GSE182953
Inflammation of gill epithelia in fish causes increased permeation of polar organic chemicals from OSPW via disruption of tight junctions
The epithelial cell layer that lines the fish gill controls the paracellular permeation of chemicals through tight junctions. The integrity of tight junctions can be affected by inflammation, which is likely to impact the branchial bioavailability of chemicals. In this study, we experimentally induced inflammation in the rainbow trout gill cell line RTgill-W1 via exposure to bacterial lipopolysaccharides (LPS). We then co-exposed the cells to extracts of oil sands process-affected water (OSPW), which contain a complex mixture of toxicologically relevant chemicals. Cells exposed to LPS showed a significant reduction in transepithelial electrical resistance (TEER), an indicator of tight junction integrity, after 24 h of exposure. Quantitative RT-PCR analysis determined that the abundance of transcripts of genes coding for tight junction proteins (Claudin 28b and 10e) was significantly decreased in cells exposed to 20, 50, and 100 mg L-1 LPS. Chemical analysis revealed a significant increase in permeation of constituents of OSPW across the gill cell epithelial layer at all studied LPS concentrations. These in vitro findings were confirmed in vivo in rainbow trout fingerlings exposed to both LPS and 10% OSPW for 48 h, which similarly resulted in an increase in chemical uptake relative to fish exposed to OSPW alone. This research demonstrated that inflammation of gill epithelia and the resulting disruption of tight junction integrity could lead to significantly greater uptake of potentially harmful chemicals from the environment, which has important implications for risk assessment. Overall design: mRNA profiles of Rtgill-W1 cells exposed to L-15 media (reference/control) and 100 mg/L bacterial lipopolysaccharide (LPS; treated) for 4 hours. There were 4 replicates of control/reference and 3 replicates of LPS-treated cells.