Thymic stromal lymphopoietin enhances tight-junction barrier function of human nasal epithelial cells

2009 ◽  
Vol 338 (2) ◽  
pp. 283-293 ◽  
Author(s):  
Ryuta Kamekura ◽  
Takashi Kojima ◽  
Jun-ichi Koizumi ◽  
Noriko Ogasawara ◽  
Makoto Kurose ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Tight Junction ◽  
Barrier Function ◽  
Thymic Stromal Lymphopoietin ◽  
Nasal Epithelial Cells ◽  
Human Nasal Epithelial Cells

Protein Kinase C Enhances Tight Junction Barrier Function of Human Nasal Epithelial Cells in Primary Culture by Transcriptional Regulation

2008 ◽  
Vol 74 (2) ◽  
pp. 432-442 ◽  
Author(s):  
Jun-ichi Koizumi ◽  
Takashi Kojima ◽  
Noriko Ogasawara ◽  
Ryuta Kamekura ◽  
Makoto Kurose ◽  
...  
Keyword(s):  
Transcriptional Regulation ◽  
Protein Kinase C ◽  
Protein Kinase ◽  
Epithelial Cells ◽  
Tight Junction ◽  
Primary Culture ◽  
Barrier Function ◽  
Nasal Epithelial Cells ◽  
Kinase C ◽  
Human Nasal Epithelial Cells

PPARγ agonists upregulate the barrier function of tight junctions via a PKC pathway in human nasal epithelial cells

2010 ◽  
Vol 61 (6) ◽  
pp. 489-498 ◽  
Author(s):  
Noriko Ogasawara ◽  
Takashi Kojima ◽  
Mitsuru Go ◽  
Tsuyoshi Ohkuni ◽  
Jun-ichi Koizumi ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Tight Junctions ◽  
Barrier Function ◽  
Nasal Epithelial Cells ◽  
Human Nasal Epithelial Cells ◽  
Pparγ Agonists

scholarly journals Regulation of Tight Junctions in Upper Airway Epithelium

2013 ◽  
Vol 2013 ◽  
pp. 1-11 ◽  
Author(s):  
Takashi Kojima ◽  
Mitsuru Go ◽  
Ken-ichi Takano ◽  
Makoto Kurose ◽  
Tsuyoshi Ohkuni ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Tight Junction ◽  
Tight Junctions ◽  
Airway Epithelium ◽  
Barrier Function ◽  
Upper Airway ◽  
Mucosal Barrier ◽  
Upper Respiratory Tract ◽  
Junction Molecules ◽  
Human Nasal Epithelial Cells

The mucosal barrier of the upper respiratory tract including the nasal cavity, which is the first site of exposure to inhaled antigens, plays an important role in host defense in terms of innate immunity and is regulated in large part by tight junctions of epithelial cells. Tight junction molecules are expressed in both M cells and dendritic cells as well as epithelial cells of upper airway. Various antigens are sampled, transported, and released to lymphocytes through the cells in nasal mucosa while they maintain the integrity of the barrier. Expression of tight junction molecules and the barrier function in normal human nasal epithelial cells (HNECs) are affected by various stimuli including growth factor, TLR ligand, and cytokine. In addition, epithelial-derived thymic stromal lymphopoietin (TSLP), which is a master switch for allergic inflammatory diseases including allergic rhinitis, enhances the barrier function together with an increase of tight junction molecules in HNECs. Furthermore, respiratory syncytial virus infection in HNECsin vitroinduces expression of tight junction molecules and the barrier function together with proinflammatory cytokine release. This paper summarizes the recent progress in our understanding of the regulation of tight junctions in the upper airway epithelium under normal, allergic, and RSV-infected conditions.

Urban Particulate Matters May Affect Endoplasmic Reticulum Stress and Tight Junction Disruption in Nasal Epithelial Cells

2021 ◽  
pp. 194589242110040
Author(s):  
Soo Kyoung Park ◽  
Sun Hee Yeon ◽  
Mi-Ra Choi ◽  
Seung Hyeon Choi ◽  
Sung Bok Lee ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Epithelial Cells ◽  
Er Stress ◽  
Stress Responses ◽  
Barrier Function ◽  
Epithelial Barrier ◽  
In Vivo Models ◽  
Nasal Epithelial Cells ◽  
Human Nasal Epithelial Cells ◽  
Mucosal Barrier Function

Background Exposure to airborne urban particulate matter (UPM) has been closely related to the development and aggravation of respiratory disease, including sinonasal disorders. Objective The aims of this study were to investigate the effect of UPM on nasal epithelial tight junctions (TJs) and mucosal barrier function and delineate the underlying mechanism by using both in vitro and in vivo models. Methods In this study, human nasal epithelial cells (hNECs) and BALB/c mice were exposed to UPMs. UPM 1648a and 1649 b were employed. TJ and endoplasmic reticulum (ER) stress marker expression was measured using western blot analysis and immunofluorescence. TJ integrity and nasal epithelial barrier function were evaluated by transepithelial electric resistance (TER) and paracellular flux. In addition, the effects of N‐acetyl‐L‐cysteine (NAC) on UPM-induced nasal epithelial cells were investigated. Results UPM significantly impaired the nasal epithelial barrier, as demonstrated by decreased protein expression of TJ and ER stress markers in human nasal epithelial cells. This finding was in parallel to reduced transepithelial electrical resistance and increased fluorescein isothiocyanate–dextran permeability. Pretreatment with NAC decreased the degree of UPM-mediated ER stress and restored nasal epithelial barrier disruption in human nasal epithelial cells (hNEC) and the nasal mucosa of experimental animals. Conclusion These data suggest that UPMs may induce nasal epithelial barrier dysfunction by targeting TJs and ER stress could be related in this process. Based on these results, we suggest that suppression of this process with an inhibitor targeting ER stress responses could represent a novel promising therapeutic target in UPM-induced sinonasal disease.

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