S100A4 Induces Neutrophilic Inflammation in Chronic Rhinosinusitis with Nasal Polyps via TLR4 Pathway.

ABSTRACT:

Background

Treating neutrophilic inflammation in chronic rhinosinusitis with nasal polyps (CRSwNP) remains a challenge. Managing excessive infiltration and activation of neutrophils in tissues is important for improving CRSwNP outcomes. S100A4, a calcium-binding protein, regulates cell migration, chemotaxis and tissue fibrosis. In this study, we sought to examine the role of S100A4 in neutrophilic inflammation in CRSwNP and its involvement in TLR4 signaling.

Methods

Quantitative RT-PCR and immunofluorescence were used to analyze the expression and cellular distribution of S100A4 in sinonasal mucosa. Primary human nasal epithelial cells (hNECs) were cultured and treated with S100A4 to assess cytokine and chemokine production. Additionally, we employed TLR4 inhibitor (TAK-242)

SUBMITTER: Tu Y 

PROVIDER: S-EPMC12619731 | biostudies-literature | 2025 Nov

REPOSITORIES: biostudies-literature