Ccl5+ Macrophages drive pro-inflammatory responses and neutrophil recruitment in sepsis-associated acute kidney injury.

Sepsis leads to dysfunctional immune responses with multi-organ damage, and acute kidney injury (AKI) is a common complication of sepsis. To gain a deeper understanding of the specific underlying mechanisms of sepsis, we investigated the effects of specific macrophages on sepsis. To gain a deeper understanding of the specific underlying mechanisms of sepsis, we investigated the effects of specific macrophages on sepsis. Single-cell sequencing of a mouse model of endotoxemia revealed that sepsis is a common complication of sepsis. Single-cell sequencing of a mouse model of endotoxemia revealed that the emerging macrophage subpopulation Ccl5+ Mac was significantly pro-inflammatory, activating a large number of pathways activating a large number of pathways associated with immune response and inflammatory response, including IL6-JAK-STAT3 signaling, TGF-β signaling, and inflammatory response. Interestingly, we found that Ccl5+ Mac recruits neutrophil through CCL5-CCR1 ligand receptor pairs by cellular communication analysis thereby further affecting sepsis. We therefore hypothesize that this macrophage subpopulation is actively involved in the underlying molecular mechanisms of AKI. We therefore hypothesize that this macrophage subpopulation is actively involved in the underlying molecular mechanisms of AKI in sepsis and provide valuable insights.