An Investigation of the Innate Immune Response in Bovine Mammary Epithelial Cells Challenged by Prototheca zopfii

2016 ◽  
Vol 181 (11-12) ◽  
pp. 823-832 ◽  
Author(s):  
Zhaoju Deng ◽  
Muhammad Shahid ◽  
Limei Zhang ◽  
Jian Gao ◽  
Xiaolong Gu ◽  
...  
Keyword(s):  
Immune Response ◽  
Epithelial Cells ◽  
Innate Immune Response ◽  
Mammary Epithelial Cells ◽  
Mammary Epithelial ◽  
Innate Immune ◽  
Prototheca Zopfii ◽  
Bovine Mammary Epithelial Cells

scholarly journals Innate immune response of bovine mammary epithelial cells toMycoplasma bovis

2018 ◽  
Vol 19 (1) ◽  
pp. 79 ◽  
Author(s):  
Satoshi Gondaira ◽  
Hidetoshi Higuchi ◽  
Hidetomo Iwano ◽  
Koji Nishi ◽  
Takanori Nebu ◽  
...  
Keyword(s):  
Immune Response ◽  
Epithelial Cells ◽  
Innate Immune Response ◽  
Mammary Epithelial Cells ◽  
Mammary Epithelial ◽  
Innate Immune ◽  
Bovine Mammary Epithelial Cells

scholarly journals Effects of Sodium Octanoate on Innate Immune Response of Mammary Epithelial Cells duringStaphylococcus aureusInternalization

2013 ◽  
Vol 2013 ◽  
pp. 1-8 ◽  
Author(s):  
Nayeli Alva-Murillo ◽  
Alejandra Ochoa-Zarzosa ◽  
Joel E. López-Meza
Keyword(s):  
Immune Response ◽  
Epithelial Cells ◽  
Mrna Expression ◽  
Innate Immune Response ◽  
Mammary Epithelial Cells ◽  
Short Chain Fatty Acids ◽  
Mammary Epithelial ◽  
Innate Immune ◽  
Sodium Octanoate ◽  
Bovine Mammary Epithelial Cells

Bovine mammary epithelial cells (bMECs) are capable of initiating an innate immune response to invading bacteria. Short chain fatty acids can reduceStaphylococcus aureusinternalization into bMEC, but it has not been evaluated if octanoic acid (sodium octanoate, NaO), a medium chain fatty acid (MCFA), has similar effects. In this study we determined the effect of NaO onS. aureusinternalization into bMEC and on the modulation of innate immune elements. NaO (0.25–2 mM) did not affectS. aureusgrowth and bMEC viability, but it differentially modulated bacterial internalization into bMEC, which was induced at 0.25–0.5 mM (~60%) but inhibited at 1-2 mM (~40%). Also, bMEC showed a basal expression of all the innate immune genes evaluated, which were induced byS. aureus. NaO induced BNBD4, LAP, and BNBD10 mRNA expression, but BNBD5 and TNF-αwere inhibited. Additionally, the pretreatment of bMEC with NaO inhibited the mRNA expression induction generated by bacteria which coincides with the increase in internalization; only TAP and BNDB10 showed an increase in their expression; it coincides with the greatest effect on the reduction of bacterial internalization. In conclusion, NaO exerts a dual effect onS. aureusinternalization in bMEC and modulates elements of innate immune response.

scholarly journals Lipid-Rich Extract from Mexican Avocado Seed (Persea americana var. drymifolia) Reduces Staphylococcus aureus Internalization and Regulates Innate Immune Response in Bovine Mammary Epithelial Cells

2019 ◽  
Vol 2019 ◽  
pp. 1-10
Author(s):  
Marisol Báez-Magaña ◽  
Alejandra Ochoa-Zarzosa ◽  
Nayeli Alva-Murillo ◽  
Rafael Salgado-Garciglia ◽  
Joel Edmundo López-Meza
Keyword(s):  
Staphylococcus Aureus ◽  
Immune Response ◽  
Epithelial Cells ◽  
Innate Immune Response ◽  
Mammary Epithelial Cells ◽  
Persea Americana ◽  
Mammary Epithelial ◽  
Innate Immune ◽  
Bovine Mammary Epithelial Cells ◽  
Avocado Seed

Bovine mammary epithelial cells (bMECs) are capable of initiating an innate immune response (IIR) to invading bacteria. Staphylococcus aureus is not classically an intracellular pathogen, although it has been shown to be internalized into bMECs. S. aureus internalizes into nonprofessional phagocytes, which allows the evasion of the IIR and turns antimicrobial therapy unsuccessful. An alternative treatment to control this pathogen is the modulation of the innate immune response of the host. The Mexican avocado (Persea americana var. drymifolia) is a source of molecules with anti-inflammatory and immunomodulatory properties. Hence, we analyze the effect of a lipid-rich extract from avocado seed (LEAS) on S. aureus internalization into bMECs and their innate immunity response. The effects of LEAS (1-500 ng/ml) on the S. aureus growth and bMEC viability were assessed by turbidimetry and MTT assays, respectively. LEAS did not show neither antimicrobial nor cytotoxic effects. S. aureus internalization into bMECs was analyzed by gentamicin protection assays. Interestingly, LEAS (1-200 ng/ml) decreased bacterial internalization (60-80%) into bMECs. This effect correlated with NO production and the induction of the gene expression of IL-10, while the expression of the proinflammatory cytokine TNF-α was reduced. These effects could be related to the inhibition of MAPK p38 (∼60%) activation by LEAS. In conclusion, our results showed that LEAS inhibits the S. aureus internalization into bMECs and modulates the IIR, which indicates that avocado is a source of metabolites for control of mastitis pathogens.

Bovine mammary epithelial cells, initiators of innate immune responses to mastitis

2005 ◽  
Vol 45 (8) ◽  
pp. 757 ◽  
Author(s):  
C. Gray ◽  
Y. Strandberg ◽  
L. Donaldson ◽  
R. L. Tellam
Keyword(s):  
Immune Response ◽  
Mammary Gland ◽  
Epithelial Cells ◽  
Mammary Epithelial Cells ◽  
Vital Role ◽  
Mammary Epithelial ◽  
Innate Immune ◽  
Mammary Tissue ◽  
Effector Cells ◽  
Bovine Mammary Epithelial Cells

Innate immunity plays a vital role in the protection of the bovine mammary gland against mastitis. Until recently, the migration of effector cells such as neutrophils and monocytes into the mammary gland was thought to provide the only defence against invading pathogens. However, mammary epithelial cells may also play an important role in the immune response, contributing to the innate defence of the mammary tissue through secretion of antimicrobial peptides and attraction of circulating immune effector cells. This paper reviews the innate immune pathways in mammary epithelial cells and examines their role in the initiation of an innate immune response to Gram-positive and Gram-negative bacteria.

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.

β-Glucan modulates the lipopolysaccharide-induced innate immune response in rat mammary epithelial cells

2013 ◽  
Vol 15 (2) ◽  
pp. 457-465 ◽  
Author(s):  
Wei Zhu ◽  
Haitian Ma ◽  
Jinfeng Miao ◽  
Guoqing Huang ◽  
Mingqing Tong ◽  
...  
Keyword(s):  
Immune Response ◽  
Epithelial Cells ◽  
Innate Immune Response ◽  
Mammary Epithelial Cells ◽  
Mammary Epithelial ◽  
Innate Immune

scholarly journals Escherichia coli and Staphylococcus aureus Differentially Regulate Nrf2 Pathway in Bovine Mammary Epithelial Cells: Relation to Distinct Innate Immune Response

Cells ◽  
2021 ◽  
Vol 10 (12) ◽  
pp. 3426
Author(s):  
Yi-Tian Ying ◽  
Jing Yang ◽  
Xun Tan ◽  
Rui Liu ◽  
Ying Zhuang ◽  
...  
Keyword(s):  
Immune Response ◽  
Epithelial Cells ◽  
Inflammatory Response ◽  
Mammary Epithelial Cells ◽  
Mammary Epithelial ◽  
Innate Immune ◽  
Bovine Mammary Epithelial Cells ◽  
E Coli ◽  
Nrf2 Activation ◽  
And Staphylococcus Aureus

Escherichia coli and Staphylococcus aureus are major mastitis causing pathogens in dairy cattle but elicit distinct immune and an inflammatory response in the udder. However, the host determinants responsible for this difference remains largely unknown. Our initial studies focused on the global transcriptomic response of primary bovine mammary epithelial cells (pbMECs) to heat-killed E. coli and S. aureus. RNA-sequencing transcriptome analysis demonstrates a significant difference in expression profiles induced by E. coli compared with S. aureus. A major differential response was the activation of innate immune response by E. coli, but not by S. aureus. Interestingly, E. coli stimulation increased transcript abundance of several genes downstream of Nrf2 (nuclear factor erythroid 2-related factor 2) that were enriched in gene sets with a focus on metabolism and immune system. However, none of these genes was dysregulated by S. aureus. Western blot analysis confirms that S. aureus impairs Nrf2 activation as compared to E. coli. Using Nrf2-knockdown cells we demonstrate that Nrf2 is necessary for bpMECs to mount an effective innate defensive response. In support of this notion, nuclear Nrf2 overexpression augmented S. aureus-stimulated inflammatory response. We also show that, unlike E. coli, S. aureus disrupts the non-canonical p62/SQSTM1-Keap1 pathway responsible for Nrf2 activation through inhibiting p62/SQSTM1 phosphorylation at S349. Collectively, our findings provide important insights into the contribution of the Nrf2 pathway to the pathogen-species specific immune response in bovine mammary epithelial cells and raise a possibility that impairment of Nrf2 activation contributes to, at least in part, the weak inflammatory response in S. aureus mastitis.

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