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Vitamin D 3 as a novel regulator of basic fibroblast growth factor in chronic rhinosinusitis with nasal polyposis
Author(s) -
Sansoni E. Ritter,
Sautter Nathan B.,
Mace Jess C.,
Smith Timothy L.,
Yawn James R.,
Lawrence Lauren A.,
Schlosser Rodney J.,
Soler Zachary M.,
Mulligan Jennifer K.
Publication year - 2015
Publication title -
international forum of allergy and rhinology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.503
H-Index - 46
eISSN - 2042-6984
pISSN - 2042-6976
DOI - 10.1002/alr.21474
Subject(s) - medicine , regulator , chronic rhinosinusitis , sinusitis , chronic sinusitis , nasal polyps , growth regulator , vitamin d and neurology , vitamin , fibroblast growth factor , gastroenterology , dermatology , immunology , gene , biochemistry , receptor , biology , chemistry , botany
Background The immunopathogenesis of chronic rhinosinusitis (CRS) is largely unknown, but it is thought that different inflammatory profiles are responsible for the different CRS subtypes. 25‐Hydroxyvitamin‐D (25‐VD3) has been shown to alter inflammatory mediators in other disease processes and 25‐VD3 deficiency is associated with CRS with nasal polyps (CRSwNP), but it is unknown if 25‐VD3 levels impact local inflammation in CRS. This study investigated the correlation between plasma 25‐VD3 and sinonasal mucus monocyte chemoattractant protein‐1 (MCP‐1), regulated upon activation normal T cell expressed and secreted (RANTES), and basic fibroblast growth factor (bFGF) levels in patients with CRS. Methods Study subjects undergoing endoscopic sinus surgery (ESS) for CRS were prospectively enrolled from January 2012 to August 2014. Control subjects included patients undergoing ESS for noninflammatory pathology. Blood and sinonasal mucus were collected at the time of ESS. Plasma 25‐VD3 was measured by enzyme‐linked immunosorbent assay (ELISA) and mucus levels of MCP‐1, RANTES, and bFGF by cytometric bead array (CBA). Results A total of 57 patients were enrolled and categorized as CRS without nasal polyps (CRSsNP) (n = 31), CRSwNP (n = 14), and controls (n = 12). No significant correlation was found between MCP‐1 and 25‐VD3. There was a significant negative correlation between 25‐VD3 and RANTES ( r = −0.612; p = 0.026) and bFGF ( r = −0.578; p = 0.039) in CRSwNP patients; however, there was no significant correlation in CRSsNP patients. Conclusion This data suggests that 25‐VD3 may play a role in regulation of RANTES and bFGF expression in CRSwNP. This may occur through regulation of NP fibroblasts or other immune cells. Further investigation is warranted to better elucidate the role of RANTES, bFGF, and 25‐VD3 in CRSwNP.