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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.
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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