Phosphatidylinositol-Specific Phospholipase C can decreases Müller cells viability and suppress its phagocytic activity by modulating PI3K/AKT signaling pathway.
Bianjin SunShudan LinMengmeng ZhengBeijia ZhengLiping MaoYunfeng GuJiabei CaiYiran DaiMeiqin ZhengLou YongliangPublished in: Canadian journal of microbiology (2023)
Bacillus cereus endophthalmitis is a devastating eye infection that causes rapid blindness through the release of extracellular tissue-destructive exotoxins. The phagocytic and antibacterial functions of ocular cells are the keys to limiting ocular bacterial infections. In a previous study, we identified a new virulence gene, plcA-2 (different from the original plcA-1 gene), that was strongly associated with the plcA gene of Listeria monocytogenes. This plcA gene had been confirmed to play an important role in phagocytosis. However, how the BcPI-PLC proteins encoded by the plcA-1/2 genes affect phagocytes remains unclear in B. cereus endophthalmitis. Here, we found that the enzymatic activity of Bc-PI-PLC-A2 was approximately 2-fold higher than that of Bc-PI-PLC-A1, and both proteins inhibited the viability of Müller cells. In addition, PI-PLC proteins reduced phagocytosis of Müller cells by decreasing the phosphorylation levels of key proteins in the PI3K/AKT signaling pathway. In conclusion, we showed that PI-PLC proteins contribute to inhibit the viability of and suppress the phagocytosis of Müller cells, providing new insights into the pathogenic mechanism of B. cereus endophthalmitis.
Keyphrases
- induced apoptosis
- signaling pathway
- cell cycle arrest
- pi k akt
- genome wide
- oxidative stress
- escherichia coli
- cell proliferation
- epithelial mesenchymal transition
- copy number
- pseudomonas aeruginosa
- genome wide identification
- hydrogen peroxide
- cystic fibrosis
- quantum dots
- genome wide analysis
- anti inflammatory
- wound healing