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Human Nasal Epithelial Cells (human + nasal_epithelial_cell)

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Medical Sciences100%

Kinds of Human Nasal Epithelial Cells

  • primary human nasal epithelial cell
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    Selected Abstracts

    Time-series nasal epithelial transcriptomics during natural pollen exposure in healthy subjects and allergic patients

    ALLERGY, Issue 2 2010
    P. Mattila
    To cite this article: Mattila P, Renkonen J, Toppila-Salmi S, Parviainen V, Joenväärä S, Alff-Tuomala S, Nicorici D, Renkonen R. Time-series nasal epithelial transcriptomics during natural pollen exposure in healthy subjects and allergic patients. Allergy 2010; 65: 175,183. Abstract Background:, The role of epithelium has recently awakened interest in the studies of type I hypersensitivity. Objective:, We analysed the nasal transcriptomics epithelial response to natural birch pollen exposure in a time series manner. Methods:, Human nasal epithelial cell swabs were collected from birch pollen allergic patients and healthy controls in winter season. In addition, four specimens at weekly intervals were collected from the same subjects during natural birch pollen exposure in spring and transcriptomic analyses were performed. Results:, The nasal epithelium of healthy subjects responded vigorously to allergen exposure. The immune response was a dominating category of this response. Notably, the healthy subjects did not display any clinical symptoms regardless of this response detected by transcriptomic analysis. Concomitantly, the epithelium of allergic subjects responded also, but with a different set of responders. In allergic patients the regulation of dyneins, the molecular motors of intracellular transport dominated. This further supports our previous hypothesis that the birch pollen exposure results in an active uptake of allergen into the epithelium only in allergic subjects but not in healthy controls. Conclusion:, We showed that birch pollen allergen causes a defence response in healthy subjects, but not in allergic subjects. Instead, allergic patients actively transport pollen allergen through the epithelium to tissue mast cells. Our study showed that new hypotheses can arise from the application of discovery driven methodologies. To understand complex multifactorial diseases, such as type I hypersensitivity, this kind of hypotheses might be worth further analyses. [source]

    Nod1, Nod2 and Nalp3 receptors, new potential targets in treatment of allergic rhinitis?

    ALLERGY, Issue 10 2010
    J. Bogefors
    To cite this article: Bogefors J, Rydberg C, Uddman R, Fransson M, Månsson A, Benson M, Adner M, Cardell LO. Nod1, Nod2 and Nalp3 receptors, new potential targets in treatment of allergic rhinitis? Allergy 2010; 65: 1222,1226. Abstract Background:, Recently, a new set of pattern-recognition receptors, the nucleotide-binding oligomerization domain (Nod)-like receptors (NLRs), have emerged. Their activation, either by allergens or microbes, triggers an inflammatory response. The knowledge about NLRs in human airways is limited. Aim of the study:, To investigate presence of NLRs in the human nose of healthy individuals and patients with intermittent allergic rhinitis outside and during pollen season. Methods:, The expression of Nod1, Nod2, and Nalp3 in nasal biopsies was determined with real-time RT-PCR and immunohistochemistry. Cultured primary human nasal epithelial cells (HNECs) were analyzed using real-time RT-PCR and flow cytometry to further verify the presence of NLRs in the epithelium. Results:, Immunohistochemical analysis revealed presence of Nod1, Nod2, and Nalp3 in the nasal epithelium. This was corroborated in cultured HNECs. Patients suffering from symptomatic allergic rhinitis exhibited lower Nod1 and Nalp3 mRNA levels than both controls and patients during pollen season. Nod2 expression was found in all specimens tested, but no differences were seen between the three groups. Conclusion:, Nod1, Nod2, and Nalp3 receptors were found to be present in the human nose. The expression of Nod1 and Nalp3 were down-regulated during pollen season among patients with allergic rhinitis. This opens up for new insights and novel therapeutic strategies in inflammatory airway disease. [source]

    Staphylococcus aureus enterotoxin B augments granulocyte migration and survival via airway epithelial cell activation

    ALLERGY, Issue 8 2010
    W. Huvenne
    To cite this article: Huvenne W, Callebaut I, Reekmans K, Hens G, Bobic S, Jorissen M, Bullens DMA, Ceuppens JL, Bachert C, Hellings PW. Staphylococcus aureus enterotoxin B augments granulocyte migration and survival via airway epithelial cell activation. Allergy 2010; 65: 1013,1020. Abstract Background:,Staphylococcus aureus enterotoxin B (SEB) has recently been postulated to be involved in the pathology of granulocyte-dominated disease. Studying the immunologic interaction between SEB and airway epithelial cells in immortalized cell lines or long-term epithelial cell cultures has obvious disadvantages. Methods:, We used a novel technique of freshly isolated and purified human nasal epithelial cells (HNEC) from healthy, nonallergic individuals, which were incubated for 24 h without/with SEB at different concentrations. Chemokine production was evaluated in the supernatant using Cytometric Bead Array. The chemotactic activity of the supernatant was studied in vitro using a Boyden chamber. Survival was evaluated with flow cytometry, using propidium iodide to identify dead cells. Results:,Staphylococcus aureus enterotoxin B showed a dose-dependent induction of interferon-inducible protein-10, monokine induced by interferon-,, regulated upon activation normal T cell expressed and secreted, monocyte chemoattractant protein 1 (MCP-1) and granulocyte colony stimulating factor production by epithelial cells in vitro. The supernatant of epithelial cells had chemotactic activity for granulocytes in vitro, which was enhanced in the supernatant of SEB-stimulated epithelial cells. Reduced number of propidium iodide positive granulocytes was found in the conditions where supernatant of SEB-stimulated epithelial cells was applied. Conclusion:,Staphylococcus aureus enterotoxin B exerts a direct pro-inflammatory effect on HNEC, with induction of chemokine and growth factor release, resulting in the migration and prolonged survival of granulocytes in vitro. [source]

    Opposing roles of IL-17A and IL-25 in the regulation of TSLP production in human nasal epithelial cells

    ALLERGY, Issue 5 2010
    G. Xu
    To cite this article: Xu G, Zhang L, Wang DY, Xu R, Liu Z, Han DM, Wang XD, Zuo KJ, Li HB. Opposing roles of IL-17A and IL-25 in the regulation of TSLP production in human nasal epithelial cells. Allergy 2010; 65: 581,589. Abstract Background:, The importance of IL-17A, IL-17F, and IL-25 in allergic rhinitis (AR), as well as their possible role in regulation on thymic stromal lymphopoietin (TSLP) production in nasal epithelial cells, is not well understood. Objective:, To determine the possible regulation of IL-17A, IL-17F, and IL-25 on TSLP production in the initiation of allergic responses. Methods:, The levels of IL-17A, IL-17F, IL-25, and TSLP in nasal lavages of patients with AR were measured using an enzyme-linked immunosorbent assay (ELISA) and compared with that in normal controls. Then, primary human nasal epithelial cells (HNECs) were stimulated with dsRNA (0,75 ,g/ml), as well as IL-17A (100 ng/ml), IL-17F (100 ng/ml), and IL-25(100 ng/ml). The mRNA expression of IL-17A, IL-17F, IL-25, TSLP, as well as the chemokines CCL20, IL-8, and eotaxin was analyzed using quantitative real-time PCR, and their protein levels in the supernatants of cultured HNECs were determined by ELISA. Results:, Both TSLP and IL-17 cytokines are significantly elevated in patients with AR. dsRNA was found to increase the production of IL-17F, IL-25, TSLP, CCL20, and IL-8 in HNECs. Furthermore, IL-25 significantly enhanced dsRNA-induced TSLP production in primary HNECs and was dominant to the inhibitory effect of IL-17A on TSLP regulation. Conclusions:, Our study provides the first evidence that both IL-17F and IL-25 can be induced by dsRNA in HNECs. Despite of the opposing effects of IL-17A and IL-25 on TSLP regulation in HNECs, IL-25 was dominant to IL-17A, providing a plausible explanation for the simultaneous upregulation of IL-17 cytokines and TSLP in patients with AR. [source]

    Muco-ciliary differentiation of nasal epithelial cells is decreased after wound healing in vitro

    ALLERGY, Issue 8 2009
    D. S. Lazard
    Background:, Epithelial damage and modifications of cell differentiation are frequent in airway diseases with chronic inflammation, in which transforming growth factor-,1 (TGF-,1) plays an important role. The aim of this study was to evaluate the differentiation of human nasal epithelial cells (HNEC) after wound healing and the potential effects of TGF-,1. Methods:, Basal, mucus, and ciliated cells were characterized by cytokeratin-14, MUC5AC, and ,IV tubulin immunodetection, respectively. Their expression was evaluated in situ in nasal polyps and in an in vitro model of wound healing in primary cultures of HNEC after wound closure, under basal conditions and after TGF-,1 supplementation. Using RT-PCR, the effects of TGF-,1 on MUC5AC and DNAI1 genes, specifically transcribed in mucus and ciliated cells, were evaluated. Results:,In situ, high TGF-,1 expression was associated with low MUC5AC and ,IV tubulin expression. In vitro, under basal conditions, MUC5AC expression remained stable, cytokeratin-14 expression was strong and decreased with time, while ,IV tubulin expression increased. Transforming growth factor-,1 supplementation downregulated MUC5AC and ,IV tubulin expression as well as MUC5AC and DNAI1 transcripts. Conclusion:, After a wound, differentiation into mucus and ciliated cells was possible and partially inhibited in vitro by TGF-,1, a cytokine that may be involved in epithelial remodeling observed in chronic airway diseases. [source]

    Rhinovirus infection-induced alteration of tight junction and adherens junction components in human nasal epithelial cells

    THE LARYNGOSCOPE, Issue 2 2010
    Nam-Kyung Yeo MD
    Abstract Objectives/Hypothesis: Manifestations of rhinovirus (RV) infections include mucus overproduction, increased vascular permeability, and secondary bacterial infection. These effects may reflect disrupted epithelial barrier functions, which are mainly regulated by intercellular junctions, referred to as tight junctions (TJs) and adherens junctions (AJs). The objective of this study was to investigate changes in the components of TJs (ZO-1, occluding, and claudin-1) and AJs (E-cadherin) after RV infection in cultured nasal epithelial cells. Methods: Primary human nasal epithelial cells grown at an air-liquid interface were infected apically with RV. RV-induced changes in the expression of epithelial TJ and AJ proteins were determined using real-time reverse transcriptase-polymerase chain reaction, confocal microscopy, and Western blot analyses. Functional changes in the integrity of junctional proteins were assessed by measuring transepithelial resistance (TER) using a voltmeter. Results: RV infection decreased mRNA levels of ZO-1, occludin, claudin-1, and E-cadherin to 64.2%, 51.8%, 56.2%, and 56.3%, respectively, of those in controls (P < .05). Decreases in ZO-1, occludin, claudin-1, and E-cadherin protein levels in RV-infected cells were evident in immunofluorescent confocal microscopic images. Expression levels of these proteins were also lower in the RV-infected group in Western blot analyses. RV infection reduced the mean TER from 143.1 ,/cm2 (controls) to 122.6 ,/cm2. Conclusions: RV infection decreased the expression of TJ and AJ components and reduced TER in primary cultured human nasal epithelial cells, indicating that RV infection may exert a harmful effect on nasal epithelial barrier function. Laryngoscope, 2010 [source]

    Rhinovirus enhances various bacterial adhesions to nasal epithelial cells simultaneously

    THE LARYNGOSCOPE, Issue 7 2009
    Jong Hwan Wang MD
    Abstract Objectives/Hypothesis: Viral upper respiratory tract infections are often followed by secondary bacterial infections in the form of acute rhinosinusitis. We investigate the effect of rhinovirus infection on the expression of cell adhesion molecules and bacterial adherence to primary human nasal epithelial cells. Methods: Cells were infected with rhinovirus serotype 16 (RV-16), and then Staphylococcus aureus, Streptococcus pneumoniae, or Hemophilus influenzae were added to the culture. Rhinovirus-induced expression of fibronectin, platelet-activating factor receptor, and carcinoembryonic antigen-related cell adhesion molecule, was assayed by confocal microscopy, real-time polymerase chain reaction, and Western blot analysis. Bacterial adhesion to cells was assessed by confocal microscopy and the fluorescence intensity of adherent bacteria was analyzed using Image-Pro Plus 5.1 (Media Cybernetics, Inc., Bethesda, MD). Results: RV-16 infection significantly increased the gene and protein expression of fibronectin, platelet-activating factor receptor, and carcinoembryonic antigen-related cell adhesion molecule in nasal epithelial cells. Compared with rhinovirus-uninfected control cells, the adhesion of S. aureus, S. pneumoniae, and H. influenzae increased significantly to 2.53-fold, 1.51-fold, and 2.74-fold of control levels, respectively, in rhinovirus-infected nasal epithelial cells. Conclusions: These findings suggest that increased expression of host cell adhesion molecules may be the mechanism accounting for the increase in susceptibility to bacterial rhinosinusitis associated with rhinovirus-induced upper respiratory infections. Laryngoscope, 2009 [source]

    Increased nitric oxide production in nasal epithelial cells from allergic patients , RT-PCR analysis and direct imaging by a fluorescence indicator: DAF-2 DA*

    CLINICAL & EXPERIMENTAL ALLERGY, Issue 6 2001
    S. Takeno
    Background Nitric oxide (NO) is believed to participate in the regulation of airway clearance and non-specific cellular immunity. Recent studies have suggested that airway epithelial cells of allergic and non-allergic individuals may differ in their ability to produce this molecule. Objective The aim of this study was to detect the difference in NO production in human nasal epithelial cells between normal subjects and patients with perennial allergic rhinitis (AR), and to assess the relationship between the expression of nitric oxide synthase (NOS) isoforms and the severity of the disease. Methods Nasal epithelial cells were obtained from the inferior turbinate. The expression of mRNAs encoding constitutive endothelial NOS (eNOS) and inducible NOS (iNOS) was studied by reverse transcription-polymerase chain reaction (RT-PCR). Direct NO production in living cells was visualized and quantified by a fluorescent indicator, DAF-2 DA. Results RT-PCR analysis demonstrated that AR patients with a RAST score of 5 or 6 showed significant increases in the levels of iNOS mRNA and slight reductions in those of eNOS mRNA. Patients with a RAST score of 2,4 also revealed the same tendency however, the difference was not significant. DAF-2 DA imaging demonstrated that epithelial cells, especially the ciliated cells, produced a larger amount of NO than non-epithelial inflammatory cells. Preincubation with L-NAME resulted in an approximate 40% decrease in both groups. Conclusion These results directly indicate that nasal epithelial cells of AR patients overall produce higher levels of NO through the concomitant expression of different NOS isoforms. Continuous NO production by the epithelial cells in normal subjects further support the hypothesis that NO derived from epithelium may play dual roles in the regulation of nasal airway clearance and in the host defense. In addition, the use of DAF-2 DA provides a reliable method to visualize and quantify the direct NO production of living cells. [source]