International immunopharmacology · 2025
ADAM28 promotes epithelial mesenchymal transition and impairs tight junctions in non-eosinophilic chronic rhinosinusitis with nasal polyps by inducing M1 polarization of macrophages.
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Zi Jiajia, Yu Longgang, Wang Lin, Li Danyang, Du Xiaoyun, Chen Han, Zhang Jisheng, Jiang Yan
Аннотация
BACKGROUND: Chronic rhinosinusitis with nasal polyps (CRSwNP) is characterized by tight junction dysfunction associated with epithelial-mesenchymal transition (EMT) processing. ADAM28 participates in the pathogenic process of inflammatory airway diseases.
METHODS: The effects of ADAM28 knockdown on the expression levels of the M1-type macrophage markers were examined using M1-type macrophage polarization model established with the THP1 cells. An inflammation model was established by collecting cell supernatants from M1-polarized macrophages with stable ADAM28 knockdown to stimulate HNEPC and primary nasal mucosal epithelial cells (pHNECs).The expression levels of EMT markers and tight junction proteins were detected.
RESULTS: ADAM28 was highly expressed in non-eosinophilic CRSwNP (NE-CRSwNP) and correlated with NE-CRSwNP clinical scores. Immunofluorescence assay demonstrated that the number of ADAM28-positive macrophages significantly increased in the NE-CRSwNP group compared with the control group. In addition, ADAM28 levels were significantly elevated in M1-type macrophages. ADAM28 knockdown significantly reduced the expression levels of M1-type macrophage polarization markers in M1 macrophages. Furthermore, ADAM28 knockdown elevated the expression of EMT marker E-cadherin and decreased the expression of α-SMA in HNEPC and pHNECs. Additionally, ADAM28 knockdown increased the expression levels of tight junction proteins in pHNECs cultured at an air-liquid interface.
CONCLUSION: ADAM28 is markedly elevated in NE-CRSwNP and is correlated with the clinical scores of NE-CRSwNP. ADAM28 induces the M1-type polarization of macrophages. ADAM28 promotes EMT and impairs tight junctions of nasal epithelia by inducing M1-type polarization of macrophages.
METHODS: The effects of ADAM28 knockdown on the expression levels of the M1-type macrophage markers were examined using M1-type macrophage polarization model established with the THP1 cells. An inflammation model was established by collecting cell supernatants from M1-polarized macrophages with stable ADAM28 knockdown to stimulate HNEPC and primary nasal mucosal epithelial cells (pHNECs).The expression levels of EMT markers and tight junction proteins were detected.
RESULTS: ADAM28 was highly expressed in non-eosinophilic CRSwNP (NE-CRSwNP) and correlated with NE-CRSwNP clinical scores. Immunofluorescence assay demonstrated that the number of ADAM28-positive macrophages significantly increased in the NE-CRSwNP group compared with the control group. In addition, ADAM28 levels were significantly elevated in M1-type macrophages. ADAM28 knockdown significantly reduced the expression levels of M1-type macrophage polarization markers in M1 macrophages. Furthermore, ADAM28 knockdown elevated the expression of EMT marker E-cadherin and decreased the expression of α-SMA in HNEPC and pHNECs. Additionally, ADAM28 knockdown increased the expression levels of tight junction proteins in pHNECs cultured at an air-liquid interface.
CONCLUSION: ADAM28 is markedly elevated in NE-CRSwNP and is correlated with the clinical scores of NE-CRSwNP. ADAM28 induces the M1-type polarization of macrophages. ADAM28 promotes EMT and impairs tight junctions of nasal epithelia by inducing M1-type polarization of macrophages.