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- W2591967546 abstract "Background Exposure to elevated concentrations of particulate matter (PM) pollution is associated with increased mortality and exacerbation of cardiopulmonary disease. The toxicological basis for this has been attributed to its capacity to induce oxidative stress in vivo, triggering activation of both the innate and adaptive immune systems. Recent studies have demonstrated evidence of an enhanced impact of PM during periods of increased photochemistry, characterised by high ozone; suggesting that ozonation of PM may enhance its toxicity. Methods We examined the oxidative potential of PM10 (less than 10μm in diameter) collected within London, UK, during periods of high and low ozone concentrations. PM10 samples were extracted from filters collected, between Mar-July 2014 (n=6, elevated ozone, 102±20 μg/m3) and Dec 2013-Apr 2014 (n=8, low ozone, 24±14 μg/m3), from roadside and urban background sites across London. PM10 oxidative potential (OP) was assessed by quantifying its capacity to oxidise ascorbate (AA) and glutathione (GSH) in a synthetic human respiratory tract lining fluid, over a 4 hour period (37oC, pH 7). Results are expressed as the percentage loss of AA and GSH per μg of PM10 (OPAA and OPGSH/μg respectively). The PM10 effect on the immune system was quantified by examining its capacity to drive the maturation of monocyte derived dendritic cells (MDDCs) from healthy non asthmatic donors (n=6) following a 24 hour incubation (2.5-20 μg/mL). Cell maturation was assessed by examining the expression of CD83, CD86, MHC class I and MHC class II by flow-cytometry. Results PM10 collected during a high ozone period exhibited enhanced OPAA (0.94±0.01 vs. 0.81±0.01 %/μg, P Conclusion These data suggest that urban PM collected during high ozone periods has an enhanced capacity to activate the adaptive immune system." @default.
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- W2591967546 date "2016-11-01" @default.
- W2591967546 modified "2023-09-27" @default.
- W2591967546 title "Urban Particulate Matter Collected During Ozone Episodes Has an Enhanced Capacity to Drive Dendritic Cell Maturation" @default.
- W2591967546 doi "https://doi.org/10.1016/j.freeradbiomed.2016.10.134" @default.
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