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ORIGINAL RESEARCH

Inhibitory Effect of Apolipoprotein A-I on Eosinophils in Allergic Rhinitis in vitro and in vivo

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Pages 89-96 | Received 24 Nov 2023, Accepted 08 Feb 2024, Published online: 13 Feb 2024
 

Abstract

Purpose

Eosinophils have pivotal roles in the development of allergic rhinitis (AR) through the release of cytotoxic substances. Apolipoprotein A-I (Apo-AI) exhibits a strong inhibitory effect on eosinophil infiltration in allergic diseases. Nevertheless, the precise impact of Apolipoprotein A-I on eosinophils remains uncertain.

Methods

Our study recruited a total of 15 AR children and 15 controls. The correlation between Apo-AI expression and the counts of blood eosinophils was examined. Flow cytometry was employed to assess the role of Apo-AI in eosinophil apoptosis and adhesion. The Transwell system was performed to conduct the migration assay. An animal model using AR mice was established to test the effect of Apo-AI on eosinophils.

Results

Serum Apo-AI were negatively related to eosinophils counts and eosinophil chemotactic protein levels in AR. Apo-AI exerts a pro-apoptotic effect while also impeding the processes of adhesion, migration, and activation of eosinophils. The apoptosis triggered by Apo-AI was facilitated through the phosphoinositide 3-kinase (PI3K) pathway. The chemotaxis and activation of eosinophils, which are influenced by Apolipoprotein A-I, are regulated through the PI3K and MAPK signaling pathways. Apo-AI treated mice presented with decreased blood and nasal eosinophilic inflammation as well as down-regulated eosinophil related cytokines.

Conclusion

Our findings provide confirmation that Apo-AI exhibits inhibitory effects on the function of eosinophils in allergic rhinitis. This suggests that Apo-AI holds potential as a therapeutic target for future treatment strategies.

Acknowledgments

Yinhui Zeng, Jinyuan Li and Yueqiang Wen are co-first authors for this study. This study was supported by grants from the National Natural Science Grant of China (No.81970861, No.82271142), the Guangdong Province Natural Science Grant (No. 2021A1515010940), and the Science and Technology Program of Guangzhou (No. 202201020600, No.202201011844), Scientific Research Capacity Improvement Project of Guangzhou Medical University (02-410-2302151XM).

Disclosure

The authors declare that they have no relevant conflicts of interest in this work.