Deletion of sua gene reduces the ability of Streptococcus uberis to adhere to and internalize into bovine mammary epithelial cells

2011 ◽  
Vol 147 (3-4) ◽  
pp. 426-434 ◽  
Author(s):  
Xueyan Chen ◽  
Oudessa Kerro Dego ◽  
Raul A. Almeida ◽  
Troy E. Fuller ◽  
Douglas A. Luther ◽  
...  
2010 ◽  
Vol 2010 ◽  
pp. 1-8 ◽  
Author(s):  
Raul A. Almeida ◽  
John R. Dunlap ◽  
Stephen P. Oliver

We showed that internalization ofStreptococcus uberisinto bovine mammary epithelial cells occurred through receptor- (RME) and caveolae-mediated endocytosis (CME). We reported also that treatment ofS. uberiswith host proteins including lactoferrin (LF) enhanced its internalization into host cells. Since the underlying mechanism(s) involved in such enhancement was unknown we investigated if preincubation ofS. uberiswith host proteins drives internalization of this pathogen into host cells through CME. Thus, experiments involving coculture of collagen-, fibronectin-, and LF-pretreatedS. uberiswith bovine mammary epithelial cells treated with RME and CME inhibitors were conducted. Results showed that internalization of host proteins-pretreatedS. uberisinto mammary epithelial cells treated with RME inhibitors was higher than that of untreated controls. These results suggest that pretreatment with selected host proteins commitsS. uberisto CME, thus avoiding intracellular bactericidal mechanisms and allowing its persistence into bovine mammary epithelial cells.


2018 ◽  
Vol 85 (1) ◽  
pp. 53-56 ◽  
Author(s):  
Raúl A. Almeida ◽  
Oudessa Kerro-Dego ◽  
Agustín G. Rius

Heat stress (HS) negatively affects milk production and has been associated with decreased immune function, and increased rate of intramammary infections (IMI). Research has shown that HS affects gene expression, cell cycle, and cell metabolism in bovine mammary epithelial cells (BMEC). Since BMEC are an initial target of mastitis pathogens, we studied adherence to and internalisation of S. uberis into HS-BMEC, as well as the effect that this interaction has on host cells by measuring HS-BMEC viability and membrane integrity. Results reported in this Research Communication showed that HS reduced cell viability and induced membrane damage. However, these pathological changes, as well as the rate of adherence and internalisation of S. uberis into BMEC, were augmented when S. uberis was cocultured with HS-BMEC. These results may help to understand the pathogenesis of S. uberis IMI as well as the increased susceptibility of mammary glands to IMI in cows subjected to HS.


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