CD36
TLR4型
信号转导
促炎细胞因子
清道夫受体
细胞生物学
内化
吞噬作用
脂多糖
生物
受体
激活剂(遗传学)
化学
炎症
免疫学
生物化学
胆固醇
脂蛋白
作者
Duo-Yao Cao,Jun Luo,Dekun Chen,Huifen Xu,Huaiping Shi,Xiaoqi Jing,Wenjuan Zang
摘要
Abstract The scavenger receptor CD36 is involved in pathogen recognition, phagocytosis, and pathogen-induced signaling. This study investigated the relationship between CD36 and TLR4 in modifying lipopolysaccharide (LPS)-induced signaling pathways and mediating Escherichia coli ( E. coli ) endocytosis in primary goat mammary epithelial cells (pGMECs). The manipulation of CD36 expression significantly influenced TLR4 and nuclear factor kappa B (NF-κB) mRNA expression in pGMECs stimulated with LPS for 12 h. NF-κB and activator protein-1 (AP-1) activity was regulated by the manipulation of CD36 expression in LPS-induced pGMECs. However, CD36-mediated AP-1 activation occurred primarily through c-Jun N-terminal kinase (c-JNK). Adaptor proteins and proinflammatory cytokines were also involved in these signaling pathways and acted by regulating CD36 expression in LPS-stimulated cells. Moreover, CD36 cooperated with TLR4 in TLR4-mediated phagocytosis following E. coli simulation, but this complex was not induced by LPS treatment. Our study is the first to illuminate CD36 as a scavenger receptor in ruminants. Additionally, this study indicates that CD36 plays a vital role in the LPS-induced activation of downstream signaling cascades and mediates E. coli phagocytosis via TLR4 in pGMECs, which offers a novel treatment strategy for mastitis.
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