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PM 2.5 Extracts Induce INFγ-Independent Activation of CIITA, MHCII, and Increases Inflammation in Human Bronchial Epithelium.

Authors :
Jirau-Colón, Héctor
Jiménez-Vélez, Braulio D.
Source :
Toxics; Apr2024, Vol. 12 Issue 4, p292, 20p
Publication Year :
2024

Abstract

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 PM<subscript>2.5</subscript> (from Puerto Rico) and CuSO<subscript>4</subscript>, 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 PM<subscript>2.5</subscript> 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 CuSO<subscript>4</subscript> 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 PM<subscript>2.5</subscript> extract exposure in human bronchial epithelia can be induced early via an alternate non-canonical pathway in the absence of INFγ. [ABSTRACT FROM AUTHOR]

Details

Language :
English
ISSN :
23056304
Volume :
12
Issue :
4
Database :
Complementary Index
Journal :
Toxics
Publication Type :
Academic Journal
Accession number :
176874910
Full Text :
https://doi.org/10.3390/toxics12040292