Key findings:
- No loss of cell viability or barrier integrity
- No induction of classical inflammatory or fibrotic markers
- But: activation of markers for fibroblast proliferation and migration was detected
The results suggest that “silent” epithelial stress from mixed airborne pollutants may initiate early lung damage through unconventional epithelial–mesenchymal crosstalk—an aspect that may be missed by standard toxicity endpoints.
This work underscores the need for repeated (chronic) exposure scenarios to capture the full scope of respiratory hazard assessment.
Did you observe pre-inflammatory effects in your own research as well?
Read the full publication here: https://lnkd.in/dNrvcbGD
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