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Review
. 2013:2013:947072.
doi: 10.1155/2013/947072. Epub 2012 Dec 29.

Regulation of tight junctions in upper airway epithelium

Takashi Kojima  1 , Mitsuru Go, Ken-ichi Takano, Makoto Kurose, Tsuyoshi Ohkuni, Jun-ichi Koizumi, Ryuta Kamekura, Noriko Ogasawara, Tomoyuki Masaki, Jun Fuchimoto, Kazufumi Obata, Satoshi Hirakawa, Kazuaki Nomura, Takashi Keira, Ryou Miyata, Nobuhiro Fujii, Hiroyuki Tsutsumi, Tetsuo Himi, Norimasa Sawada
Affiliations
Review

Regulation of tight junctions in upper airway epithelium

Takashi Kojima et al. Biomed Res Int. 2013.

Abstract

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 HNECs in vitro induces 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.

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Figures

Figure 1
Figure 1
Schema of putative sealing intercellular spaces by tight junction molecules in the upper airway epithelium including epithelial cells, M cells, and dendritic cells.
Figure 2
Figure 2
SEM image (a), immunostaining (b) for occludin, claudin-1 and tricellulin, and freeze-fracture image (c) in human nasal mucosa in vivo. Scanning electron microscopy (SEM) image (d), phase contrast (e), immunostaining (f) for occludin, claudin-1 and tricellulin, and freeze-fracture image (g) in human nasal epithelial cells in vitro (hTERT-HNECs). Scale bars: (a) and (d) = 800 nm, (b) and (f) = 10 μm, (c) and (g) = 200 nm, and (e) = 20 μm.
Figure 3
Figure 3
RT-PCR (a) for mRNAs of tight junction molecules in human nasal mucosa in vivo and two types of human nasal epithelial cells in vitro (primary and hTERT-HNECs). M, 100-bp ladder DNA marker; Oc, occludin; CL, claudin. SEM image (b) and immunostaining for Ck20 (c), Ck20, and occludin (d) in human adenoidal epithelium in vivo. Immunostaining for occludin and HLA-DR (e), occludin and CD11c (f), and claudin-1 and HLA-DR (g) in human nasal epithelium in vivo. M: M-like cell. Scale bars: (a) = 20 μm, (b) = 5 μm, (c) and (d) = 20 μm, and (e)–(g) = 10 μm.
Figure 4
Figure 4
(a) Phase contrast, immunostaining for RSV/G-protein and claudin-4, and freeze-fracture image in human nasal epithelial cells in vitro (hTERT-HNECs) at 24 h after infection with RSV. Scale bars: white bars = 20 μm, black bars = 100 nm. (b) Transepithelial electrical resistance (TER) values in hTERT-HNECs at 24 h after infection with RSV. N = 3, *P < 0.01 versus control.
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