Annexin A2 regulates Mycoplasma bovis adhesion and invasion to embryo bovine lung cells affecting molecular expression essential to inflammatory response.
Annexin A2 regulates Mycoplasma bovis adhesion and invasion to embryo bovine lung cells affecting molecular expression essential to inflammatory response.
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DOI：
10.3389/fimmu.2022.974006
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发表时间：
2022
影响因子：
7.3
通讯作者：
中科院分区：
文献类型：
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作者：
牛支原体（M. bovis）是牛呼吸道疾病复合体的重要病原体，侵入下呼吸道并引起严重的肺炎。然而，其分子机制在很大程度上仍然未知。宿主膜联蛋白A2（ANXA 2）是一种钙依赖性磷脂结合蛋白。目前的研究试图确定ANXA 2是否可以介导M.从而影响其诱导炎症反应。ANXA 2在M.牛感染的牛肺上皮细胞（EBL），并用抗ANXA 2抗体阻断ANXA 2减少M.牛对EBL的粘附。与未感染细胞相比，M.牛传染病此外，RNA干扰敲低EBL细胞中ANXA 2表达导致M.牛侵袭和F-肌动蛋白聚合。其次，对M.进行ANXA 2敲减和未敲减的牛感染的EBL细胞。数据显示，ANXA 2敲低的EBL细胞具有2487个差异表达基因（DEG），与对照相比，1175个上调，1312个下调。根据GO和KEGG分析，50个可能与炎症反应相关的基因、23个参与细胞外基质（ECM）受体相互作用的基因和48个与PI 3 K-AKT信号通路相关的基因上调，而38个mRNA结合基因、16个mRNA 3′-UTR结合基因和34个RNA转运基因下调。此外，选择了19个具有不同变化倍数的基因进行qPCR验证，结果与RNA-seq结果一致。总之，在ANXA 2敲低的细胞中，IL-17信号通路中的两种趋化因子（IL-8和CXCL 5）和关键的牛β-防御素TAP的转录显著增加。此外，ANXA 2敲除或敲除可增加NF-κB和MAPK的磷酸化活性。牛传染病此外，ANXA 2敲低也显著降低了M后通过外显子V3和V7跳跃的CD 44转录物。牛传染病我们的结论是M.牛借宿主ANXA 2介导其粘附和侵袭，从而负调控IL-17信号通路必需的分子表达。此外，CD 44 V3和V7亚型可能参与了M中ANXA 2介导的过程。牛感染EBL细胞。这些发现揭示了对M.牛传染病
Mycoplasma bovis (M. bovis) is an important pathogen of the bovine respiratory disease complex, invading lower respiratory tracts and causing severe pneumonia. However, its molecular mechanism largely remains unknown. Host annexin A2 (ANXA2) is a calcium-dependent phospholipid-binding protein. The current study sought to determine whether ANXA2 could mediate M. bovis adhesion and invasion thereby affecting its induction of inflammatory response. ANXA2 expression was upregulated in M. bovis-infected bovine lung epithelial cells (EBL), and blocking ANXA2 with an anti-ANXA2 antibody reduced M. bovis adhesion to EBL. Compared with uninfected cells, more ANXA2 was translocated from the cytoplasm to the cell surface after M. bovis infection. Furthermore, RNA interference knockdown of ANXA2 expression in EBL cells resulted in a significant decrease in M. bovis invasion and F-actin polymerization. Next, the transcriptomic study of M. bovis-infected EBL cells with and without ANXA2 knockdown were performed. The data exhibited that ANXA2 knockdown EBL cells had 2487 differentially expressed genes (DEGs), with 1175 upregulated and 1312 downregulated compared to control. According to GO and KEGG analyses, 50 genes potentially linked to inflammatory responses, 23 involved in extracellular matrix (ECM) receptor interaction, and 48 associated with PI3K-AKT signal pathways were upregulated, while 38 mRNA binding genes, 16 mRNA 3′-UTR binding genes, and 34 RNA transport genes were downregulated. Furthermore, 19 genes with various change-folds were selected for qPCR verification, and the results agreed with the RNA-seq findings. Above all, the transcription of two chemokines (IL-8 and CXCL5) and a key bovine β-defensin TAP in IL-17 signaling pathway were significantly increased in ANXA2 knockdown cells. Moreover, ANXA2 knockdown or knockout could increase NF-κB and MAPK phosphorylation activity in response to M. bovis infection. Additionally, ANXA2 knockdown also significantly decreased the CD44 transcripts via exon V3 and V7 skipping after M. bovis infection. We concluded that M. bovis borrowed host ANXA2 to mediate its adhesion and invasion thereby negatively regulating molecular expression essential to IL-17 signal pathway. Furthermore, CD44 V3 and V7 isoforms might contribute to this ANXA2 meditated processes in M. bovis infected EBL cells. These findings revealed a new understanding of pathogenesis for M. bovis infection.
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影响因子：
5.2
作者：
Josse J;Laurent F;Diot A
通讯作者：
Diot A
影响因子：
--
作者：
Madureira PA;Hill R;Miller VA;Giacomantonio C;Lee PW;Waisman DM
通讯作者：
Waisman DM
影响因子：
3.1
作者：
Bower, K;Djordjevic, SP;Ranson, M
通讯作者：
Ranson, M
DOI：
10.3390/pathogens10121628
发表时间：
2021-12-15
期刊：
Pathogens (Basel, Switzerland)
影响因子：
--
作者：
Lu D;Zhang H;Zhang Y;Zhao G;Anwar Khan F;Chen Y;Hu C;Yang L;Chen H;Guo A
通讯作者：
Guo A
影响因子：
3.7
作者：
Hakobyan D;Gerke V;Heuer A
通讯作者：
Heuer A