Developmental exposure to mercury chloride impairs social behavior in male offspring dependent on genetic background and maternal autoimmune environment

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To date, the connection between inorganic mercury (Hg) and social behavior remains incompletely understood. The aim of this study was to investigate the influence of maternal autoimmunity by inorganic Hg (Hg2+) exposure on social behavior of offspring. Wild-type (WT) and immunoglobulin deficient (Ig−/−) B10.S dams fertilized by male WT B10.S or SJL mice were treated with 50 μM Hg chloride (HgCl2). Non-pregnant female WT B10.S mice were used to investigate factors regulating HgCl2-induced autoimmunity to brain. HgCl2 selectively impaired social behavior in male offspring, but not female offspring from WT B10.S dams × male SJL, in that only male offspring displayed reduced time distribution with the stranger mouse, decreased sniffing to the stranger mouse and increased self-grooming. HgCl2 did not disrupt social behavior of male or female offspring from WT B10.S dams × male WT B10.S or Ig−/− B10.S dams × male SJL. The offspring from WT and Ig−/− B10.S dams × male SJL had equivalent autoimmunity to brain antigens during HgCl2 exposure, indicating that maternal, but not offspring-derived anti-brain antibodies (Ab) impaired social behavior of the offspring. Non-pregnant WT B10.S mice treated with HgCl2 had increased anti-brain Ab dependent on increase in CD4 T cell activation and IFNγ signaling to macrophages. IFNγ interaction with macrophages drove B cells and plasma cells to produce IgG. Therefore, HgCl2 selectively impaired social behavior in males with certain genetic background via maternally derived anti-brain Ab production, thus providing a novel insight into our current understanding of Hg toxicity.HighlightsHgCl2 impairs social behavior in male offspring of B10.S dams × male SJL mice.HgCl2-impaird social behavior depends on maternal anti-brain Ab production.HgCl2-induced anti-brain Ab requires increased CD4 T cell activation and IFNγ.IFNγ acts on macrophages to drive anti-brain Ab production during HgCl2 exposure.

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