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Microplastic exposure aggravates pneumococcus-induced inflammation in macrophages by activating ferroptosis
Ko-Wei Chang1, Jo-Tsen Chen2, Chun-Ning Chuang3
1Department of Thoracic Medicine, Chang Gung Memorial Hospital at Linkou, Taoyuan, Taiwan; Graduate Institute of Clinical Medical Sciences, College of Medicine, Chang Gung University, Taoyuan, Taiwan; School of Medicine, National Tsing Hua University, Hsinchu, Taiwan.
Abstract:
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.
Insights
Microplastics (MPs) impair macrophage ability to clear Streptococcus pneumoniae, worsening inflammation. MPs promote M1 macrophage polarization and ferroptosis, highlighting risks of plastic pollution during bacterial infections.
Area of Science:
- Environmental Health
- Immunology
- Toxicology
Background:
- Microplastics (MPs) are pervasive pollutants with potential health risks.
- These particles can carry chemicals and pathogens, impacting biological systems.
- Streptococcus pneumoniae causes pneumonia, but its interaction with MPs in macrophages is unknown.
Purpose of the Study:
- Investigate how MPs affect macrophage function during pneumococcal infection.
- Elucidate the mechanisms behind MP-induced inhibition of bacterial clearance and inflammation.
Main Methods:
- Assessed macrophage phagocytosis of Streptococcus pneumoniae under MP exposure.
- Analyzed C-C motif chemokine ligand 2 (CCL2) production.
- Examined the roles of PI3K/Akt and MAPK/ERK signaling pathways.
- Investigated M1 macrophage polarization and ferroptosis pathway activation.
Main Results:
- MP exposure significantly reduced macrophage phagocytosis and pneumococcal engulfment.
- MPs synergistically increased CCL2 production via PI3K/Akt and MAPK/ERK pathways.
- MP-exposed macrophages showed enhanced M1 polarization and ferroptosis activation during infection.
Conclusions:
- Microplastics disrupt macrophage immune functions, hindering bacterial clearance.
- MPs exacerbate pneumococcal infection by promoting pro-inflammatory M1 polarization and ferroptosis.
- Findings offer insights into managing MP-related pulmonary diseases.
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