The destruction of mucosal barriers, epithelial remodeling, and impaired mucociliary clearance: possible pathogenic mechanisms of Pseudomonas aeruginosa and Staphylococcus aureus in chronic rhinosinusitis

Abstract Chronic rhinosinusitis (CRS) is a pathological condition characterized by persistent inflammation in the upper respiratory tract and paranasal sinuses. The epithelium serves as the first line of defense against potential threats and protects the nasal mucosa. The fundamental mechanical barr...

Full description

Bibliographic Details
Main Authors: Zahra Chegini, Milad Noei, Jaber Hemmati, Mohammad Reza Arabestani, Aref Shariati
Format: Article
Language:English
Published: BMC 2023-10-01
Series:Cell Communication and Signaling
Subjects:
Online Access:https://doi.org/10.1186/s12964-023-01347-2
_version_ 1797636740716953600
author Zahra Chegini
Milad Noei
Jaber Hemmati
Mohammad Reza Arabestani
Aref Shariati
author_facet Zahra Chegini
Milad Noei
Jaber Hemmati
Mohammad Reza Arabestani
Aref Shariati
author_sort Zahra Chegini
collection DOAJ
description Abstract Chronic rhinosinusitis (CRS) is a pathological condition characterized by persistent inflammation in the upper respiratory tract and paranasal sinuses. The epithelium serves as the first line of defense against potential threats and protects the nasal mucosa. The fundamental mechanical barrier is formed by the cell-cell contact and mucociliary clearance (MCC) systems. The physical-mechanical barrier is comprised of many cellular structures, including adhesion junctions and tight junctions (TJs). To this end, different factors, such as the dysfunction of MCC, destruction of epithelial barriers, and tissue remodeling, are related to the onset and development of CRS. Recently published studies reported the critical role of different microorganisms, such as Staphylococcus aureus and Pseudomonas aeruginosa, in the induction of the mentioned factors. Bacteria could result in diminished ciliary stimulation capacity, and enhance the chance of CRS by reducing basal ciliary beat frequency. Additionally, bacterial exoproteins have been demonstrated to disrupt the epithelial barrier and induce downregulation of transmembrane proteins such as occludin, claudin, and tricellulin. Moreover, bacteria exert an influence on TJ proteins, leading to an increase in the permeability of polarized epithelial cells. Noteworthy, it is evident that the activation of TLR2 by staphylococcal enterotoxin can potentially undermine the structural integrity of TJs and the epithelial barrier through the induction of pro-inflammatory cytokines. The purpose of this article is an attempt to investigate the possible role of the most important microorganisms associated with CRS and their pathogenic mechanisms against mucosal surfaces and epithelial barriers in the paranasal sinuses. Video Abstract
first_indexed 2024-03-11T12:39:25Z
format Article
id doaj.art-2e454cf5877c456a971c31b11f35e5ad
institution Directory Open Access Journal
issn 1478-811X
language English
last_indexed 2024-03-11T12:39:25Z
publishDate 2023-10-01
publisher BMC
record_format Article
series Cell Communication and Signaling
spelling doaj.art-2e454cf5877c456a971c31b11f35e5ad2023-11-05T12:25:05ZengBMCCell Communication and Signaling1478-811X2023-10-0121111410.1186/s12964-023-01347-2The destruction of mucosal barriers, epithelial remodeling, and impaired mucociliary clearance: possible pathogenic mechanisms of Pseudomonas aeruginosa and Staphylococcus aureus in chronic rhinosinusitisZahra Chegini0Milad Noei1Jaber Hemmati2Mohammad Reza Arabestani3Aref Shariati4Department of Microbiology, School of Medicine, Hamadan University of Medical SciencesDepartment of Genetics, Faculty of Advanced Science and Technology, Tehran Medical Sciences, Islamic Azad UniversityDepartment of Microbiology, School of Medicine, Hamadan University of Medical SciencesDepartment of Microbiology, School of Medicine, Hamadan University of Medical SciencesStudent Research Committee, Khomein University of Medical SciencesAbstract Chronic rhinosinusitis (CRS) is a pathological condition characterized by persistent inflammation in the upper respiratory tract and paranasal sinuses. The epithelium serves as the first line of defense against potential threats and protects the nasal mucosa. The fundamental mechanical barrier is formed by the cell-cell contact and mucociliary clearance (MCC) systems. The physical-mechanical barrier is comprised of many cellular structures, including adhesion junctions and tight junctions (TJs). To this end, different factors, such as the dysfunction of MCC, destruction of epithelial barriers, and tissue remodeling, are related to the onset and development of CRS. Recently published studies reported the critical role of different microorganisms, such as Staphylococcus aureus and Pseudomonas aeruginosa, in the induction of the mentioned factors. Bacteria could result in diminished ciliary stimulation capacity, and enhance the chance of CRS by reducing basal ciliary beat frequency. Additionally, bacterial exoproteins have been demonstrated to disrupt the epithelial barrier and induce downregulation of transmembrane proteins such as occludin, claudin, and tricellulin. Moreover, bacteria exert an influence on TJ proteins, leading to an increase in the permeability of polarized epithelial cells. Noteworthy, it is evident that the activation of TLR2 by staphylococcal enterotoxin can potentially undermine the structural integrity of TJs and the epithelial barrier through the induction of pro-inflammatory cytokines. The purpose of this article is an attempt to investigate the possible role of the most important microorganisms associated with CRS and their pathogenic mechanisms against mucosal surfaces and epithelial barriers in the paranasal sinuses. Video Abstracthttps://doi.org/10.1186/s12964-023-01347-2CRSStaphylococcus aureousPseudomonas aeruginosaMucociliary clearanceEpithelial remodelingMucosal barriers
spellingShingle Zahra Chegini
Milad Noei
Jaber Hemmati
Mohammad Reza Arabestani
Aref Shariati
The destruction of mucosal barriers, epithelial remodeling, and impaired mucociliary clearance: possible pathogenic mechanisms of Pseudomonas aeruginosa and Staphylococcus aureus in chronic rhinosinusitis
Cell Communication and Signaling
CRS
Staphylococcus aureous
Pseudomonas aeruginosa
Mucociliary clearance
Epithelial remodeling
Mucosal barriers
title The destruction of mucosal barriers, epithelial remodeling, and impaired mucociliary clearance: possible pathogenic mechanisms of Pseudomonas aeruginosa and Staphylococcus aureus in chronic rhinosinusitis
title_full The destruction of mucosal barriers, epithelial remodeling, and impaired mucociliary clearance: possible pathogenic mechanisms of Pseudomonas aeruginosa and Staphylococcus aureus in chronic rhinosinusitis
title_fullStr The destruction of mucosal barriers, epithelial remodeling, and impaired mucociliary clearance: possible pathogenic mechanisms of Pseudomonas aeruginosa and Staphylococcus aureus in chronic rhinosinusitis
title_full_unstemmed The destruction of mucosal barriers, epithelial remodeling, and impaired mucociliary clearance: possible pathogenic mechanisms of Pseudomonas aeruginosa and Staphylococcus aureus in chronic rhinosinusitis
title_short The destruction of mucosal barriers, epithelial remodeling, and impaired mucociliary clearance: possible pathogenic mechanisms of Pseudomonas aeruginosa and Staphylococcus aureus in chronic rhinosinusitis
title_sort destruction of mucosal barriers epithelial remodeling and impaired mucociliary clearance possible pathogenic mechanisms of pseudomonas aeruginosa and staphylococcus aureus in chronic rhinosinusitis
topic CRS
Staphylococcus aureous
Pseudomonas aeruginosa
Mucociliary clearance
Epithelial remodeling
Mucosal barriers
url https://doi.org/10.1186/s12964-023-01347-2
work_keys_str_mv AT zahrachegini thedestructionofmucosalbarriersepithelialremodelingandimpairedmucociliaryclearancepossiblepathogenicmechanismsofpseudomonasaeruginosaandstaphylococcusaureusinchronicrhinosinusitis
AT miladnoei thedestructionofmucosalbarriersepithelialremodelingandimpairedmucociliaryclearancepossiblepathogenicmechanismsofpseudomonasaeruginosaandstaphylococcusaureusinchronicrhinosinusitis
AT jaberhemmati thedestructionofmucosalbarriersepithelialremodelingandimpairedmucociliaryclearancepossiblepathogenicmechanismsofpseudomonasaeruginosaandstaphylococcusaureusinchronicrhinosinusitis
AT mohammadrezaarabestani thedestructionofmucosalbarriersepithelialremodelingandimpairedmucociliaryclearancepossiblepathogenicmechanismsofpseudomonasaeruginosaandstaphylococcusaureusinchronicrhinosinusitis
AT arefshariati thedestructionofmucosalbarriersepithelialremodelingandimpairedmucociliaryclearancepossiblepathogenicmechanismsofpseudomonasaeruginosaandstaphylococcusaureusinchronicrhinosinusitis
AT zahrachegini destructionofmucosalbarriersepithelialremodelingandimpairedmucociliaryclearancepossiblepathogenicmechanismsofpseudomonasaeruginosaandstaphylococcusaureusinchronicrhinosinusitis
AT miladnoei destructionofmucosalbarriersepithelialremodelingandimpairedmucociliaryclearancepossiblepathogenicmechanismsofpseudomonasaeruginosaandstaphylococcusaureusinchronicrhinosinusitis
AT jaberhemmati destructionofmucosalbarriersepithelialremodelingandimpairedmucociliaryclearancepossiblepathogenicmechanismsofpseudomonasaeruginosaandstaphylococcusaureusinchronicrhinosinusitis
AT mohammadrezaarabestani destructionofmucosalbarriersepithelialremodelingandimpairedmucociliaryclearancepossiblepathogenicmechanismsofpseudomonasaeruginosaandstaphylococcusaureusinchronicrhinosinusitis
AT arefshariati destructionofmucosalbarriersepithelialremodelingandimpairedmucociliaryclearancepossiblepathogenicmechanismsofpseudomonasaeruginosaandstaphylococcusaureusinchronicrhinosinusitis