ABSTRACT
The declaration of COVID-19 pandemic by the WHO initiated a series of lockdowns globally that varied in stringency and duration; however, the spatiotemporal effects of these lockdowns on air quality remain understudied. This study evaluates the global impact of lockdowns on air pollutants using tropospheric and ground-level indicators over a five-month period. Moreover, the relationship between air pollution and COVID-19 cases and mortalities was examined. Changes in the global tropospheric (NO2, aerosols, and O3) and ground-level (PM2.5, PM10, NO2, and O3) pollutants were observed, and the maximum air quality improvement was observed immediately after lockdown. Except for a few countries, a decline in air pollutants correlated with a reduction in Land Surface Temperature (LST). Notably, regions with higher tropospheric NO2 and aerosol concentrations were also COVID-19 hotspots. Our analysis showed moderate positive correlation for NO2 with COVID-19 cases (R2 = 0.33; r = 0.57, P = 0.006) and mortalities (R2 = 0.40; r = 0.63, P = 0.015), while O3 showed a weak-moderate positive correlation with COVID-19 cases (R2 = 0.22; r = 0.47, P = 0.003) and mortalities (R2 = 0.12; r = 0.35, P = 0.012). However, PM2.5, and PM10 showed no significant correlation with either COVID-19 cases or mortality. This study reveals that humans living under adverse air pollution conditions are at higher risk of COVID-19 infection and mortality.
ABSTRACT
MicroRNAs (miRNAs) regulate the synthesis of cytokines in response to Toll-like receptor (TLR) activation. Our recent microarray study comparing normal and inflamed human dental pulps showed that miRNA-181 (miR-181) family is differentially expressed in the presence of inflammation. Prior studies have reported that the dental pulp, which is composed primarily of TLR4/2+ fibroblasts, expresses elevated levels of cytokines including interleukin-8 (IL-8) when inflamed. In this study, we employed an in-vitro model to determine the role of the miRNA-181 family in the TLR agonist-induced response in human fibroblasts. TLR4/2+ primary human dental pulp fibroblasts were stimulated with lipopolysaccharide from Porphyromonas gingivalis (Pg LPS), a known oral pathogen, and IL-8 and miR-181 expression measured. An inversely proportional relationship between IL-8 and miR-181a was observed. In-silico analysis identified a miR-181a-binding site on the 3' untranslated region (UTR) of IL-8, which was confirmed by dual-luciferase assays. MiR-181a directly binds to the 3'UTR of IL-8, an important inflammatory component of the immune response, and modulates its levels. This is the very first report demonstrating miR-181a regulation of IL-8.
