Upregulated-gene expression of pro-inflammatory cytokines (TNF-α, IL-1β and IL-6) via TLRs following NF-κB and MAPKs in bovine mastitis
Upregulated-gene expression of pro-inflammatory cytokines (TNF-α, IL-1β and IL-6) via TLRs following NF-κB and MAPKs in bovine mastitis
复制标题
DOI：
10.1016/j.actatropica.2020.105458
复制
发表时间：
2020-07-01
期刊：
影响因子：
2.7
通讯作者：
Guo, Mengyao
中科院分区：
文献类型：
--
作者：
Akhtar, Muhammad;Guo, Shuai;Guo, Mengyao
乳腺炎是奶牛乳房的炎症，给奶牛带来巨大的经济损失。奶牛乳房中的炎症、任何组织损伤和病原体均可激活Toll样受体（TLR）。金黄色葡萄球菌(S.金黄色葡萄球菌）是乳腺炎的主要原因。在乳腺炎中，活化的TLRs启动NF-κ B/MAPKs通路，其进一步触发与乳腺炎相关的基因表达，随后是先天性免疫应答。在本研究中，研究了病原体诱导的乳腺组织中促炎性细胞因子的基因表达谱。苏木精和伊红（H & E）结果表明，感染组织中存在严重的组织病理学变化。Western blot结果提示，TLR 2/TLR 4在感染组织中的过度表达与NF-κ B/MAPKs通路的激活有关。qRT-PCR结果显示，与未感染组织相比，感染组织中与TLR 2/TLR 4介导的NF-κ B/MAPK信号通路相关的基因表达。mRNA和相对蛋白质表达水平的统计学分析表明，在感染组织中促炎性细胞因子（TNF-α、IL-1 β和IL-6）的上调，而不是在非感染组织中。这些结果表明，基因表达水平的上调涉及乳腺正常免疫功能的潜在调节途径。结论：本研究为进一步研究乳腺病理生理学及TLRs和NF-κ B/MAPKs介导的促炎性细胞因子基因表达提供了新的思路。
Mastitis is the inflammation of mammary glands which causes huge economic loss in dairy cows. Inflammation, any tissue injury and pathogens in cow udder activate Toll-like Receptors (TLRs). Staphylococcus aureus (S. aureus) is the major cause of mastitis. In mastitis, activated TLRs initiate the NF-kappa B/MAPKs pathways which further trigger the gene expression associated with mastitis followed by innate immune response. In this study, pathogenic-induced gene expression profile of pro-inflammatory cytokines in mammary gland tissues, was investigated in mastitis. The Hematoxylin and Eosin (H & E) results indicated severe histopathological changes in infected tissues. Western blot results suggested the over expressions of TLR2/TLR4 with NF-kappa B/MAPKs pathways activation in infected tissues. qRT-PCR results revealed the gene expression associated with TLR2/TLR4-mediated NF-kappa B/MAPKs pathways in infected tissues in comparison with non-infected. Statistical analysis of mRNA and relative protein expression levels indicated the up-regulation of pro-inflammatory cytokines (TNF-alpha, IL-1 beta and IL-6) in infected tissues rather than non-infected tissues. These results suggested that the up-regulation of gene expression levels implicated the underlying regulatory pathways for proper immune function in mammary glands. In conclusion, our study might give new insights for investigation and better understanding of mammary gland pathophysiology and TLRs and NF-kappa B/MAPKs-mediated gene expression of pro-inflammatory cytokines.