Related Experiment Video
Updated: May 30, 2025
Investigation of Macrophage Polarization Using Bone Marrow Derived Macrophages
Published on: June 23, 2013
Signaling lymphocytic activation molecule family 8 disrupts epithelial barrier in chronic rhinosinusitis with nasal
Danyang Li1, Longgang Yu1, Jiajia Zi1
1Department of Otorhinolaryngology Head and Neck Surgery, The Affiliated Hospital of Qingdao University, Qingdao, People's Republic of China.
Background:
Recent studies reveal that M1 macrophages accumulate predominantly in noneosinophilic chronic rhinosinusitis with nasal polyps (neCRSwNP). However, the precise mechanisms regulating M1 macrophages and their impact on the epithelial barrier remain unclear.
Objective:
To investigate the expression and regulatory role of signaling lymphocytic activation molecule family (SLAMF)8, a molecule exclusively expressed in myeloid cells, in M1 macrophage polarization and its potential contribution to neCRSwNP development.
Methods:
We evaluated SLAMF8 expression and its correlation with clinical variables using real-time quantitative polymerase chain reaction and Western blot in sinonasal mucosa samples from CRSwNP and control subjects. Immunofluorescence staining confirmed the co-expression of SLAMF8 with macrophages. After SLAMF8 knockdown, we explored the influence on macrophage M1 polarization and the effect on epithelial-mesenchymal transition (EMT) process and tight junction integrity in epithelial cells through an indirect co-culture system of M1 macrophages with human nasal epithelial cells.
Results:
SLAMF8 was highly expressed on M1 macrophages in polyp tissues, notably in neCRSwNP, and correlated with disease severity indices only in neCRSwNP. SLAMF8 knockdown in THP-1 cells reduced M1 macrophage markers (CD86, iNOS, and NLRP3) and decreased secretion of inflammatory cytokines (interleukin-1 beta, interleukin-6, and tumor necrosis factor alpha). Co-culture with M1 macrophage supernatant after SLAMF8 knockdown enhanced epithelial viability, reduced EMT and apoptosis, and up-regulated tight junction markers, occludin and claudin-4, in nasal epithelial cells.
Conclusion:
SLAMF8 elevation correlates with the EMT, epithelial tight junction, and disease severity in neCRSwNP. SLAMF8 up-regulation promotes M1 macrophage polarization, which facilitates EMT and impairs nasal epithelial barrier function. SLAMF8 may represent a novel therapeutic target for neCRSwNP.
Insights
Signaling lymphocytic activation molecule family (SLAMF)8 promotes M1 macrophage polarization in noneosinophilic chronic rhinosinusitis with nasal polyps (neCRSwNP). Targeting SLAMF8 may improve nasal epithelial barrier function and disease severity.
Area of Science:
- Immunology and Inflammation Research
- Epithelial Biology and Barrier Function
- Rhinology and Sinonasal Diseases
Background:
- M1 macrophages are prevalent in noneosinophilic chronic rhinosinusitis with nasal polyps (neCRSwNP), but regulatory mechanisms and epithelial impact are unknown.
- Signaling lymphocytic activation molecule family (SLAMF)8, expressed in myeloid cells, is investigated for its role in M1 macrophage polarization and neCRSwNP pathogenesis.
Purpose of the Study:
- To examine SLAMF8 expression in neCRSwNP.
- To determine SLAMF8's role in M1 macrophage polarization.
- To assess SLAMF8's contribution to nasal epithelial barrier dysfunction and epithelial-mesenchymal transition (EMT) in neCRSwNP.
Main Methods:
- SLAMF8 expression was quantified in sinonasal tissues using RT-qPCR and Western blot.
- Immunofluorescence confirmed SLAMF8 co-localization with macrophages.
- SLAMF8 knockdown was performed in THP-1 cells, followed by co-culture with human nasal epithelial cells to assess M1 polarization, EMT, and tight junction integrity.
Main Results:
- SLAMF8 was highly expressed on M1 macrophages in neCRSwNP tissues and correlated with disease severity.
- SLAMF8 knockdown reduced M1 markers and inflammatory cytokine secretion.
- Reduced SLAMF8 in M1 macrophages improved epithelial viability, decreased EMT and apoptosis, and restored tight junction proteins (occludin, claudin-4).
Conclusions:
- Elevated SLAMF8 is linked to EMT, compromised epithelial tight junctions, and disease severity in neCRSwNP.
- SLAMF8 promotes M1 macrophage polarization, contributing to epithelial barrier impairment.
- SLAMF8 represents a potential therapeutic target for neCRSwNP.
More Related Videos
06:08Author Spotlight: Advancing Allergic Rhinitis Research with Multicolor Immunofluorescence
Published on: September 22, 2023
10:43Polarization of M1 and M2 Human Monocyte-Derived Cells and Analysis with Flow Cytometry upon Mycobacterium tuberculosis Infection
Published on: September 18, 2020
