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C. sakazakii activates AIM2 pathway accompanying with excessive ER stress response in mammalian mammary gland epithelium.
Cell Stress and Chaperones ( IF 3.3 ) Pub Date : 2020-01-10 , DOI: 10.1007/s12192-019-01065-0
Wenjuan Song 1, 2 , Le Sheng 1, 2 , Fanghui Chen 1, 2 , Yu Tian 3 , Lian Li 1, 2 , Genlin Wang 1, 2 , Honglin Li 4 , Yafei Cai 1, 2
Affiliation  

Bovine mastitis is a common inflammatory disease caused by various factors. The main factor of mastitis is pathogenic microorganism infection, such as Staphylococcus aureus, Escherichia coli, and Streptococcus. Cronobacter sakazakii (C. sakazakii) is a newly discovered pathogenic bacteria in milk products, which seriously threat human health in recent years. At present, it has not been reported that the pathogenesis of mastitis is caused by C. sakazakii. This study investigated the inflammation of mammary gland epithelium, which was induced by C. sakazakii for the first time. We focused on bacterial isolation, histological observation, AIM2 inflammasome pathways, endoplasmic reticulum stress, and apoptosis. The results showed that C. sakazakii–induced inflammation caused damage of tissue, significantly increased the production of pro-inflammatory cytokines (including TNF-α, IL-1β, and IL-6), activated the AIM2 inflammasome pathway (increased the expression of AIM2 and cleaved IL-1β), and induced endoplasmic reticulum stress (increased the expression of ERdj4, Chop, Grp78) and apoptosis (increased the ratio of Bax/Bcl-2, a marker of apoptosis). In conclusion, it is suggested that it maybe inhibite AIM2 inflammasome pathways and alleviate endoplasmic reticulum stress (ER stress) against the C. sakazakii–induced inflammation.

中文翻译:


C. sakazakii 激活 AIM2 通路并伴随哺乳动物乳腺上皮细胞的过度 ER 应激反应。



牛乳腺炎是由多种因素引起的常见炎症性疾病。乳腺炎的主要因素是病原微生物感染,如金黄色葡萄球菌大肠杆菌链球菌等。阪崎克罗诺杆菌C. sakazakii )是近年来在乳制品中新发现的致病菌,严重威胁人类健康。目前尚未见乳腺炎的发病机制是由坂崎棒状杆菌引起的报道。本研究首次研究了坂崎棒状杆菌诱导的乳腺上皮炎症。我们重点关注细菌分离、组织学观察、AIM2 炎症小体途径、内质网应激和细胞凋亡。结果显示,坂崎棒杆菌诱导的炎症引起组织损伤,显着增加促炎细胞因子(包括TNF-α、IL-1β和IL-6)的产生,激活AIM2炎症小体通路(增加AIM2 和裂解的 IL-1β),并诱导内质网应激(ERdj4、Chop、Grp78 的表达增加)和细胞凋亡(细胞凋亡标志物 Bax/Bcl-2 的比率增加)。总之,它可能抑制 AIM2 炎症小体途径并减轻内质网应激(ER 应激),以对抗坂崎棒状杆菌诱导的炎症。
更新日期:2020-01-10
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