Center for Gastrointestinal Biology, Department of Morphology, Institute of Biological Sciences, Federal University of Minas Gerais, Belo Horizonte, Brazil.
Department of Biochemistry and Immunology, Institute of Biological Sciences, Federal University of Minas Gerais, Belo Horizonte, Brazil.
Front Immunol. 2022 Jul 28;13:892114. doi: 10.3389/fimmu.2022.892114. eCollection 2022.
Kupffer cells are the primary liver resident immune cell responsible for the liver firewall function, including clearance of bacterial infection from the circulation, as they are strategically positioned inside the liver sinusoid with intimate contact with the blood. Disruption in the tissue-resident macrophage niche, such as in Kupffer cells, can lead to a window of susceptibility to systemic infections, which represents a significant cause of mortality in patients with acetaminophen (APAP) overdose-induced acute liver injury (ALI). However, how Kupffer cell niche disruption increases susceptibility to systemic infections in ALI is not fully understood. Using a mouse model of ALI induced by APAP overdose, we found that Kupffer cells upregulated the apoptotic cell death program and were markedly reduced in the necrotic areas during the early stages of ALI, opening the niche for the infiltration of neutrophils and monocyte subsets. In addition, during the resolution phase of ALI, the remaining tissue macrophages with a Kupffer cell morphology were observed forming replicating cell clusters closer to necrotic areas devoid of Kupffer cells. Interestingly, mice with APAP-induced liver injury were still susceptible to infections despite the dual cellular input of circulating monocytes and proliferation of remaining Kupffer cells in the damaged liver. Therapy with bone marrow-derived macrophages (BMDM) was shown to be effective in occupying the niche devoid of Kupffer cells following APAP-induced ALI. The rapid BMDM migration to the liver and their positioning within necrotic areas enhanced the healing of the tissue and restored the liver firewall function after BMDM therapy. Therefore, we showed that disruption in the Kupffer cell niche and its impaired function during acute liver injury are key factors for the susceptibility to systemic bacterial infections. In addition, modulation of the liver macrophage niche was shown to be a promising therapeutic strategy for liver injuries that reduce the Kupffer cell number and compromise the organ function.
库普弗细胞是主要的肝脏驻留免疫细胞,负责肝脏防火墙功能,包括从循环中清除细菌感染,因为它们位于肝窦内,与血液密切接触。组织驻留巨噬细胞龛位的破坏,如库普弗细胞,可导致对全身感染的易感性窗口,这是乙酰氨基酚 (APAP) 过量诱导的急性肝损伤 (ALI) 患者死亡的主要原因。然而,库普弗细胞龛位破坏如何增加 ALI 患者对全身感染的易感性尚不完全清楚。我们使用 APAP 过量诱导的 ALI 小鼠模型发现,库普弗细胞上调了细胞凋亡程序,并在 ALI 的早期阶段在坏死区域明显减少,为中性粒细胞和单核细胞亚群的浸润开辟了龛位。此外,在 ALI 的消退阶段,观察到具有库普弗细胞形态的剩余组织巨噬细胞在没有库普弗细胞的坏死区域附近形成复制细胞簇。有趣的是,尽管循环单核细胞的双重细胞输入和受损肝脏中剩余库普弗细胞的增殖,APAP 诱导肝损伤的小鼠仍然容易感染。骨髓来源的巨噬细胞 (BMDM) 治疗显示在 APAP 诱导的 ALI 后有效占据缺乏库普弗细胞的龛位。BMDM 快速迁移到肝脏并定位于坏死区域内,增强了组织的愈合,并在 BMDM 治疗后恢复了肝脏防火墙功能。因此,我们表明,库普弗细胞龛位的破坏及其在急性肝损伤期间的功能障碍是易患全身细菌感染的关键因素。此外,调节肝脏巨噬细胞龛位被证明是一种有前途的治疗策略,可减少库普弗细胞数量并损害器官功能的肝损伤。