Human sinonasal epithelial cells direct dendritic function and T‐cell T helper 1/T helper 2 skewing following <i>Aspergillus</i> exposure

Self Cite

Section: Methodsmentioning

confidence: 99%

Reduced sinonasal levels of 1α‐hydroxylase are associated with worse quality of life in chronic rhinosinusitis with nasal polyps

Schlosser

Carroll

Soler

et al. 2015

Self Cite

“…Control HSNEC cell cultures were established as previously described from 16 individuals who reported to have never smoked and were confirmed by hair nicotine. Given our earlier studies showing that CRSwNP HSNECs are hyperresponsive to inhaled stimuli, in these studies we focused solely on control subject‐derived HSNECs. CSE was generated as previously described and used at concentration of 5% or 10%.…”

Section: Methodsmentioning

confidence: 99%

“…Monocytes from control patients were differentiated into moDCs, as described elsewhere . For controls, moDCs were treated with either their own culture medium (RPMI with no fetal bovine serum [FBS]) or HSNEC medium (BEGM).…”

Section: Methodsmentioning

confidence: 99%

Impact of tobacco smoke on upper airway dendritic cell accumulation and regulation by sinonasal epithelial cells

Mulligan

O’Connell

Pasquini

et al. 2017

Self Cite

Background These studies examined the impact of environmental tobacco smoke (ETS) and active smoking on sinonasal dendritic cell (DCs) subsets in controls or patients with chronic rhinosinusitis with nasal polyps (CRSwNP). In subsequent in vitro investigations, we examined the influence of cigarette smoke extract (CSE) on human sinonasal epithelial cells’ (HSNECs) ability to regulate DC functions. Methods Sinonasal tissue, blood and hair were collected from patients undergoing sinus surgery. Smoking status and ETS exposure were determined by hair nicotine. DC subsets were examined by flow cytometric analysis. Monocyte-derived dendritic cells (moDCs) were treated with conditioned medium from non-smoked exposed HSNEC (NS-HSNEC) or cigarette smoke extract-exposed HSNEC (CSE-HSNEC) to assess the impact of CSE exposure on HSNEC regulation of moDCs functions. Results Control subjects who were active smokers displayed increased sinonasal moDC and mDC1 and reduced mDC2 cells, while in those with CRSwNP only moDC and mDC2 were altered. ETS was found to increase only moDCs in patients with CRSwNP. In vitro, CSE stimulated HSNEC secretion of the moDC regulatory products CCL20, PGE2 and GM-CSF. CSE-exposure also promoted HSNECs to stimulate monocyte and moDC migration. MoDCs treated with CSE-HSNEC media stimulated an increase in antigen uptake and expression of CD80 and CD86. Lastly, CSE-HSNEC treated moDCs secreted increased levels of IL-10, IFN-γ and TSLP compared Conclusions Active smoking and to a lesser degree ETS, alters the sinonasal composition of DCs. A potential mechanism to account for this is that cigarette smoke stimulates HSNEC to induce moDC migration, maturation and activation.

“…Immunostaining and flow cytometric analysis of human sinonasal fibroblasts was conducted as described. 34,35 Antibodies were used according to manufacturer instructions, and included FSP (Abcam, Cambridge, MA) and MUC1-FITC (BD Biosciences, San Jose, CA). An anti-Immunoglobulin M Phycoerythrin-Cyanide 7 (IgM PE-Cy7) secondary antibody (Biolegend, San Diego, CA) was added at a concentration of 1:250.…”

Section: Tissue Processing Immunostaining and Flow Cytometric Analysismentioning

confidence: 99%

Fibroblast levels are increased in chronic rhinosinusitis with nasal polyps and are associated with worse subjective disease severity

Carroll

O’Connell

Schlosser

et al. 2015

Self Cite