Vocal fold fibroblasts immunoregulate activated macrophage phenotype

Area of Science:

• Immunology
• Cell Biology
• Otolaryngology

Background:

• Fibroblasts are crucial in wound healing, producing inflammatory mediators.
• Dysregulated inflammation in vocal folds can lead to scarring and functional impairment.

Purpose of the Study:

• To investigate the immunomodulatory effects of vocal fold fibroblasts (VFFs) from normal, polyp, and scar tissues on macrophages.
• To understand fibroblast-macrophage interactions in the context of lipopolysaccharide (LPS)-induced inflammation.

Main Methods:

• Co-culture of VFFs with CD14+ monocytes.
• Stimulation with LPS for 24 and 72 hours.
• Quantification of inflammatory cytokines (TNF-α, IL-6, IL-8, IL-10, IL-12, IL-1β, MCP-1) via ELISA.

Main Results:

• Macrophages co-cultured with polyp VFFs showed significantly increased pro-inflammatory cytokines (TNF-α, IL-1β, IL-12) and IL-10 at 24h.
• Macrophages co-cultured with scar VFFs exhibited decreased TNF-α, IL-1β, IL-12, and increased IL-10 at 24h.
• At 72h, polyp VFFs enhanced multiple cytokines, while scar VFFs continued to suppress IL-1β and IL-12.

Conclusions:

• VFFs modulate macrophage inflammatory responses differently based on tissue origin (normal, polyp, scar).
• Polyp VFFs may promote excessive inflammation, while scar VFFs may dampen it.
• These interactions could contribute to abnormal extracellular matrix deposition and vocal fold dysfunction.