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Fine Particulate Matter (PM2.5) Promotes CD146 Expression in Alveolar Epithelial Cells and Cryptococcus neoformans
Zhixiao Sun1, Ningfei Ji1, Jingxian Jiang1
1Department of Respiratory and Critical Care Medicine, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Abstract:
Air pollution is a leading cause of increasing infectious lung diseases. Pulmonary cryptococcosis is a fatal fungal pneumonia in acquired immunodeficiency syndrome patients. In some cases, the pathogen Cryptococcus neoformans also develops dormant nodules in immunocompetent individuals. In the present study, we demonstrated that fine particulate matter (PM2.5) increased CD146 expression in alveolar epithelial cells and promoted C. neoformans pulmonary infection. Aryl hydrocarbon receptor (AhR) signaling was required for increased expression of CD146 in epithelial cells treated with PM2.5. In a murine model of pulmonary infection, PM2.5 promoted fungal infection, and CD146 deficiency decreased the fugal burden of C. neoformans. Our study may highlight the importance of air pollution to lung mycosis and CD146 as a target for preventing infectious lung diseases.
Insights
Fine particulate matter (PM2.5) worsens lung fungal infections by increasing CD146 expression in alveolar cells. Targeting CD146 may help prevent air pollution-linked lung mycosis.
Area of Science:
- Environmental Health
- Infectious Diseases
- Pulmonology
Background:
- Air pollution, particularly fine particulate matter (PM2.5), is linked to increased infectious lung diseases.
- Pulmonary cryptococcosis, caused by *Cryptococcus neoformans*, is a severe fungal pneumonia, especially in immunocompromised individuals.
Purpose of the Study:
- To investigate the role of PM2.5 in promoting pulmonary fungal infections.
- To explore the involvement of CD146 and Aryl hydrocarbon receptor (AhR) signaling in PM2.5-induced exacerbation of *C. neoformans* infection.
Main Methods:
- Assessed CD146 expression in alveolar epithelial cells exposed to PM2.5.
- Utilized a murine model to study the impact of PM2.5 on *C. neoformans* pulmonary infection.
- Investigated the role of AhR signaling and CD146 deficiency in the infection model.
Main Results:
- PM2.5 exposure increased CD146 expression in alveolar epithelial cells.
- AhR signaling mediated the PM2.5-induced upregulation of CD146.
- PM2.5 promoted *C. neoformans* pulmonary infection in mice.
- CD146 deficiency significantly reduced the fungal burden in a murine model of pulmonary cryptococcosis.
Conclusions:
- PM2.5 exacerbates pulmonary fungal infections, potentially by upregulating CD146 via AhR signaling.
- CD146 is identified as a key factor in PM2.5-driven lung mycosis.
- Targeting CD146 presents a potential strategy for preventing infectious lung diseases exacerbated by air pollution.
