摘要：SummaryActivin A levels are elevated during multiple severe infections and associated with an increased risk of death. However, the role of activin A in bacterial infection is still unclear. Here, we found that activin A levels were increased duringS. aureusskin infection in mice. Administration of activin A increased the bacterial burden and promoted the spread of bacteriain vivo. Moreover, activin A inhibited neutrophil chemotaxis to N-formylmethionine-leucyl-phenylalanine via the type IIA activin receptor (ActRIIA)in vitroand impaired ActRIIA+neutrophil recruitment to infection fociin vivo. Additionally, we identified a novel subpopulation of neutrophils, ActRIIA+neutrophils, which exhibit superior phagocytic capacity compared to ActRIIA−neutrophils and possess an N2-like immunoregulatory activity via secreting IL-10 and TGF-β. Taken together, these findings indicate that activin A inhibits the recruitment of ActRIIA+neutrophils to infected foci, leading to the impairment of bacterial clearance, and thus may hamper early infection control.Graphical abstractDisplay OmittedHighlights•A novel activin A-responsitive subpopulation of neutrophils (ActRIIA+) was identified•ActRIIA+neutrophils exhibit N2-like immunoregulatory properties•Activin A inhibits ActRIIA+neutrophil recruitment to infected skinBiological sciences; immunology; microbiology
