Abstract
It is increasingly recognised that vitamin D is important in both adaptive and innate immunity with significant immunomodulatory effects. Patients undergoing oesophagectomy are at significant risk of post-operative Acute Lung Injury. They are severely vitamin d deficient and those with the lowest levels of vitamin D have a greater systemic inflammation with increased epithelial damage and extra-vascular lung water. We hypothesised that vitamin d has a trophic role to protect against alveolar epithelial damage.
Methods: A549 cells were mechanically wounded using a pipette tip and then wound repair after 24 hours culture with or without 25 D3 was assessed by videomicroscopy. Cell proliferation was measured by BRDU incorporation. Cells were incubated with FasL alone or with 25 D3 for 24 hours. Cell viability was measured using a Celltiter Aqueous solution (Promega).
Results: A549 and primary alveolar type II cells increased wound repair in response to a physiological dose of vitamin 25D3. BRDU incorporation was similarly increased supporting proliferative effect of vitamin D. sFasL induced cell death was reduced by addition of 50nmol/L 25-OH vitamin D (p=0.001) when added before or up to 1.5 hours after addition of sFasL suggesting that vitamin d reduced apoptotic cell death. sFasl inhibited proliferation of ATII in actions that were blocked by vitamin d.
Conclusions: Our data suggests that Vitamin D plays a role in the maintenance of an intact alveolar epithelial barrier through effects on wound repair and is protective against apoptotic cell death.
- © 2011 ERS
