Abstract
Background: Myocarditis is an inflammatory heart disease caused by viral infections that can lead to heart failure, and occurs more often in men than women. Since animal studies have shown that myocarditis is influenced by sex hormones, we hypothesized that endocrine disruptors, which interfere with natural hormones, may play a role in the progression of the disease. The human population is exposed to the endocrine disruptor bisphenol A (BPA) from plastics, such as water bottles and plastic food containers. Methods: Male and female adult BALB/c mice were housed in plastic versus glass caging, or exposed to BPA in drinking water versus control water. Myocarditis was induced with coxsackievirus B3 on day 0, and the endpoints were assessed on day 10 post infection. Results: We found that male BALB/c mice that were exposed to plastic caging had increased myocarditis due to complement activation and elevated numbers of macrophages and neutrophils, whereas females had elevated mast cell activation and fibrosis. Conclusions: These findings show that housing mice in traditional plastic caging increases viral myocarditis in males and females, but using sex-specific immune mechanisms.
Highlights
In order to assess the effect of plastic caging on myocarditis, in this study we examined the effect of exposure to plastics from traditional plastic cages and plastic water bottles, and control glass cages and glass water bottles, in 6–8-weekold male and female BALB/c mice with coxsackie virus B3 (CVB3) myocarditis, using control water
The male and female BALB/c mice were given 250 μg bisphenol A (BPA)/L in their drinking water, which is equivalent to an estimated intake of 50 μg BPA/kg body weight (BW), which is equivalent to the EPA reference dose or the maximum daily oral exposure dose that is likely to occur over a lifetime without deleterious effects [65]
We found that exposure to plastic caging in BALB/c female mice did not significantly alter myocardial inflammation histologically, at day 10 post infection, during peak myocarditis (p = 0.34) (Figure 1a)
Summary
The development of fibrosis has been associated with the release of Th2 cytokines that include interleukin (IL)-4, IL-5, and IL-13 [17] Other proinflammatory cells, such as Th17 cells, have been demonstrated to link inflammation and fibrosis, through the secretion of IL-17A, which was observed to promote hypertension-induced fibrosis, and to promote remodeling and fibrosis that lead to DCM in animal models and patients with myocarditis [18,19,20]. Results: We found that male BALB/c mice that were exposed to plastic caging had increased myocarditis due to complement activation and elevated numbers of macrophages and neutrophils, whereas females had elevated mast cell activation and fibrosis. Conclusions: These findings show that housing mice in traditional plastic caging increases viral myocarditis in males and females, but using sex-specific immune mechanisms
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