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The capacity of particulate matter (PM) to enhance and stimulate the expression of pro-inflammatory mediators has been previously demonstrated in non-antigen-presenting cells (human bronchial epithelia). Nonetheless, many proposed mechanisms for this are extrapolated from known canonical molecular pathways. This work evaluates a possible mechanism for inflammatory exacerbation after exposure to PM2.5 (from Puerto Rico) and CuSO4, using human bronchial epithelial cells (BEAS-2B) as a model. The induction of CIITA, MHCII genes, and various pro-inflammatory mediators was investigated. Among these, the phosphorylation of STAT1 Y701 was significantly induced after 4 h of PM2.5 exposure, concurrent with a slight increase in CIITA and HLA-DRα mRNA levels. INFγ mRNA levels remained low amidst exposure time, while IL-6 levels significantly increased at earlier times. IL-8 remained low, as expected from attenuation by IL-6 in the known INFγ-independent inflammation pathway. The effects of CuSO4 showed an increase in HLA-DRα expression after 8 h, an increase in STAT1 at 1 h, and RF1 at 8 h We hypothesize and show evidence that an inflammatory response due to PM2.5 extract exposure in human bronchial epithelia can be induced early via an alternate non-canonical pathway in the absence of INFγ. [ABSTRACT FROM AUTHOR]

Particle pollution from urban and industrialized regions in Rio de Janeiro (RJ), Brazil was analyzed for toxic and pro-inflammatory (cytokines: IL-6, IL-8, IL-10) responses in human bronchial epithelial cells. Trace elements contribution was studied. Airborne particulate matter was collected at: three industrial sites Ind-1 (PM 10 ) and Ind-2a and 2b (PM 2.5 ); Centro urban area (PM 10 ) and two rural sites (PM 2.5 , PM 10 ). PM 10 acetone extracts were toxic and did not elicit cytokine release; aqueous extracts were less toxic and stimulated the release of IL-6 and IL-8. PM 2.5 aqueous extracts from Ind-2 decreased the release of IL-6 and IL-8. Zinc concentration was higher at the industrial and rural reference sites (Ref-1-2) although metals were not associated to cytokines changes. These results demonstrate that PM from RJ can either increase or decrease cytokine secretion in vitro while being site specific and time dependent. [ABSTRACT FROM AUTHOR]

Exposure to airborne particulate matter (PM) has been associated with the transcriptional up-regulation of pro-inflammatory mediators. However, the effect of PM on post-transcriptional regulation of pro-inflammatory mediators has not been fully explored. In this study, we examined the acute effect of organic extracts from urban PM, rural PM and diesel exhaust particles (DEP) on the post-transcriptional control of interleukin-6 (IL-6) and interleukin-8 (CXCL8) using a human bronchial epithelial cell line. Both PM and DEP extracts induced the release of IL-6 and CXCL8 after 24 h of exposure. Time-course experiments were conducted to examine changes in mRNA steady-state levels and half-lives. The steady-state levels of CXCL8 mRNA increase at 15 min on cells exposed to both PM and DEP extracts. Meanwhile only the urban extract induced significant increases of IL-6 mRNA levels at 15 min. Indirect measurements of IL-6 mRNA half-life showed a dramatic increase in cells exposed to the organic extracts. CXCL8 mRNA half-life increases in cells exposed to PM extracts and not DEP extract. Nuclear run-ons demonstrated that the urban PM and DEP extracts promoted an up-regulation in the transcription rate of CXCL8 at 15 min but not for IL-6. Urban and rural PM influences the post-transcriptional control of CXCL8. [ABSTRACT FROM AUTHOR]