Data from: Single cell RNA-seq analysis reveals that prenatal arsenic exposure results in long-term, adverse effects on immune gene expression in response to Influenza A infection

Arsenic exposure via drinking water is a serious environmental health
concern. Epidemiological studies suggest a strong association between
prenatal arsenic exposure and subsequent childhood respiratory infections,
as well as morbidity from respiratory diseases in adulthood, long after
systemic clearance of arsenic. We investigated the impact of exclusive
prenatal arsenic exposure on the inflammatory immune response and
respiratory health after an adult influenza A (IAV) lung infection.
C57BL/6J mice were exposed to 100 ppb sodium arsenite in utero, and
subsequently infected with IAV (H1N1) after maturation to adulthood.
Assessment of lung tissue and bronchoalveolar lavage fluid (BALF) at
various time points post IAV infection reveals greater lung damage and
inflammation in arsenic exposed mice versus control mice. Single-cell RNA
sequencing analysis of immune cells harvested from IAV infected lungs
suggests that the enhanced inflammatory response is mediated by
dysregulation of innate immune function of monocyte derived macrophages,
neutrophils, NK cells, and alveolar macrophages. Our results suggest that
prenatal arsenic exposure results in lasting effects on the adult host
innate immune response to IAV infection, long after exposure to arsenic,
leading to greater immunopathology. This study provides the first direct
evidence that exclusive prenatal exposure to arsenic in drinking water
causes predisposition to a hyperinflammatory response to IAV infection in
adult mice, which is associated with significant lung damage.