Social sensing of infection reprograms peripheral immunity in healthy mice

Abstract

In plants and insects, social immunity enables individuals to detect infection in neighbors and mount protective, community-level responses. Whether mammals possess analogous mechanisms remains unknown. Here, we asked how the presence of sick cage-mates influences the physiology of uninfected neighbors. We found that healthy mice co-housed with conspecifics infected with the non-communicable murine pathogen Toxoplasma gondii undergo a shift in peripheral immune responses that establishes a primed immune state. This exposure-induced priming conferred physiological resilience to a sublethal lipopolysaccharide (LPS)-inflammatory challenge and was mediated by increased myeloid-derived IL-10 production. Blocking IL-10 signaling abrogated exposure-induced protection against a subsequent immune challenge. Thus, our findings show that immune state in healthy mammals can be shaped by exposure to infected conspecifics, hinting at social immunity-based protective mechanisms in mammals. One sentence summaryImmune responses in healthy mammals are shaped by exposure to infected conspecifics.