# PM2.5 Extracts Induce INFγ-Independent Activation of CIITA, MHCII, and Increases Inflammation in Human Bronchial Epithelium

## TL;DR

This study shows that PM2.5 exposure can trigger inflammation in human bronchial cells through a non-canonical pathway that does not rely on INFγ.

## Contribution

The paper identifies an INFγ-independent mechanism by which PM2.5 induces inflammation in bronchial epithelium.

## Key findings

- PM2.5 exposure significantly induced phosphorylation of STAT1 Y701 and increased CIITA and HLA-DRα mRNA levels.
- IL-6 levels rose early after PM2.5 exposure, while INFγ mRNA levels remained low.
- CuSO4 exposure increased HLA-DRα and STAT1 expression at different time points.

## 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 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.