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.

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 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.

scholarly journals Immune relevant gene expression of mammary epithelial cells and their influence on leukocyte chemotaxis in response to different mastitis pathogens

2012 ◽  
Vol 51 (No. 4) ◽  
pp. 125-132 ◽  
Author(s):  
O. Wellnitz ◽  
P. Reith ◽  
Haas SC ◽  
Meyer HHD
Keyword(s):  
Immune Response ◽  
Epithelial Cells ◽  
Mrna Expression ◽  
Mammary Epithelial Cells ◽  
Mammary Epithelial ◽  
E Coli ◽  
Amyloid A ◽  
Streptococcus Uberis ◽  
Leukocyte Chemotaxis ◽  
Mastitis Pathogens

Different mastitis pathogens induce different courses of infection, i.e. more or less severe. Mammary epithelial cells play an important role in the initial combat against microorganisms by expression of cytokines and acute phase proteins that regulate the immune response. The objective of the present study was to investigate the involvement of the epithelial cells into the outcome of mastitis induced by different pathogens. Primary epithelial cell cultures isolated from milk were used to test the immune response by measuring the mRNA expression of immunomodulators and their influence on polymorph nuclear chemotaxis. Because the cells showed different responses to isolated bacterial endotoxins (lipopolysaccharide, lipoteichoic acid, and peptidoglycans) compared to whole bacteria, they were treated with heat inactivated (10 MOI) gram-negative Escherichia coli, a very common pathogen causing acute intra-mammary infections, with Staphylococcus aureus, a prevalent cause of chronic, and, Streptococcus uberis, an inducer of acute and chronic mastitis. E. coli induced an increased mRNA expression of interleukin (IL)-8 within a 1 h treatment. A treatment for 6 h with E. coli and S. aureus induced increased mRNA expression of IL-6, IL-8, TNF-&aacute; and serum amyloid A (SAA). After a 24 h treatment the expression of these immunomodulators was still elevated, except in the E. coli treatment the SAA expression showed no differences to control cells anymore. Interestingly, Str. uberis in the same concentration did only induce the expression of IL-8 after a 6 h treatment but had no influence on other immunomodulator mRNA expression. Cell culture supernatants of E. coli and S. aureus treated cells for 12 h increased leukocyte chemotaxis in a 96-well MultiScreen<sup>TM</sup>MIC-plate. S. aureus seemed to induce increased chemotaxis after shorter treatments than E. coli. In conclusion, mammary epithelial cells are involved in the different immune response to various mastitis pathogens, and the induction of chemotaxis of leukocytes from blood to milk during mastitis. Therefore, most likely epithelial cells play a role in the differential pattern of immunomediators stimulated by different pathogens.

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