bacterial Infection Induces Hematopoietic Stem and Progenitor Cell Expansion in the Absence of TLR Signaling
Cutting Edge: Bacterial Infection Induces Hematopoietic Stem and Progenitor Cell Expansion in the Absence of TLR Signaling
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DOI：
10.4049/jimmunol.0903652
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发表时间：
2010-03-01
影响因子：
4.4
通讯作者：
Moldawer, Lyle L.
中科院分区：
文献类型：
--
作者：
Scumpia, Philip O.;Kelly-Scumpia, Kindra M.;Moldawer, Lyle L.
骨髓（BM）造血干细胞和祖细胞（HSPC）可以被IIFN型、TLR激动剂、病毒和细菌激活以增加造血。在这项研究中，我们报告了体内内毒素处理诱导TLR 4，MyD 88和Toll/IL-1抗性结构域含有衔接子诱导IFN-β（TRIF）的BM HSPC依赖性扩增。由金黄色葡萄球菌或盲肠结扎和穿刺引起的细菌感染也诱导HSPC扩增，但MyD 88、TRIF、IIFN型、细胞因子、PG或氧化应激途径不是其扩增所需的。S. MyD 88（-/-）TRIF（-/-）小鼠中金黄色葡萄球菌诱导的HSPC扩增也是正常的，但与BM重塑相关，因为粒细胞储存在外周释放。重要的是，单独的BM细胞结构的减少可以再现HSPC扩增。这些数据表明，体内HSPC对细菌感染的反应是复杂的，并不绝对依赖于关键的炎症信号传导途径。免疫学杂志，2010，184：2247-2251。
Bone marrow (BM) hematopoietic stem and progenitor cells (HSPCs) can be activated by type IIFNs, TLR agonists, viruses, and bacteria to increase hematopoiesis. In this study, we report that endotoxin treatment in vivo induces TLR4, MyD88, and Toll/IL-1 resistance domain-containing adaptor-inducing IFN-beta (TRIF)dependent expansion of BM HSPCs. Bacterial infection by Staphylococcus aureus or cecal ligation and puncture also induces HSPC expansion, but MyD88, TRIF, type IIFN, cytokine, PG, or oxidative stress pathways are not required for their expansion. S. aureus-induced HSPC expansion in MyD88(-/-)TRIF(-/-) mice is also normal, but is associated with BM remodeling as granulocyte stores are released peripherally. Importantly, reduction in BM cellularity alone can reproduce HSPC expansion. These data show in vivo HSPC responses to bacterial infection are complex and not absolutely dependent upon key inflammatory signaling pathways. The Journal of Immunology, 2010, 184: 2247-2251.