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Microplastic exposure aggravates pneumococcus-induced inflammation in macrophages by activating ferroptosis
Summary
Researchers investigated how microplastic exposure affects the immune response of macrophages to pneumococcal (Streptococcus pneumoniae) infection. They found that microplastics impaired macrophage phagocytosis, inhibited bacterial clearance, and amplified inflammation by activating ferroptosis and promoting M1 macrophage polarization through PI3K/Akt and MAPK/ERK signaling pathways. The study suggests that microplastic exposure may worsen bacterial lung infections by compromising immune cell function.
Microplastics (MPs) are ubiquitous environmental pollutants posing serious concerns owing to their potential health implications. MPs exert detrimental effects via the plastic particles, MP-bound chemicals, and MP-carrying pathogens. Streptococcus pneumoniae (pneumococcus) is a major pathogen causing bacterial pneumonia and respiratory inflammation. However, specific immune responses of macrophages to pneumococcus under MP exposure remain unclear. In this study, we aimed to investigate the mechanisms by which MPs inhibit macrophage functions, bacterial clearance, and inflammation during pneumococcal infection. Our results showed that MP exposure significantly impaired macrophage phagocytosis and inhibited pneumococcal engulfment. Furthermore, MPs synergistically enhanced C-C motif chemokine ligand 2 (CCL2) production via the phosphoinositide 3-kinase/protein kinase B (PI3K/Akt) and mitogen-activated protein kinase/extracellular signal-regulated kinase (MAPK/ERK) pathways, promoting M1 macrophage polarization and activating the ferroptosis pathway upon pneumococcal infection. Understanding the roles of MPs in the exacerbation of macrophage-driven inflammation will facilitate the development of new strategies to manage and treat pneumococcus-induced pulmonary diseases.
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