Effects of PM 10 Airborne Particles from Different Regions of a Megacity on In Vitro Secretion of Cytokines by a Monocyte Line during Different Seasons.
Noemi Meraz-CruzNatalia Manzano-LeónDaniel Eduardo Sandoval-ColinMaría Del Carmen García de León MéndezRaúl Quintana-BelmaresLaura Sevilla TapiaAlvaro R Osornio-VargasMiatta A BuxtonMarie S O'NeillFelipe Vadillo-OrtegaPublished in: Toxics (2024)
Several epidemiological studies have demonstrated that particulate matter (PM) in air pollution can be involved in the genesis or aggravation of different cardiovascular, respiratory, perinatal, and cancer diseases. This study assessed the in vitro effects of PM 10 on the secretion of cytokines by a human monocytic cell line (THP-1). We compared the chemotactic, pro-inflammatory, and anti-inflammatory cytokines induced by PM 10 collected for two years during three different seasons in five different Mexico City locations. MIP-1α, IP-10, MCP-1, TNF-α, and VEGF were the main secretion products after stimulation with 80 μg/mL of PM 10 for 24 h. The THP-1 cells showed a differential response to PM 10 obtained in the different sites of Mexico City. The PM 10 from the north and the central city areas induced a higher pro-inflammatory cytokine response than those from the south. Seasonal pro-inflammatory cytokine secretion always exceeded anti-inflammatory secretion. The rainy-season-derived particles caused the lowest pro-inflammatory effects. We concluded that toxicological assessment of airborne particles provides evidence supporting their potential role in the chronic exacerbation of local or systemic inflammatory responses that may worsen the evolution of some chronic diseases.
Keyphrases
- particulate matter
- air pollution
- endothelial cells
- lung function
- anti inflammatory
- chronic obstructive pulmonary disease
- squamous cell carcinoma
- young adults
- pregnant women
- dendritic cells
- drug induced
- vascular endothelial growth factor
- high glucose
- cystic fibrosis
- immune response
- signaling pathway
- oxidative stress
- risk assessment
- polycyclic aromatic hydrocarbons
- cell cycle arrest
- extracorporeal membrane oxygenation
- cell death
- case control