Frontiers in immunology · 2026
ANKRD22 contributes to NF-κB-associated inflammatory responses in alveolar type II epithelial cells during PM2.5-triggered airway inflammation.
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Jin Yan, Zhao Yun, Wei Shihui, Chen Xingyu, Zhu Ke, Xiong Juan, Qi Rongbin, Zhang Wen, Lai Tianwen, Cao Chao
Аннотация
BACKGROUND: PM2.5 causes multifaceted detrimental effects on human health. Alveolar type II epithelial (AT-II) cells serve critical function in PM2.5-induced airway inflammation. However, the mechanism remains unclear.
METHODS: ANKRD22 expression in AT-II cells was assessed in a PM2.5-induced mouse airway inflammation model using immunofluorescence, qRT-PCR and Western blot. AT-II cell-specific ANKRD22 knockout (AT-II-ANKRD22△/△ ) mice were generated and exposed to PM2.5. Inflammation was evaluated by BALF leukocyte and neutrophil counts, lung H&E staining, and qRT-PCR/ELISA for IL-6 and CXCL1. In vitro, ANKRD22 knockdown in A549 cells was performed prior to PM2.5 stimulation, and cytokine levels (IL-6, IL-8, IL-1β, CXCL1, CXCL2) were measured by qRT-PCR and ELISA. RNA sequencing was used to explore the regulatory mechanisms of ANKRD22 in AT-II cells during PM2.5-induced airway inflammation.
RESULTS: Our study demonstrated that PM2.5 promoted ANKRD22 expression in AT-II cells both in vivo and in vitro. PM2.5-induced inflammation was alleviated in AT-II- ANKRD22△/△ mice. The expression of IL6, IL8, IL1B, CXCL1, and CXCL2 was downregulated by ANKRD22 siRNA in A549 cells. Mechanistically, PM2.5 exposure significantly enhanced the protein expression of P50 and the phosphorylation of IKKβ, IκBα and RELA. Moreover, these PM2.5-induced changes were markedly attenuated following ANKRD22 deficiency. Similarly, PM2.5 exposure induced significant upregulation of p52 protein levels and RELB phosphorylation, which were substantially reduced by ANKRD22 knockdown.
CONCLUSION: In conclusion, PM2.5 stimulation promoted the ANKRD22 expression in AT-II cells, thereby contributing to NF-κB-associated inflammatory responses during PM2.5-induced airway inflammation.
METHODS: ANKRD22 expression in AT-II cells was assessed in a PM2.5-induced mouse airway inflammation model using immunofluorescence, qRT-PCR and Western blot. AT-II cell-specific ANKRD22 knockout (AT-II-ANKRD22△/△ ) mice were generated and exposed to PM2.5. Inflammation was evaluated by BALF leukocyte and neutrophil counts, lung H&E staining, and qRT-PCR/ELISA for IL-6 and CXCL1. In vitro, ANKRD22 knockdown in A549 cells was performed prior to PM2.5 stimulation, and cytokine levels (IL-6, IL-8, IL-1β, CXCL1, CXCL2) were measured by qRT-PCR and ELISA. RNA sequencing was used to explore the regulatory mechanisms of ANKRD22 in AT-II cells during PM2.5-induced airway inflammation.
RESULTS: Our study demonstrated that PM2.5 promoted ANKRD22 expression in AT-II cells both in vivo and in vitro. PM2.5-induced inflammation was alleviated in AT-II- ANKRD22△/△ mice. The expression of IL6, IL8, IL1B, CXCL1, and CXCL2 was downregulated by ANKRD22 siRNA in A549 cells. Mechanistically, PM2.5 exposure significantly enhanced the protein expression of P50 and the phosphorylation of IKKβ, IκBα and RELA. Moreover, these PM2.5-induced changes were markedly attenuated following ANKRD22 deficiency. Similarly, PM2.5 exposure induced significant upregulation of p52 protein levels and RELB phosphorylation, which were substantially reduced by ANKRD22 knockdown.
CONCLUSION: In conclusion, PM2.5 stimulation promoted the ANKRD22 expression in AT-II cells, thereby contributing to NF-κB-associated inflammatory responses during PM2.5-induced airway inflammation.