Defensin γ-thionin from Capsicum chinense has immunomodulatory effects on bovine mammary epithelial cells during Staphylococcus aureus internalization

Díaz-Murillo, Violeta; Medina-Estrada, Ivan; López‐Meza, Joel E.; Ochoa‐Zarzosa, Alejandra

doi:10.1016/j.peptides.2016.02.008

Cited by 22 publications

(28 citation statements)

References 41 publications

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“…To determine the number of S. aureus invading BMEC under different conditions, we followed a previously described method (Díaz-Murillo et al, 2016). The BMEC grown in 24-well plates were infected using DMEM/F12 medium containing S. aureus (1 × 10 5 cfu/well) at a multiplicity of infection of 1, and treated with 0 (control group), 10, 20, or 30 μg/mL CGA (n = 3) at 37°C, 5% CO 2 for 3 h. Cells were then washed 5 times with sterile PBS.…”

Section: S Aureus Invasion Assaymentioning

confidence: 99%

The protective effect of chlorogenic acid on bovine mammary epithelial cells and neutrophil function

Gong

Zhan

et al. 2018

Journal of Dairy Science

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Chlorogenic acid (CGA) is the ester of caffeic acid and quinic acid and plays an important role in antibacterial activity and anti-inflammatory properties. The objective of this study was to examine the effects of CGA on the growth of Staphylococcus aureus and the mRNA levels of the genes encoding the inflammatory response cytokines, κ-casein, and neutrophil function in bovine mammary epithelial cells (BMEC) exposed to S. aureus. Chlorogenic acid has important antibacterial, antioxidant, and anti-inflammatory functions; however, the effect of CGA on BMEC and neutrophils exposed to S. aureus has not been investigated previously. Our results demonstrated that 10, 20, and 30 μg/mL CGA had no cytotoxic effects on BMEC in culture, and that 20 μg/mL CGA enhanced the viability of BMEC exposed to S. aureus, whereas 30 μg/mL CGA reduced S. aureus growth after 9 h compared with controls. The rate of S. aureus invasion into BMEC was also attenuated by 30 μg/mL CGA compared with controls, whereas this treatment led to reduced abundance of IL6, IL8, and TLR2 mRNA in S. aureus-exposed BMEC. Migration of bovine polymorphonuclear leukocytes was significantly decreased in S. aureus-exposed BMEC with 10 and 20 μg/mL CGA treatment when compared with S. aureus treatment alone. In addition, incubation with 20 or 30 μg/mL CGA enhanced the phagocytic ability of polymorphonuclear leukocytes compared with the control group. Importantly, levels of κ-casein were enhanced by treatment of S. aureus-exposed BMEC with CGA. Our results suggest that the use of CGA may be a potent therapeutic tool against bovine mastitis caused by S. aureus.

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Section: S Aureus Invasion Assaymentioning

confidence: 99%

The protective effect of chlorogenic acid on bovine mammary epithelial cells and neutrophil function

Gong

Zhan

et al. 2018

Journal of Dairy Science

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“…Staphylococcus aureus ( S. aureus ) in the udder of dairy cows causes harmful clinical symptoms and is associated with poor cure rates (7). The insufficient recognition of the infecting S. aureus in the mammary compartment is believed to hinder the host in raising an adequate innate immune response and the pathogen may, therefore, persist in the tissue (8, 9). In addition, these Gram-positive bacteria may infiltrate the mammary epithelial cell (MEC) layers and induce complicating factors such as biofilms formation (10, 11).…”

Section: Introductionmentioning

confidence: 99%

Preconditioning with Lipopolysaccharide or Lipoteichoic Acid Protects against Staphylococcus aureus Mammary Infection in Mice

et al. 2017

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Staphylococcus aureus is one of the most causative agents of mastitis and is associated with chronic udder infections. The persistency of the pathogen is believed to be the result of an insufficient triggering of local inflammatory signaling. In this study, the preclinical mastitis model was used, aiming to evaluate if lipopolysaccharide (LPS) or lipoteichoic acid (LTA) preconditioning could aid the host in more effectively clearing or at least limiting a subsequent S. aureus infection. A prototypic Gram-negative virulence factor, i.e., LPS and Gram-positive virulence factor, i.e., LTA were screened whether they were able to boost the local immune compartment. Compared to S. aureus-induced inflammation, both toxins had a remarkable high potency to efficiently induce two novel selected innate immunity biomarkers i.e., lipocalin 2 (LCN2) and chitinase 3-like 1 (CHI3L1). When combining mammary inoculation of LPS or LTA prior to a local S. aureus infection, we were able to modulate the innate immune response, reduce local bacterial loads, and induce either LCN2 or CHI3L1 at 24 h post-infection. Clodronate depletion of mammary macrophages also identified that macrophages contribute only to a limited extend to the LPS/LTA-induced immunomodulation upon S. aureus infection. Based on histological neutrophil influx evaluation, concomitant local cytokine profiles and LCN2/CHI3L1 patterns, the macrophage-independent signaling plays a major role in the LPS- or LTA-pretreated S. aureus-infected mouse mammary gland. Our results highlight the importance of a vigilant microenvironment during the innate immune response of the mammary gland and offer novel insights for new approaches concerning effective immunomodulation against a local bacterial infection.

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“…Antimicrobial peptides (AMPs) are a diverse group of molecules with a broad range of activities, including cytotoxic, antifungal, antibacterial, or immunomodulatory effects. In mammals, these molecules are produced by different types of cells, highlighting those that are in intimate contact with pathogens such as epithelial cells [ 54 ]. In different models of infection, E2 exerts antibacterial activity against many pathogens because it favors the expression and secretion of AMPs.…”

Section: Functions Of E2 In Epithelial Cellsmentioning

confidence: 99%

Immunomodulatory Effects of 17β-Estradiol on Epithelial Cells during Bacterial Infections

Medina-Estrada

Alva-Murillo

López‐Meza

et al. 2018

Journal of Immunology Research

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The innate immune system can function under hormonal control. 17β-Estradiol (E2) is an important sexual hormone for the reproductive cycle of mammals, and it has immunomodulatory effects on epithelial cells, which are the first line of defense against incoming bacteria. E2 regulates various pathophysiological processes, including the response to infection in epithelial cells, and its effects involve the regulation of innate immune signaling pathways, which are mediated through estrogen receptors (ERs). E2 modulates the expression of inflammatory and antimicrobial elements such as cytokines and antimicrobial peptides. The E2 effects on epithelial cells during bacterial infections are characterized by an increase in the production of antimicrobial peptides and by the diminution of the inflammatory response to abrogate proinflammatory cytokine induction by bacteria. Here, we review several novel molecular mechanisms through which E2 regulates the innate immune response of epithelial cells against bacterial infections.

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Defensin γ-thionin from Capsicum chinense has immunomodulatory effects on bovine mammary epithelial cells during Staphylococcus aureus internalization

Cited by 22 publications

References 41 publications

The protective effect of chlorogenic acid on bovine mammary epithelial cells and neutrophil function

The protective effect of chlorogenic acid on bovine mammary epithelial cells and neutrophil function

Preconditioning with Lipopolysaccharide or Lipoteichoic Acid Protects against Staphylococcus aureus Mammary Infection in Mice

Immunomodulatory Effects of 17β-Estradiol on Epithelial Cells during Bacterial Infections

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