Photo Credit: wildpixel
The following is a summary of “Signaling lymphocytic activation molecule family 8 disrupts epithelial barrier in chronic rhinosinusitis with nasal polyps through M1 macrophage polarization,” published in the January 2025 issue of Annals of Allergy, Asthma & Immunology by Li et al.
M1 macrophages accumulate in non-eosinophilic chronic rhinosinusitis with nasal polyps (neCRSwNP), but their regulation and impact on the epithelial barrier remain unclear.
Researchers conducted a retrospective study to examine the role of SLAMF8 in M1 macrophage polarization and its impact on neCRSwNP.
They evaluated SLAMF8 expression in sinonasal mucosa from CRSwNP and control subjects using real-time quantitative PCR and Western blot. Immunofluorescence confirmed SLAMF8 co-expression with macrophages. After SLAMF8 knockdown, they assessed its effect on M1 polarization, epithelial-mesenchymal transition (EMT), and tight junction integrity in an indirect co-culture of M1 macrophages with human nasal epithelial cells.
The results showed SLAMF8 was highly expressed on M1 macrophages in polyp tissues, especially in neCRSwNP, and correlated with disease severity in neCRSwNP. SLAMF8 knockdown in THP-1 cells reduced M1 macrophage markers (CD86, iNOS, NLRP3) and decreased inflammatory cytokines (IL-1β, IL-6, TNF-α). Co-culture with M1 macrophage supernatant after SLAMF8 knockdown enhanced epithelial viability, reduced EMT and apoptosis, and upregulated tight junction markers Occludin and Claudin-4 in nasal epithelial cells.
Investigators found that SLAMF8 elevation correlated with EMT, tight junctions, and disease severity in neCRSwNP. SLAMF8 upregulation promoted M1 polarization, impairing the nasal epithelial barrier and suggesting it as a therapeutic target.
Source: annallergy.org/article/S1081-1206(25)00047-X/abstract
