NDLI: Cigarette smoke exposure is associated with vitamin D3 deficiencies in patients with chronic rhinosinusitis.

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Cigarette smoke exposure is associated with vitamin D3 deficiencies in patients with chronic rhinosinusitis.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Mulligan, Jennifer K. Nagel, Whitney O'Connell, Brendan P. Wentzel, Jennifer Atkinson, Carl Schlosser, Rodney J.
Description	Author Affiliation: Mulligan JK ( Department of Otolaryngology-Head & Neck Surgery, Medical University of South Carolina, Charleston, SC); Nagel W ( Department of Otolaryngology-Head & Neck Surgery, Medical University of South Carolina, Charleston, SC.); O'Connell BP ( Department of Otolaryngology-Head & Neck Surgery, Medical University of South Carolina, Charleston, SC.); Wentzel J ( Department of Otolaryngology-Head & Neck Surgery, Medical University of South Carolina, Charleston, SC.); Atkinson C ( Department of Microbiology and Immunology, Medical University of South Carolina, Charleston, SC.); Schlosser RJ ( Department of Otolaryngology-Head & Neck Surgery, Medical University of South Carolina, Charleston, SC)
Abstract	BACKGROUND: Cigarette smoke (CS) plays a role in the exacerbation of chronic rhinosinusitis (CRS); however, the mechanism for this is unknown. We hypothesize that CS impairs human sinonasal epithelial cell (HSNEC) conversion of 25(OH)D3 (25VD3) to 1,25-dihydroxyvitamin D3 (1,25VD3) and, furthermore, that supplementation with 1,25VD3 will reverse smoke-induced inflammatory responses by HSNECs. OBJECTIVE: We sought to determine the effect of CS on vitamin D3 (VD3) levels, conversion, and regulation of CS-induced inflammation in control subjects and patients with CRS. METHODS: Blood and sinus tissue explants were collected at the time of surgery from control subjects, patients with chronic rhinosinusitis without nasal polyps, and patients with chronic sinusitis with nasal polyps (CRSwNP). Expression of VD3 metabolizing enzymes were measured by using RT-PCR. Primary HSNECs were cultured from tissue explants. 25VD3 with and without cigarette smoke extract (CSE) was used to examine conversion of 25VD3 to 1,25VD3, as well as HSNEC production of proinflammatory cytokines. RESULTS: CS exposure was associated with reduced circulating and sinonasal 25VD3 levels in all groups compared with those seen in CS-naive, disease-matched counterparts. CS exposure decreased expression of CYP27B1 and was especially pronounced in patients with CRSwNP. CSE impairs control HSNEC conversion of 25VD3. HSNECs from patients with CRSwNP also demonstrate an intrinsic reduction in conversion of 25VD3 to 1,25VD3. Exogenous 1,25VD3 reduces CSE-induced cytokine production by HSNECs. CONCLUSIONS: Exposure to CS is associated with reduced 25VD3 levels and an impaired ability of HSNECs to convert 25VD3 to 1,25VD3. Addition of 1,25VD3 reduces the proinflammatory effects of CS on HSNECs. Impaired VD3 conversion by CS exposure represents a novel mechanism through which CS induces its proinflammatory effects.
File Format	HTM / HTML
ISSN	00916749
e-ISSN	10976825
Journal	Journal of Allergy and Clinical Immunology
Issue Number	2
Volume Number	134
Language	English
Publisher	Elsevier
Publisher Date	2014-08-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Discipline Immunology Calcitriol Deficiency Rhinitis Metabolism Sinusitis Tobacco Chemistry Vitamin D Deficiency 25-hydroxyvitamin D3 1-alpha-hydroxylase Genetics Calcifediol Pharmacology Case-control Studies Chronic Disease Complex Mixtures Isolation & Purification Epithelial Cells Cytology Drug Effects Gene Expression Regulation Nasal Polyps Complications Pathology Primary Cell Culture Respiratory Mucosa Research Support, N.i.h., Extramural Research Support, Non-u.s. Gov't
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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