Related Experiment Video
Updated: May 19, 2026
06:08
Immunofluorescent Labeling in Nasal Mucosa Tissue Sections of Allergic Rhinitis Rats via Multicolor Immunoassay
Published on: September 22, 2023
HDAC8 impairs tight junctions in allergic rhinitis through Smad7 deacetylation
Huan-Huan Chang1, Zi-Ne Cao1, Pan-Hong Dang1
1Department of Otolaryngology-Head and Neck Surgery, The Affiliated Children's Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi, China.
Frontiers in Immunology
|May 18, 2026
Summary
Histone deacetylase 8 (HDAC8) reduces Smad7 acetylation, disrupting the nasal epithelial barrier in allergic rhinitis (AR). Inhibiting HDAC8 restores barrier function, suggesting HDAC8 as a therapeutic target for AR.
Area of Science:
- Immunology
- Molecular Biology
- Cell Biology
Background:
- Allergic rhinitis (AR) is characterized by immune imbalance (Th2/Th17) and impaired nasal epithelial barrier function.
- The precise molecular links between immune dysregulation and barrier defects in AR remain incompletely understood.
Purpose of the Study:
- To investigate the role of histone deacetylase 8 (HDAC8) in disrupting the nasal epithelial tight junction (TJ) barrier in AR.
- To determine if HDAC8 modulates Smad7 acetylation, thereby affecting TJ integrity.
Main Methods:
- Utilized primary human nasal epithelial cells and a house dust mite-induced AR mouse model.
- Manipulated HDAC8 levels via overexpression, siRNA, or pharmacological inhibition (PCI-34051).
- Assessed Smad7 acetylation status, protein interactions, TJ protein expression (ZO-1, Occludin, Claudin-1), nasal pathology, and serum cytokines.
Main Results:
- HDAC8 expression and binding to Smad7 were elevated in AR models, correlating with decreased Smad7 acetylation and TJ proteins.
- HDAC8 inhibition or knockdown restored Smad7 acetylation and TJ protein levels.
- An acetylation-mimetic Smad7 mutant rescued HDAC8-induced TJ disruption, confirming the role of Smad7 acetylation.
- In vivo, PCI-34051 treatment improved nasal epithelial integrity and modulated key immune cytokine profiles.
Conclusions:
- HDAC8-induced reduction in Smad7 acetylation contributes significantly to epithelial barrier dysfunction in AR.
- HDAC8 represents a promising therapeutic target for restoring mucosal homeostasis in allergic rhinitis.
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