Environmental cadmium exposure following respiratory syncytial virus infection stimulated lung inflammation and disrupted essential metal homeostasis 2326

Abstract Description Cadmium (Cd) accumulates in humans due to dietary, environmental exposure and occupational sources, and has a long biological half-life. Most individuals have pre-existing immunity from early-life exposure to respiratory syncytial virus (RSV), which causes serious lung disease and hospitalizations among high-risk infants and the elderly. Little is known, however, about the effects of early-life RSV infection on low environmental levels of Cd, essential metals and subsequent lung pathology. In this study, we examined the impact of low-dose Cd exposure after RSV infection in infancy on essential metals and lung inflammation in a mouse model. C57BL/6 mice at 8 days were exposed to RSV or unexposed. A subset of these mice then received low-dose Cd (3.0 mg CdCl2/L) in drinking water for 16 weeks (RSV+Cd). Lung tissues were analyzed for essential metals using inductively coupled plasma mass spectrometry, and inflammation was assessed by ELISA. The results show Mg, Zn, and Se levels were reduced, while Fe levels were elevated in both male and female mice after RSV, Cd or RSV+Cd treatment compared to the control group (n = 10 per group). Lung inflammation was substantially higher in the RSV+Cd group than RSV or Cd treatment alone, as measured by the cytokines TNFα, IL-6, and IL-1β, as well as the chemokine KC. In conclusion, our study shows that cumulative Cd burden following RSV infection promotes inflammation, disrupts essential metal regulation, and contributes to lung pathology. Funding Sources NIH/NIEHS ES031980 Topic Categories Viral Immunology (VIR)