Bone marrow (BM)-resident hematopoietic stem and progenitor cells (HSPCs) are often activated following bacterial insults to replenish the host hemato-immune system, but how they integrate the associated tissue damage signals to initiate distal tissue repair is largely unknown. Here, we show that acute gut inflammation expands HSPCs in the BM and directs them to inflamed mesenteric lymph nodes through GM–CSFR activation for further expansion and potential differentiation into Ly6C⁺/G⁺ myeloid cells specialized in gut tissue repair. We identified this process to be mediated by Bacteroides, a commensal gram-negative bacteria that activates innate immune signaling. These findings establish cross-organ communication between the BM and distant inflamed sites, whereby a certain subset of multipotent progenitors is specified to respond to imminent hematopoietic demands and to alleviate inflammatory symptoms.

中文翻译：

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造血干细胞和祖细胞整合微生物信号以促进炎症后肠道组织修复

骨髓（BM）驻留的造血干细胞和祖细胞（HSPC）通常在细菌损伤后被激活，以补充宿主的血液免疫系统，但它们如何整合相关的组织损伤信号以启动远端组织修复尚不清楚。在这里，我们发现急性肠道炎症会扩增 BM 中的 HSPC，并通过 GM-CSFR 激活将它们引导至发炎的肠系膜淋巴结，以进一步扩增并潜在分化为专门负责肠道组织修复的 Ly6C + /G ⁺骨髓^细胞。我们发现这个过程是由拟杆菌介导的，拟杆菌是一种共生的革兰氏阴性细菌，可以激活先天免疫信号。这些发现在骨髓和远处炎症部位之间建立了跨器官通讯，从而指定多能祖细胞的某个子集来响应迫在眉睫的造血需求并减轻炎症症状。