Role of Toll-like receptor 2 against Streptococcus uberis infection in primary mouse mammary epithelial cells

2020 ◽  
Vol 79 ◽  
pp. 106142 ◽  
Author(s):  
Zhixin Wan ◽  
Xudong Wang ◽  
Ming Liu ◽  
Jiakun Zuo ◽  
Yuanyuan Xu ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Mammary Epithelial Cells ◽  
Mammary Epithelial ◽  
Toll Like Receptor ◽  
Streptococcus Uberis ◽  
Primary Mouse ◽  
Toll Like Receptor 2

scholarly journals Taurine Alleviates Streptococcus uberis-Induced Inflammation by Activating Autophagy in Mammary Epithelial Cells

2021 ◽  
Vol 12 ◽  
Author(s):  
Zhenglei Wang ◽  
Riguo Lan ◽  
Yuanyuan Xu ◽  
Jiakun Zuo ◽  
Xiangan Han ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Theoretical Basis ◽  
Mammary Epithelial Cells ◽  
Bacterial Load ◽  
Mammary Epithelial ◽  
Invasive Pathogens ◽  
Streptococcus Uberis ◽  
Theoretical Support ◽  
And Control

Streptococcus uberis infection can cause serious inflammation and damage to mammary epithelial cells and tissues that can be significantly alleviated by taurine. Autophagy plays an important role in regulating immunity and clearing invasive pathogens and may be regulated by taurine. However, the relationships between taurine, autophagy, and S. uberis infection remain unclear. Herein, we demonstrate that taurine augments PTEN activity and inhibits Akt/mTOR signaling, which decreases phosphorylation of ULK1 and ATG13 by mTOR and activates autophagy. Activating autophagy accelerates the degradation of intracellular S. uberis, reduces intracellular bacterial load, inhibits over-activation of the NF-κB pathway, and alleviates the inflammation and damage caused by S. uberis infection. This study increases our understanding of the mechanism through which taurine regulates autophagy and is the first to demonstrate the role of autophagy in S. uberis infected MAC-T cells. Our study also provides a theoretical basis for employing nutritional elements (taurine) to regulate innate immunity and control S. uberis infection. It also provides theoretical support for the development of prophylactic strategies for this important pathogen.

scholarly journals Toll-like receptor-4, but not toll-like receptor-2 mediates secretion of tumour necrosis factor α and interleukin-8 in lipopolysaccharide-stimulated mouse mammary epithelial cells

2013 ◽  
Vol 57 (3) ◽  
pp. 393-397 ◽  
Author(s):  
Chang-Liang He ◽  
Qiong Yi ◽  
Yuan-Fang Li ◽  
Hang Yang ◽  
Lu Wang
Keyword(s):  
Epithelial Cells ◽  
Tumour Necrosis ◽  
Mammary Epithelial Cells ◽  
Mammary Epithelial ◽  
Tumour Necrosis Factor Α ◽  
Toll Like Receptor ◽  
Tnf Α ◽  
Toll Like Receptor 2 ◽  
Factor Α ◽  
Necrosis Factor

Abstract Mammary epithelial cells (MECs) from Kunming mice were isolated and stimulated in vitro with 10 μg/mL of Escherichia coli lipopolysaccharide (LPS). The release of tumour necrosis factor α (TNF-α) and interleukin-8 (IL-8) into culture supernatants was measured by ELISA. Furthermore, blocking experiments with Toll-like receptor 2 (TLR2) and TLR4 antibodies were performed to verify whether cytokine secretion depended on LPS-induced activation of TLR2 or TLR4. The results revealed that LPS-stimulated mouse MECs significantly secreted TNF-α and IL-8. Blocking of the TLR4 pathway inhibited the secretion of TNF-α and IL-8, while inhibition of LPS-induced TNF-α and IL-8 production was not observed when TLR2 was blocked. Thus, TLR4 can mediate the LPS-induced expression of cytokines such as TNF-α and IL-8 in mouse MECs.

Cytotoxic effects of cadmium in mammary epithelial cells: Protective role of the macrocycle [15]pyN5

2012 ◽  
Vol 50 (6) ◽  
pp. 2180-2187 ◽  
Author(s):  
Sandrina Gonçalves ◽  
Ana Sofia Fernandes ◽  
Nuno G. Oliveira ◽  
Joana Marques ◽  
Judite Costa ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Mammary Epithelial Cells ◽  
Protective Role ◽  
Mammary Epithelial ◽  
Cytotoxic Effects

scholarly journals Metalloproteinase axes increase beta-catenin signaling in primary mouse mammary epithelial cells lacking TIMP3

2007 ◽  
Vol 120 (6) ◽  
pp. 1050-1060 ◽  
Author(s):  
C. V. Hojilla ◽  
I. Kim ◽  
Z. Kassiri ◽  
J. E. Fata ◽  
H. Fang ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Mammary Epithelial Cells ◽  
Mammary Epithelial ◽  
Beta Catenin ◽  
Primary Mouse

scholarly journals MiR-125b regulates inflammation in bovine mammary epithelial cells by targeting the NKIRAS2 gene

2021 ◽  
Vol 52 (1) ◽  
Author(s):  
Zhuo-Ma Luoreng ◽  
Da-Wei Wei ◽  
Xing-Ping Wang
Keyword(s):  
T Cells ◽  
Epithelial Cells ◽  
Dairy Cows ◽  
Mammary Epithelial Cells ◽  
Mammary Epithelial ◽  
Luciferase Reporter ◽  
Regulation Mechanism ◽  
Bovine Mammary Epithelial Cells ◽  
Tnf Α

AbstractMastitis is a complex inflammatory disease caused by pathogenic infection of mammary tissue in dairy cows. The molecular mechanism behind its occurrence, development, and regulation consists of a multi-gene network including microRNA (miRNA). Until now, there is no report on the role of miR-125b in regulating mastitis in dairy cows. This study found that miR-125b expression is significantly decreased in lipopolysaccharide (LPS)-induced MAC-T bovine mammary epithelial cells. Also, its expression is negatively correlated with the expression of NF-κB inhibitor interacting Ras-like 2 (NKIRAS2) gene. MiR-125b target genes were identified using a double luciferase reporter gene assay, which showed that miR-125b can bind to the 3′ untranslated region (3′ UTR) of the NKIRAS2, but not the 3′UTR of the TNF-α induced protein 3 (TNFAIP3). In addition, miR-125b overexpression and silencing were used to investigate the role of miR-125b on inflammation in LPS-induced MAC-T. The results demonstrate that a reduction in miR-125b expression in LPS-induced MAC-T cells increases NKIRAS2 expression, which then reduces NF-κB activity, leading to low expression of the inflammatory factors IL-6 and TNF-α. Ultimately, this reduces the inflammatory response in MAC-T cells. These results indicate that miR-125b is a pro-inflammatory regulator and that its silencing can alleviate bovine mastitis. These findings lay a foundation for elucidating the molecular regulation mechanism of cow mastitis.

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