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抗菌肽CATH-2通过NF-κB/NLRP3/MAPK信号通路及巨噬细胞溶酶体功能障碍减轻禽致病性诱导的炎症反应

Antimicrobial Peptide CATH-2 Attenuates Avian Pathogenic -Induced Inflammatory Response via NF-κB/NLRP3/MAPK Pathway and Lysosomal Dysfunction in Macrophages.

作者信息

Xu Yating, Xu Liuyi, Zhang Tingting, Tian Hongliang, Lu Yi, Jiang Sha, Cao Xuefeng, Li Zhiwei, Hu Xiaoxiang, Fang Rendong, Peng Lianci

机构信息

Joint International Research Laboratory of Animal Health and Animal Food Safety, College of Veterinary Medicine, Southwest University, Chongqing 400715, China.

National Center of Technology Innovation for Pigs, Chongqing 402460, China.

出版信息

Int J Mol Sci. 2024 Nov 22;25(23):12572. doi: 10.3390/ijms252312572.

DOI:10.3390/ijms252312572
PMID:39684284
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11641483/
Abstract

Cathelicidins have anti-inflammatory activity and chicken cathelicidin-2 (CATH-2) has shown to modulate immune response, but the underlying mechanism of its anti-inflammation is still unclear. Therefore, in this study, we investigated the anti-inflammatory activity of CATH-2 on murine peritoneal macrophages during avian pathogenic (APEC) infection. The results showed that CATH-2 priming significantly reduced the production of IL-1β, IL-6, IL-1α, and IL-12. In addition, CATH-2 significantly attenuated APEC-induced caspase-1 activation and the formation of an adaptor (ASC) of NLRP3 inflammasome, indicating that CATH-2 inhibits APEC-induced NLRP3 inflammasome activation. Furthermore, CATH-2 remarkably inhibited NF-κB and MAPK signaling pathways activation. Moreover, CATH-2 significantly inhibited mRNA expression of cathepsin B and inhibited lysosomal acidification, demonstrating that CATH-2 disrupts lysosomal function. In addition, promoting lysosomal acidification using ML-SA1 hampered the anti-inflammatory effect of CATH-2 on APEC-infected cells. In conclusion, our study reveals that CATH-2 inhibits APEC-induced inflammation via the NF-κB/NLRP3/MAPK pathway through the dysfunction of lysosome.

摘要

抗菌肽具有抗炎活性，鸡抗菌肽-2（CATH-2）已显示出可调节免疫反应，但其抗炎的潜在机制仍不清楚。因此，在本研究中，我们研究了CATH-2在禽致病性大肠杆菌（APEC）感染期间对小鼠腹腔巨噬细胞的抗炎活性。结果表明，CATH-2预处理显著降低了IL-1β、IL-6、IL-1α和IL-12的产生。此外，CATH-2显著减弱了APEC诱导的半胱天冬酶-1激活和NLRP3炎性小体衔接蛋白（ASC）的形成，表明CATH-2抑制了APEC诱导的NLRP3炎性小体激活。此外，CATH-2显著抑制了NF-κB和MAPK信号通路的激活。此外，CATH-2显著抑制组织蛋白酶B的mRNA表达并抑制溶酶体酸化，表明CATH-2破坏了溶酶体功能。此外，使用ML-SA1促进溶酶体酸化阻碍了CATH-2对APEC感染细胞的抗炎作用。总之，我们的研究表明，CATH-2通过溶酶体功能障碍经由NF-κB/NLRP3/MAPK途径抑制APEC诱导的炎症。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/53ad/11641483/1d2e9bcfd740/ijms-25-12572-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/53ad/11641483/8a76965fd51e/ijms-25-12572-g001.jpg
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