Effect of PM2.5 on invasion and proliferation of HeLa cells and the expression of inflammatory cytokines IL‑1 and IL‑6

Abstract

Effects of different levels of PM2.5 on invasion and proliferation of HeLa cells and the expression levels of inflammatory cytokines IL-1 and IL-6 under 10 µg/ml PM2.5 were investigated. Different groups of HeLa cells were treated with PM2.5 at 0, 10, 25, 50, 100 and 200 µg/ml for 36 h, respectively. Cell proliferation was detected by MTT assay. Transwell assay was performed to detect the invasion of HeLa cells. Enzyme-linked immunosorbent assay (ELISA), RT-qPCR and western blotting were used to detect the expression levels of inflammatory cytokines IL-1 and IL-6 in PM2.5-stimulated HeLa cells. It was observed that proliferation of cells treated with PM2.5 at a concentration of 10 µg/ml was basically the same as that of untreated cells, while high concentration of PM2.5 inhibited the proliferation of HeLa cells in a dose-dependent manner in the range from 25 to 200 µg/ml (P<0.05). Transwell invasion assay showed that the number of migrating HeLa cells stimulated by 10 µg/ml PM2.5 was significantly greater than that of NC group cells (P<0.05). Western blotting showed that IL-1 and IL-6 protein expression levels in HeLa cells after stimulation with 10 µg/ml PM2.5 were significantly higher than that in NC group (P<0.05). RT-qPCR results also showed that IL-1 mRNA and IL-6 mRNA expression levels in HeLa cells stimulated by 10 µg/ml PM2.5 were significantly higher than those in the NC group (P<0.05). Additionally, ELISA results showed that IL-1 and IL-6 levels in HeLa cells stimulated by 10 µg/ml PM2.5 were significantly higher than those in NC group (P<0.05). We conclude that high concentrations of PM2.5 can inhibit the proliferation of HeLa cells to a certain extent. Stimulation with 10 µg/ml PM2.5 increases the invasion ability of HeLa cells and promotes the expression of inflammatory cytokines IL-1 and IL-6.

Pathogenic Mechanisms of Secondary Organic Aerosols

“…Other potential SOA-mediated mechanisms could be envisioned if we reason that SOA are part of PM. It has been demonstrated that PM, especially PM2.5, have the capacity to reduce cell proliferation , through cell cycle arrest in different types of cells. ,,,− PM are also known to induce apoptosis and autophagy. ,− Interestingly, a crosstalk between the latter has been documented, , and both can be explained by PM2.5 implication concerning a decrease of mRNA and protein level of mammalian target of rapamycin (mTOR). − Quite relevant, PM2.5-induced apoptosis was found to be mediated by an increase of known apoptotic factors like p53 and a decrease of its inhibitor, SGK1 usually activated by mTOR, resulting in a cascade of different steps and involving a series of molecules such as Bax, cytochrome c , APAF-1, and caspases (Figure ). − Of course, additional studies are required in order to determine the relevance of these speculations.…”

A Combination of α-Lipoic Acid (ALA) and Palmitoylethanolamide (PEA) Blocks Endotoxin-Induced Oxidative Stress and Cytokine Storm: A Possible Intervention for COVID-19

“…Another 100 µl/well chromogenic substrate TMB was added, and incubated in the dark at room temperature for 20 min. Finally, a 50 µl/well stop buffer was added, and the maximum absorption wavelength of 450 nm was measured (48).…”

Tanshinone IIA‐regulation of IL‐6 antagonizes PM2.5‐induced proliferation of human bronchial epithelial cells via a STAT3/miR‐21 reciprocal loop

“…Thus, for HBE cells, PM 2.5 ‐induced changes had biphasic effects. Previous reports show that low concentrations (10 μg/ml and 50 μg/cm 2 ) of PM 2.5 induce cell proliferation 34,35 and that a high concentration (100 μg/ml) causes apoptosis 36,37 . Another study shows that, for HBE cells, PM 2.5 (25 μg/ml) accelerates cell proliferation 38 …”

“…A low concentration of PM 2.5 (25 μg/cm 2 ) promoted cell viability, whereas high concentrations (250 and 500 μg/cm 2 ) lowered cell viability. Thus, for HBE cells, cell proliferation 34,35 and that a high concentration (100 μg/ml) causes apoptosis. 36,37 Another study shows that, for HBE cells, PM 2.5 (25 μg/ml) accelerates cell proliferation.…”