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  • Wiley  (2)
  • O'Connell, Brendan P.  (2)
  • 1
    In: International Forum of Allergy & Rhinology, Wiley, Vol. 1, No. 4 ( 2011-07), p. 296-302
    Abstract: The aim of this study was to determine if there is a link between local dendritic cells (DCs) and various subtypes of chronic rhinosinusitis (CRS): CRS with nasal polyposis (CRSwNP), CRS without nasal polyposis (CRSsNP), and allergic fungal rhinosinusitis (AFRS). Once DC presence was established we considered possible mechanisms for DC recruitment to the sinuses. Methods Biopsy specimens were taken from the osteomeatal complex during endoscopic sinus surgery in patients with AFRS (n ≥ 5), CRSsNP (n ≥ 6), and CRSwNP (n ≥ 6). Control patients (n ≥ 5) were undergoing either tumor resection or repair of cerebrospinal fluid leak and had no radiographic or endoscopic evidence of inflammatory sinus disease. Tissue samples were immunohistochemically stained for DC marker, CD209, costimulatory molecules, CD80 and CD86, and chemokine receptors, CCR2 and CCR6. Sinus tissue lysates were examined for levels of the DC chemoattractants, chemokine ligand 2 (CCL2) and CCL20. Results Analysis of sinus tissue from AFRS and CRSwNP revealed elevated numbers of cells staining positive for CD209, CD80, CD86, CCR2, and CCR6 compared to controls. CCL2 and CCL20 levels were elevated in AFRS and CRSwNP compared to controls, similar to increases in their receptors, CCR2 and CCR6, respectively. While there were trends toward increases in all markers in CRSsNP, none was statistically significant compared to control. Conclusion AFRS and CRSwNP have increased numbers of DCs displaying costimulatory molecules, DC chemoattractants, and their corresponding receptors in the sinus mucosa compared to controls. These differences represent a possible mechanism for increased numbers of DCs with a T helper 2 (Th2)‐skewed profile seen in CRSwNP and AFRS. © 2011 ARS‐AAOA, LLC.
    Type of Medium: Online Resource
    ISSN: 2042-6976 , 2042-6984
    URL: Issue
    Language: English
    Publisher: Wiley
    Publication Date: 2011
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  • 2
    In: International Forum of Allergy & Rhinology, Wiley, Vol. 7, No. 8 ( 2017-08), p. 777-785
    Abstract: In these studies we examined the impact of environmental tobacco smoke (ETS) and active smoking on sinonasal dendritic cell (DC) 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 HSNECs (NS‐HSNECs) or cigarette‐smoke‐extract‐exposed HSNECs (CSE‐HSNECs) to assess the impact of CSE exposure on HSNEC regulation of moDC functions. Results Control subjects who were active smokers displayed increased sinonasal moDC and myeloid dendritic 1 (mDC1) cells and reduced mDC2 cells, whereas, in CRSwNP patients, only moDC and mDC2 cells were altered. ETS was found to increase only moDCs in the CRSwNP patients. In vitro, CSE stimulated HSNEC secretion of the moDC regulatory products chemokine (C‐C motif) ligand 20, prostaglandin E 2 , and granulocyte‐macrophage colony‐stimulating factor. 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. Last, CSE‐HSNEC‐treated moDCs secreted increased levels of interleukin‐10, interferon‐γ, and thymic stromal lymphopoietin. Conclusion 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 HSNECs to induce moDC migration, maturation, and activation.
    Type of Medium: Online Resource
    ISSN: 2042-6976 , 2042-6984
    URL: Issue
    Language: English
    Publisher: Wiley
    Publication Date: 2017
    detail.hit.zdb_id: 2604059-1
    Location Call Number Limitation Availability
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