scholarly journals Nasal Epithelial Barrier Integrity and Tight Junctions Disruption in Allergic Rhinitis: Overview and Pathogenic Insights

2021 ◽  
Vol 12 ◽  
Author(s):  
Siti Muhamad Nur Husna ◽  
Hern-Tze Tina Tan ◽  
Norasnieda Md Shukri ◽  
Noor Suryani Mohd Ashari ◽  
Kah Keng Wong
Keyword(s):  
Allergic Rhinitis ◽  
Tight Junctions ◽  
Lymphoid Cells ◽  
Cell Junctions ◽  
Epithelial Barrier ◽  
Epigenetic Changes ◽  
T Helper ◽  
Therapeutic Approaches ◽  
First Line ◽  
T Helper 2

Allergic rhinitis (AR) is a common disorder affecting up to 40% of the population worldwide and it usually persists throughout life. Nasal epithelial barrier constitutes the first line of defense against invasion of harmful pathogens or aeroallergens. Cell junctions comprising of tight junctions (TJs), adherens junctions, desmosomes and hemidesmosomes form the nasal epithelial barrier. Impairment of TJ molecules plays causative roles in the pathogenesis of AR. In this review, we describe and discuss the components of TJs and their disruption leading to development of AR, as well as regulation of TJs expression by epigenetic changes, neuro-immune interaction, epithelial-derived cytokines (thymic stromal lymphopoietin, IL-25 and IL-33), T helper 2 (Th2) cytokines (IL-4, IL-5, IL-6 and IL-13) and innate lymphoid cells. These growing evidence support the development of novel therapeutic approaches to restore nasal epithelial TJs expression in AR patients.

Cholinergic neuron‐like D‐U87 cells promote polarization of allergic rhinitis T‐helper 2 cells

2019 ◽  
Vol 10 (2) ◽  
pp. 233-242
Author(s):  
Honghui Liu ◽  
Tiansheng Wang ◽  
Jinye Xia ◽  
Jingang Ai ◽  
Wei Li ◽  
...  
Keyword(s):  
Allergic Rhinitis ◽  
Cholinergic Neuron ◽  
T Helper ◽  
T Helper 2 ◽  
U87 Cells

T-helper 2 cytokine-induced heat shock protein 70 secretion and its potential association with allergic rhinitis

2017 ◽  
Vol 7 (5) ◽  
pp. 530-535 ◽  
Author(s):  
Hyun Jin Min ◽  
Kyung Soo Kim ◽  
Joo-Heon Yoon ◽  
Chang-Hoon Kim ◽  
Hyung-Ju Cho
Keyword(s):  
Allergic Rhinitis ◽  
Heat Shock ◽  
Heat Shock Protein ◽  
Heat Shock Protein 70 ◽  
T Helper ◽  
T Helper 2 ◽  
Potential Association

Human junction adhesion molecule regulates tight junction resealing in epithelia

2000 ◽  
Vol 113 (13) ◽  
pp. 2363-2374 ◽  
Author(s):  
Y. Liu ◽  
A. Nusrat ◽  
F.J. Schnell ◽  
T.A. Reaves ◽  
S. Walsh ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Tight Junction ◽  
Tight Junctions ◽  
Adhesion Molecule ◽  
Transmembrane Protein ◽  
Extracellular Domain ◽  
Cell Junctions ◽  
Human Neutrophils ◽  
Epithelial Barrier ◽  
Cell Cell

Epithelial cells form a highly selective barrier and line many organs. The epithelial barrier is maintained by closely apposed cell-cell contacts containing tight junctions, the regulation of which is incompletely understood. Here we report the cloning, tissue localization and evidence for a role in epithelial barrier regulation of an immunoglobulin superfamily member that likely represents the human homolog of murine junction adhesion molecule (JAM). Analysis of the primary structure of human JAM, cloned from T84 epithelial cells, predicts a transmembrane protein with an extracellular domain that contains two IgV loops. Monoclonal antibodies generated against the putative extracellular domain were reactive with a 35–39 kDa protein from both T84 epithelial cells and human neutrophils. By immunofluorescence, JAM mAbs labeled epithelial cells from intestine, lung, and kidney, prominently in the region of tight junctions (co-localization with occludin) and also along lateral cell membranes below the tight junctions. Flow cytometric studies confirmed predominant JAM expression in epithelial cells but also revealed expression on endothelial and hematopoietic cells of all lineages. Functional studies demonstrated that JAM specific mAbs markedly inhibited transepithelial resistance recovery of T84 monolayers after disruption of intercellular junctions (including tight junctions) by transient calcium depletion. Morphologic analysis revealed that, after disassembly of cell-cell junctions, anti-JAM inhibition of barrier function recovery correlated with a loss of both occludin and JAM, but not ZO-1, in reassembling tight junction structure. Reassembly of the major adherens junction component E-cadherin was not affected by JAM specific mAbs. Our findings suggest that JAM plays an important role in the regulation of tight junction assembly in epithelia. Furthermore, these JAM-mediated effects may occur by either direct, or indirect interactions with occludin.

scholarly journals Group 2 Innate Lymphoid Cells Are Critical for the Initiation of Adaptive T Helper 2 Cell-Mediated Allergic Lung Inflammation

Immunity ◽  
2014 ◽  
Vol 40 (3) ◽  
pp. 425-435 ◽  
Author(s):  
Timotheus Y.F. Halim ◽  
Catherine A. Steer ◽  
Laura Mathä ◽  
Matthew J. Gold ◽  
Itziar Martinez-Gonzalez ◽  
...  
Keyword(s):  
Lung Inflammation ◽  
Innate Lymphoid Cells ◽  
Lymphoid Cells ◽  
T Helper ◽  
T Helper 2 ◽  
Allergic Lung Inflammation ◽  
Group 2

scholarly journals HLA-DR- and CD11c-positive Dendritic Cells Penetrate beyond Well-developed Epithelial Tight Junctions in Human Nasal Mucosa of Allergic Rhinitis

2005 ◽  
Vol 53 (5) ◽  
pp. 611-619 ◽  
Author(s):  
Ken-ichi Takano ◽  
Takashi Kojima ◽  
Mitsuru Go ◽  
Masaki Murata ◽  
Shingo Ichimiya ◽  
...  
Keyword(s):  
Allergic Rhinitis ◽  
Dendritic Cells ◽  
Tight Junction ◽  
Tight Junctions ◽  
Nasal Mucosa ◽  
Epithelial Barrier ◽  
Upper Respiratory Tract ◽  
Human Nasal Mucosa ◽  
Hla Dr ◽  
Epithelial Tight Junctions

The epithelial barrier of the upper respiratory tract plays a crucial role in host defense. In this study, to elucidate whether there is antigen monitoring by dendritic cells (DCs) beyond the epithelial tight-junction barrier in allergic rhinitis, we investigated the expression and function of tight junctions and characterized DCs in the epithelium of nasal mucosa from patients with allergic rhinitis. In reverse transcription-polymerase chain reaction, mRNAs of tight-junction proteins occludin, JAM-1, ZO-1, and claudin-1, −4, −7, −8, −12, −13, and −14 were detected in the nasal mucosa. Occludin, JAM-1, and ZO-1 were colocalized in the uppermost layer in the pseudostratified epithelium of the nasal mucosa, whereas claudin-1, −4, and −7 were found throughout the epithelium. In freeze-fracture replicas of the nasal mucosa, continuous tight-junction strands formed well-developed networks. Epithelial barrier function measured by a dye tracer was well maintained in occludin-positive tight junctions in the epithelium of the nasal mucosa. HLA-DR- and CD11c-positive DCs expressed claudin-1 and penetrated beyond occludin in the epithelium of the nasal mucosa with, but not without, allergic rhinitis. These results indicate that DCs may easily access antigens beyond epithelial tight junctions in the human nasal mucosa of allergic rhinitis.

scholarly journals Histamine and T helper cytokine–driven epithelial barrier dysfunction in allergic rhinitis

2018 ◽  
Vol 141 (3) ◽  
pp. 951-963.e8 ◽  
Author(s):  
Brecht Steelant ◽  
Sven F. Seys ◽  
Laura Van Gerven ◽  
Matthias Van Woensel ◽  
Ricard Farré ◽  
...  
Keyword(s):  
Allergic Rhinitis ◽  
Epithelial Barrier ◽  
T Helper ◽  
Barrier Dysfunction ◽  
Epithelial Barrier Dysfunction

Are Cutaneous Reactions to Fly Larvae Mediated by CD4+, TIA+ NK1.1 T Cells?

2001 ◽  
Vol 5 (5) ◽  
pp. 400-405
Author(s):  
Christopher Norwood ◽  
Kathleen J. Smith ◽  
Ronald Neafie ◽  
Henry Skelton
Keyword(s):  
T Cells ◽  
T Cell ◽  
Cd4 T Cells ◽  
Cell Receptor ◽  
Lymphoid Cells ◽  
T Helper ◽  
T Helper 2 ◽  
Cutaneous Reactions ◽  
Intracellular Antigen ◽  
Fly Larvae

Background: Although there have been reports of fly larvae in wounds and as isolated primary infestations, there have been only rare reports documenting reactions to the larvae within the skin in humans and animals. There have been no reports documenting the histopathologic and immunohistochemical characteristics of the inflammatory infiltrate. Objective: We present a patient who developed local pruritus, erythema, and swelling approximately three weeks after infestation by a fly larva within the scalp. Histopathologically the biopsy site showed a mixed infiltrate containing lymphoid cells and numerous eosinophils. Immunohistochemical stains showed predominantly CD4+ T cells expressing an αβ T-cell receptor (TCR) of which approximately 30% coexpressed T-cell intracellular antigen (TIA) and CD56. In addition, there were approximately 5% of these CD4+ T cells which coexpressed CD30. Conclusions: Histopathologic and immunohistochemical findings are consistent with an effector cell population of cytotoxic CD4+ T cells that produce a T-helper 2 cytokine pattern. The phenotype of this subset of T cells is unique and among its characteristics is that antigens—usually nonprotein antigens—are presented to these CD4+, TIA+ natural killer (NK)1.1T cells by CD1d molecules.

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