Background: Adenoid hypertrophy (AH) is a chronic or acute obstruction-related ailment of the upper respiratory tract that arises as an inflammatory response to exposure of bacteria, viruses or allergies. Activation and polarization of macrophages are key processes in inflammation-related disorders like AH and CCL20/CCR6 axis is a critical therapeutic target.
Purpose: To determine that CCL20/CCR6 mediated macrophage activation and polarization can promote adenoid epithelial inflammation in AH.
Methods: To support this claim, CCL20 and CCR6 expressions were studied in clinical AH samples. In addition, the expressions of cytokines such as TNF-α, IL-1β, IL-6, IL-17, IL-10 and TGF-β were analysed. In vitro, human adenoid epithelial cells were co-cultured with polarized THP-1 and T lymphocyte H9 cells to study the expressions of several inflammatory markers.
Results: The expressions of M1 macrophage markers CD86 and IL-17 were significantly increased, whereas the expressions of M2 macrophage markers CD206 and FOXP3 were significantly decreased. The THP-1 cells were successfully polarized to M0, M1 and M2 macrophages. The survival of macrophages improved after 24 hr of induction and enhanced TGF-β expression was observed. The expressions of the inflammatory cytokines IL-6, TNF-α, IL-1β and CCL20 increased significantly.
Conclusion: Collectively, these results suggest that the CCL20/CCR6 mediated macrophage activation and polarization into M1-type macrophages can promote adenoid epithelial inflammation in AH. Further studies are warranted to determine the roles of inflammatory markers in the pathophysiology of AH and identifying potential targets.
Keywords: CCL20/CCR6 axis; adenoid hypertrophy; inflammation; macrophages; markers.
© 2022 Ye et al.