scholarly journals Inhibition of Staphylococcus aureus Invasion into Bovine Mammary Epithelial Cells by Contact with Live Lactobacillus casei

2012 ◽  
Vol 79 (3) ◽  
pp. 877-885 ◽  
Author(s):  
Damien S. Bouchard ◽  
Lucie Rault ◽  
Nadia Berkova ◽  
Yves Le Loir ◽  
Sergine Even
Keyword(s):  
Staphylococcus Aureus ◽  
Epithelial Cells ◽  
Lactobacillus Casei ◽  
Mammary Epithelial Cells ◽  
Control Strategies ◽  
Mammary Epithelial ◽  
Dairy Herds ◽  
Dependent Manner ◽  
Content Type ◽  
Bovine Mammary Epithelial Cells

ABSTRACTStaphylococcus aureusis a major pathogen that is responsible for mastitis in dairy herds.S. aureusmastitis is difficult to treat and prone to recurrence despite antibiotic treatment. The ability ofS. aureusto invade bovine mammary epithelial cells (bMEC) is evoked to explain this chronicity. One sustainable alternative to treat or prevent mastitis is the use of lactic acid bacteria (LAB) as mammary probiotics. In this study, we tested the ability ofLactobacillus caseistrains to prevent invasion of bMEC by twoS. aureusbovine strains, RF122 and Newbould305, which reproducibly induce acute and moderate mastitis, respectively.L. caseistrains affected adhesion and/or internalization ofS. aureusin a strain-dependent manner. Interestingly,L. caseiCIRM-BIA 667 reducedS. aureusNewbould305 and RF122 internalization by 60 to 80%, and this inhibition was confirmed for two otherL. caseistrains, including one isolated from bovine teat canal. The protective effect occurred without affecting bMEC morphology and viability. Once internalized, the fate ofS. aureuswas not affected byL. casei. It should be noted thatL. caseiwas internalized at a low rate but survived in bMEC cells with a better efficiency than that ofS. aureusRF122. Inhibition ofS. aureusadhesion was maintained with heat-killedL. casei, whereas contact between liveL. caseiandS. aureusor bMEC was required to preventS. aureusinternalization. This first study of the antagonism of LAB towardS. aureusin a mammary context opens avenues for the development of novel control strategies against this major pathogen.

scholarly journals Intracellular Staphylococcus aureus Control by Virulent Bacteriophages within MAC-T Bovine Mammary Epithelial Cells

2016 ◽  
Vol 61 (2) ◽  
Author(s):  
Lili Zhang ◽  
Lichang Sun ◽  
Ruicheng Wei ◽  
Qiang Gao ◽  
Tao He ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Epithelial Cells ◽  
Treatment Failure ◽  
Mammary Epithelial Cells ◽  
Recurrent Infection ◽  
Mammary Epithelial ◽  
Time Dependent ◽  
Dependent Manner ◽  
Content Type ◽  
Bovine Mammary Epithelial Cells

ABSTRACT Bacteriophages (phages) are known to effectively kill extracellular multiplying bacteria. The present study demonstrated that phages penetrated bovine mammary epithelial cells and cleared intracellular Staphylococcus aureus in a time-dependent manner. In particular, phage vB_SauM_JS25 reached the nucleus within 3 h postincubation. The phages had an endocytotic efficiency of 12%. This ability to kill intracellular host bacteria suggests the utility of phage-based therapies and may protect patients from recurrent infection and treatment failure.

scholarly journals Staphylococcus aureus Phenol-Soluble Modulins Impair Interleukin Expression in Bovine Mammary Epithelial Cells

2016 ◽  
Vol 84 (6) ◽  
pp. 1682-1692 ◽  
Author(s):  
Martine Deplanche ◽  
Ludmila Alekseeva ◽  
Ksenia Semenovskaya ◽  
Chih-Lung Fu ◽  
Frederic Dessauge ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Mammary Gland ◽  
Epithelial Cells ◽  
Mammary Epithelial Cells ◽  
Dendritic Cell Maturation ◽  
Mammary Epithelial ◽  
Content Type ◽  
Bovine Mammary Epithelial Cells ◽  
E Coli ◽  
Infected Cells

The role of the recently described interleukin-32 (IL-32) inStaphylococcus aureus-induced mastitis, an inflammation of the mammary gland, is unclear. We determined expression of IL-32, IL-6, and IL-8 inS. aureus- andEscherichia coli-infected bovine mammary gland epithelial cells. Using live bacteria, we found that inS. aureus-infected cells, induction of IL-6 and IL-8 expression was less pronounced than inE. coli-infected cells. Notably, IL-32 expression was decreased inS. aureus-infected cells, while it was increased inE. coli-infected cells. We identified the staphylococcal phenol-soluble modulin (PSM) peptides as key contributors to these effects, as IL-32, IL-6, and IL-8 expression by epithelial cells exposed topsmmutant strains was significantly increased compared to that in cells exposed to the isogenicS. aureuswild-type strain, indicating that PSMs inhibit the production of these interleukins. The use of genetically complemented strains confirmed this observation. Inasmuch as the decreased expression of IL-32, which is involved in dendritic cell maturation, impairs immune responses, our results support a PSM-dependent mechanism that allows for the development of chronicS. aureus-related mastitis.

Lactobacillus casei BL23 modulates the innate immune response in Staphylococcus aureus-stimulated bovine mammary epithelial cells

2018 ◽  
Vol 9 (6) ◽  
pp. 985-995 ◽  
Author(s):  
R.F.S. Souza ◽  
L. Rault ◽  
N. Seyffert ◽  
V. Azevedo ◽  
Y. Le Loir ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Immune Response ◽  
Mammary Gland ◽  
Epithelial Cells ◽  
Lactobacillus Casei ◽  
Mammary Epithelial Cells ◽  
Mammary Epithelial ◽  
Innate Immune ◽  
Bovine Mammary Epithelial Cells ◽  
Aureus Infection

Probiotics have been adopted to treat and prevent various diseases in humans and animals. They were notably shown to be a promising alternative to prevent mastitis in dairy cattle. This inflammation of the mammary gland is generally of infectious origin and generates extensive economic losses worldwide. In a previous study, we found that Lactobacillus casei BL23 was able to inhibit the internalisation of Staphylococcus aureus, one of the major pathogens involved in mastitis, into bovine mammary epithelial cells (bMEC). In this study, we further explored the capacity of this strain to modulate the innate immune response of bovine mammary epithelial cells during S. aureus infection. L. casei BL23 was able to decrease the expression of several pro-inflammatory cytokines, including interleukins 6, 8, 1α and 1β and tumour necrosis factor alpha, in S. aureus-stimulated bMEC, 8 h post-infection. On the other hand, L. casei did not impair the induction of defensins, such as lingual antimicrobial peptide and defensin β1 in the presence of S. aureus, and even slightly increased the induction of tracheal antimicrobial peptide during S. aureus infection. Finally, this strain did not alter the expression of the pattern recognition receptor nucleotide-binding oligomerisation domain proteins (NOD2). This study demonstrates that L. casei BL23 displayed anti-inflammatory properties on S. aureus-stimulated bMEC. These results open the way to further characterisation of the BL23 probiotic potential in a bovine mammary gland context and to a better understanding of how all these beneficial properties combine in vivo to combat mastitis pathogens.

Intracellular Staphylococcus aureus inhibits autophagy of bovine mammary epithelial cells through activating p38α

2021 ◽  
Vol 88 (3) ◽  
pp. 293-301
Author(s):  
Run Wang ◽  
Wen Zhang ◽  
Lumei Wang ◽  
Na Geng ◽  
Xiaozhou Wang ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Epithelial Cells ◽  
Mammary Epithelial Cells ◽  
Bovine Mastitis ◽  
Mammary Epithelial ◽  
Infection Model ◽  
Dependent Manner ◽  
Autophagy Flux ◽  
Bovine Mammary Epithelial Cells

AbstractStaphylococcus aureus is a common pathogen of bovine mastitis which can induce autophagy and inhibit autophagy flux, resulting in intracellular survival and persistent infection. The aim of the current study was to investigate the role of p38α in the autophagy induced by intracellular S. aureus in bovine mammary epithelial cells. An intracellular infection model of MAC-T cells was constructed, and activation of p38α was examined after S. aureus invasion. Through activating/inhibiting p38α by anisomycin/SB203580, the autophagosomes, LC3 and p62 level were analyzed by immunofluorescence and western blot. To further study the detailed mechanism of p38α, phosphorylation of ULK1ser757 was also detected. The results showed that intracellular S. aureus activated p38α, and the activation developed in a time-dependent manner. Inhibition of p38α promoted intracellular S. aureus-induced autophagy flow, up-regulated the ratio of LC3 II/I, reduced the level of p62 and inhibited the phosphorylation of ULK1ser757, whereas the above results were reversed after activation of p38α. The current study indicated that intracellular S. aureus can inhibit autophagy flow by activating p38α in bovine mammary epithelial cells.

scholarly journals Contribution of sortase SrtA2 to Lactobacillus casei BL23 inhibition of Staphylococcus aureus internalization into bovine mammary epithelial cells

PLoS ONE ◽  
2017 ◽  
Vol 12 (3) ◽  
pp. e0174060 ◽  
Author(s):  
Renata F. S. Souza ◽  
Julien Jardin ◽  
Chantal Cauty ◽  
Lucie Rault ◽  
Damien S. Bouchard ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Epithelial Cells ◽  
Lactobacillus Casei ◽  
Mammary Epithelial Cells ◽  
Mammary Epithelial ◽  
Bovine Mammary Epithelial Cells

scholarly journals Host-pathogen interactions in bovine mammary epithelial cells and HeLa cells by Staphylococcus aureus isolated from subclinical bovine mastitis

2017 ◽  
Vol 100 (8) ◽  
pp. 6414-6421 ◽  
Author(s):  
Ivana G. Castilho ◽  
Stéfani Thais Alves Dantas ◽  
Hélio Langoni ◽  
João P. Araújo ◽  
Ary Fernandes ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Epithelial Cells ◽  
Hela Cells ◽  
Mammary Epithelial Cells ◽  
Bovine Mastitis ◽  
Mammary Epithelial ◽  
Host Pathogen Interactions ◽  
Bovine Mammary Epithelial Cells ◽  
Host Pathogen

scholarly journals Plant Defensin γ-Thionin Induces MAPKs and Activates Histone Deacetylases in Bovine Mammary Epithelial Cells Infected With Staphylococcus aureus

2020 ◽  
Vol 7 ◽  
Author(s):  
Marisol Báez-Magaña ◽  
Nayeli Alva-Murillo ◽  
Ivan Medina-Estrada ◽  
María Teresa Arceo-Martínez ◽  
Joel E. López-Meza ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Epithelial Cells ◽  
Histone Deacetylases ◽  
Mammary Epithelial Cells ◽  
Mammary Epithelial ◽  
Plant Defensin ◽  
Bovine Mammary Epithelial Cells

scholarly journals Caffeic Acid Prevented LPS-Induced Injury of Primary Bovine Mammary Epithelial Cells through Inhibiting NF-κB and MAPK Activation

2019 ◽  
Vol 2019 ◽  
pp. 1-12 ◽  
Author(s):  
Mingjiang Liu ◽  
Guoqing Fang ◽  
Shaojie Yin ◽  
Xin Zhao ◽  
Chi Zhang ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Cell Viability ◽  
Signaling Pathways ◽  
Caffeic Acid ◽  
Proinflammatory Cytokines ◽  
Mammary Epithelial Cells ◽  
Mammary Epithelial ◽  
Signal Pathways ◽  
Dependent Manner ◽  
Bovine Mammary Epithelial Cells

In our previous study, lipopolysaccharide (LPS) significantly reduced the cell viability of primary bovine mammary epithelial cells (bMEC) leading to cell apoptosis, which were prevented by caffeic acid (CA) through inhibiting NF-κB activation and reducing proinflammatory cytokine expression. While the underlying mechanism remains unclear, here, we determined that LPS induced the extensive microstructural damage of bMEC, especially the mitochondria and endoplasmic reticulum. Then, the obvious reduction of mitochondrial membrane potential and expression changes of apoptosis-associated proteins (Bcl-2, Bax, and casepase-3) indicated that apoptosis signaling through the mitochondria should be responsible for the cell viability decrease. Next, the high-throughput cDNA sequencing (RNA-Seq) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis were employed to verify that the MAPK and JAK-STAT signaling pathways also were the principal targets of LPS. Following, the critical proteins (ERK, JNK, p38, and c-jun) of the MAPK signaling pathways were activated, and the release of proinflammatory cytokines (TNF-α, IL-1β, IL-6, and IL-8) regulated by NF-κB and MAPKs was significantly increased, which can promote a cascade of inflammation that induces cell injury and apoptosis. Meanwhile, CA significantly inhibited the activation of MAPKs and the release of proinflammatory cytokines in a dose-dependent manner, which were similar to its effects on the NF-κB activation that we previously published. So we concluded that CA regulates the proteins located in the upstream of multiple cell signal pathways which can reduce the LPS-induced activation of NF-κB and MAPKs, thus weakening the inflammatory response and maintaining cell structure and function, which accordingly inhibit apoptosis.

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