Vitamin D Modulates the Response of Bronchial Epithelial Cells Exposed to Cigarette Smoke Extract
Nutrients 2019, 11(9), 2138; https://doi.org/10.3390/nu11092138
- Smoking reduces vitamin D 34 studies as of Sept 2019
- Note: Inhaled Vitamin D may provide 100X high concentration of activated Vitamin D to lung cells than if taken orally
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The higher the Vitamin D concentration, the lower the inflamation
Carolien Mathyssen 1OrcID,Jef Serré 1OrcID,Annelore Sacreas 1,Stephanie Everaerts 1,Karen Maes 1,Stijn Verleden 1,Lieve Verlinden 2,Annemieke Verstuyf 2,Charles Pilette 3,Ghislaine Gayan-Ramirez 1,Bart Vanaudenaerde 1 andWim Janssens 1,
1 Lab of Respiratory Diseases, CHROMETA, KU Leuven, 3000 Leuven, Belgium
2 Clinical and Experimental Endocrinology, CHROMETA, KU Leuven, 3000 Leuven, Belgium
3 Institute of Experimental & Clinical Research—Pole of Pneumology, ENT and Dermatology, Université Catholique de Louvain (UCL), 1200 Brussels, Belgium
In chronic obstructive pulmonary disease (COPD), the bronchial epithelium is the first immune barrier that is triggered by cigarette smoke. Although vitamin D (vitD) has proven anti-inflammatory and antimicrobial effects in alveolar macrophages, little is known about the direct role of vitD on cigarette smoke-exposed bronchial epithelial cells. We examined the effects of vitD on a human bronchial epithelial cell line (16HBE) and on air–liquid culture of primary bronchial epithelial cells (PBEC) of COPD patients and controls exposed for 24 h to cigarette smoke extract (CSE). VitD decreased CSE-induced IL-8 secretion by 16HBE cells, but not by PBEC. VitD significantly increased the expression of the antimicrobial peptide cathelicidin in 16HBE and PBEC of both COPD subjects and controls. VitD did not affect epithelial to mesenchymal transition or epithelial MMP-9 expression and was not able to restore impaired wound healing by CSE in 16HBE cells. VitD increased the expression of its own catabolic enzyme CYP24A1 thereby maintaining its negative feedback.
In conclusion, vitD supplementation may potentially reduce infectious exacerbations in COPD by the upregulation of cathelicidin in the bronchial epithelium.