[NASAL MUCOSAL BARRIER FUNCTIONS].

Arerugi

Department of Otorhinolaryngology, Nippon Medical School.

Published: May 2019

Download full-text PDF

Source
http://dx.doi.org/10.15036/arerugi.67.725DOI Listing

Publication Analysis

Top Keywords

[nasal mucosal
4
mucosal barrier
4
barrier functions]
4
[nasal
1
barrier
1
functions]
1

Similar Publications

Neuroimmune signalling pathways in chronic rhinosinusitis with nasal polyps.

Curr Opin Allergy Clin Immunol

February 2025

Specialist Allergy and Clinical Immunology, Rhinology Section, Royal National ENT and Eastman Dental Hospitals, University College London Hospitals NHS Foundation Trust, London, UK.

Purpose Of Review: To evaluate the role of neuroimmune signalling pathways in the pathogenesis of chronic rhinosinusitis with nasal polyps (CRSwNP).

Recent Findings: The sinonasal mucosa is densely infiltrated by immune cells and neuronal structures that share an intimate spatial relationship within tissue compartments. Together, such neuroimmune units play a critical role in airway defence and homeostatic function.

View Article and Find Full Text PDF

Human intraepithelial mast cell differentiation and effector function are directed by TGF-β signaling.

J Clin Invest

January 2025

Jeff and Penny Vinik Center for Allergic Disease Research, Division of Allergy and Clinical Immunology, Brigham and Women's Hospital, Boston, Massachusetts, USA.

Mast cells (MCs) expressing a distinctive protease phenotype (MCTs) selectively expand within the epithelium of human mucosal tissues during type 2 (T2) inflammation. While MCTs are phenotypically distinct from subepithelial MCs (MCTCs), signals driving human MCT differentiation and this subset's contribution to inflammation remain unexplored. Here, we have identified TGF-β as a key driver of the MCT transcriptome in nasal polyps.

View Article and Find Full Text PDF

Similarly to acute intestinal helminth infection, several conditions of chronic eosinophilic type 2 inflammation of mucosal surfaces, including asthma and eosinophilic esophagitis, feature robust expansions of intraepithelial mast cells (MCs). Also the hyperplastic mucosa of nasal polyposis in the context of chronic rhinosinusitis, with or without COX1 inhibitor intolerance, contains impressive numbers of intraepithelial MCs. In this issue of the JCI, Derakhshan et al.

View Article and Find Full Text PDF

Background And Objectives: Flexible nasopharyngolaryngoscopy (F-NPLS) is a routine procedure performed in office settings. We compared two different intranasal scope navigation techniques used during F-NPLS, evaluating patient comfort and practitioner satisfaction.

Methods: This is a prospective, randomized, parallel-group controlled study.

View Article and Find Full Text PDF

Nasal mucosal mesenchymal stem cells promote repair of sciatic nerve injury in rats by modulating the inflammatory microenvironment.

Neurosci Lett

December 2024

Neuroscience Center, Wuxi School of Medicine, Jiangnan University, Wuxi, Jiangsu Province 214122, PR China; Department of Neurosurgery, Jiangnan University Medical Center ,Wuxi, Jiangsu Province, 214122, PR China; Wuxi neurosurgical Institute, Wuxi, Jiangsu Province, 214122, PR China. Electronic address:

Article Synopsis
  • Sciatic nerve injury (SNI) is a common form of peripheral nerve damage that triggers inflammation and hinders nerve recovery by activating macrophages into a harmful M1 state.
  • Ectodermal mesenchymal stem cells (EMSCs), sourced from nasal mucosa, can potentially help recover nerve function by modulating the inflammatory environment, specifically by enhancing the presence of beneficial M2 macrophages.
  • The study found that EMSCs transplantation not only improved nerve function recovery in a SNI model but also promoted an increase in M2 macrophage activity and anti-inflammatory cytokines through specific signaling pathways.
View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!