Brazilin plays an anti-inflammatory role with regulating Toll-like receptor 2 and TLR 2 downstream pathways in Staphylococcus aureus-induced mastitis in mice

Gao, Xuejiao; Wang, Tiancheng; Zhang, Zecai; Cao, Yongguo; Zhang, Naisheng; Guo, Mengyao

doi:10.1016/j.intimp.2015.04.043

Cited by 36 publications

(20 citation statements)

References 43 publications

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“…In a mouse model of S. aureus-induced mastitis, mice treated with the natural compound brazilin, present in Caesalpinia sappan heartwood, exhibited a decrease in levels of the S. aureus-induced inflammatory cytokines IL-1β, IL-6 and TNF-α, leading to a decrease in inflammatory-mediated tissue injury. In addition, an inhibition of the S. aureus-induced phosphorylation of p38, JNK and ERK in the brazilin-treated mice was observed (37). Similar regulatory mechanisms of NF-κB and MAPK signaling pathways were observed in S. aureus-infected RAW 264.7-derived macrophages treated with selenium derivatives.…”

Section: Discussionsupporting

confidence: 64%

Sulforaphane reduces intracellular survival of Staphylococcus aureus in macrophages through inhibition of JNK and p38 MAPK‑induced inflammation

Deramaudt¹,

Ali²,

Vinit³

et al. 2020

Int J Mol Med

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Macrophages are active contributors to the innate immune defense system. As macrophage activation is clearly affected by the surrounding microenvironment, the present study investigated the effect of sulforaphane (SFN) on the bactericidal activity of macrophages and the underlying molecular mechanisms involved in this process. Human THP-1-derived macrophages, primary human peripheral blood mononuclear cell-derived macrophages, and primary mouse bone marrow derived-macrophages (BMdMs) pretreated with SFN or dMSO were utilized in a model of Staphylococcus aureus infection. The results suggested that SFN pretreatment of macrophages effectively repressed the intracellular survival of S. aureus through modulation of p38/JNK signaling and decreased S. aureus-induced caspases-3/7-dependent cell apoptosis, potentially through downregulation of microRNA (miR)-142-5p and miR-146a-5p. As SFN is a well-known activator of nuclear factor erythroid 2-related factor 2 (Nrf2), Nrf2 -/-BMdMs were used to demonstrate that the SFN-mediated inhibitory effect was independent of Nrf2. Nevertheless, an increase in intracellular bacterial survival in Nrf2-deficient macrophages was observed. In addition, SFN pretreatment suppressed S. aureus-induced transcriptional expression of genes coding for the proinflammatory cytokines interleukin (IL)-1β, IL-6, and tumor necrosis factor-α (TNF-α), as well as for the M1 markers c-c motif chemokine receptor 7, IL-23 and inducible nitric oxide synthase (iNOS). Western blot analysis indicated that S. aureus challenge activated p38 mitogen-activated protein kinase (MAPK) (p38) and c-Jun N-terminal kinase (JNK) MAPK signaling pathways, while SFN pretreatment prevented p38 and JNK phosphorylation. Pretreatment with 2 specific inhibitors of p38 and JNK, SB203580 and SP600125, respectively, resulted in a decrease in S. aureus-induced proinflammatory gene expression levels compared with those observed in the SFN-pretreated macrophages. Furthermore, THP-1-derived macrophages pretreated with SB203580 or SP600125 prior to bacterial infection exhibited a significant inhibition in intracellular S. aureus survival.In conclusion, we hypothesize that concomitant targeting of the p38/JNK-inflammatory response and the S. aureus-induced apoptosis with SFN may be a promising therapeutic approach in S. aureus infection.

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Section: Discussionsupporting

confidence: 64%

Sulforaphane reduces intracellular survival of Staphylococcus aureus in macrophages through inhibition of JNK and p38 MAPK‑induced inflammation

Deramaudt¹,

Ali²,

Vinit³

et al. 2020

Int J Mol Med

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“…Host cells infected with pathogens produce a cascade of pro-inflammatory cytokines, including IL-1β, IL-6, and TNF-α (Gao et al, 2015), which are key in promoting and regulating the immune response against bacterial pathogens (Lapointe et al, 2010). Interleukin-1β and TNF-α are defined as early proinflammatory cytokines (Dinarello, 2000), whereas IL-6 is a third master proinflammatory cytokine and a vital mediator of the acute-phase response in inflammation (Heinrich et al, 2003).…”

Section: Discussionmentioning

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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“…Puerarin, a natural ingredient of R. puerariae , has been shown to inhibit LPS‐induced inflammation in the RAW264.7 macrophagocyte (Hu et al , ). Dexamethazone is a common antiinflammatory drug and often used as a standard to evaluate the antiinflammatory effect of the experimental drug (Gao et al , ). Our results demonstrated that puerarin alleviated the S. aureus ‐induced histopathological changes as effectively as dexamethazone in the mammary gland.…”

Section: Discussionmentioning

confidence: 99%

Puerarin Exerts an Antiinflammatory Effect by Inhibiting NF-kB and MAPK Activation inStaphylococcus aureus-Induced Mastitis

Zhao

Jiang

et al. 2016

Phytother. Res.

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Mastitis is defined as the inflammation of the mammary gland. There is generally no effective treatment for mastitis in animals. Puerarin, extracted from Radix puerariae, has been proven to possess many biological activities. The present study aims to reveal the potential mechanism that is responsible for the antiinflammatory action of puerarin in Staphylococcus aureus (S. aureus)-induced mastitis in mice. Histopathological changes showed that puerarin ameliorated the inflammatory injury induced by S. aureus. Quantitative real-time polymerase chain reaction and ELISA analysis indicated that puerarin not only suppressed the production of pro-inflammatory cytokines such as TNF-α, IL-1β, and IL-6 but also promoted the secretion of IL-10. Toll-like receptor 2 (TLR2) is important in the immune defense against S. aureus infection. Research in molecular biology has shown that the expression of TLR2 was inhibited with administration of puerarin. Further studies were performed on NF-kB and mitogen-activated protein kinase signaling pathways using western blot. The results demonstrated that puerarin suppressed phosphorylated IkBα, p65, p38, extracellular signal-regulated kinase 1and 2 (ERK), and c-Jun N-terminal kinase (JNK) in a dose-dependent manner. All of the results suggested that puerarin may be a potential therapy for treating mastitis. Copyright © 2016 John Wiley & Sons, Ltd.

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Brazilin plays an anti-inflammatory role with regulating Toll-like receptor 2 and TLR 2 downstream pathways in Staphylococcus aureus-induced mastitis in mice

Cited by 36 publications

References 43 publications

Sulforaphane reduces intracellular survival of Staphylococcus aureus in macrophages through inhibition of JNK and p38 MAPK‑induced inflammation

Sulforaphane reduces intracellular survival of Staphylococcus aureus in macrophages through inhibition of JNK and p38 MAPK‑induced inflammation

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

Puerarin Exerts an Antiinflammatory Effect by Inhibiting NF-kB and MAPK Activation inStaphylococcus aureus-Induced Mastitis

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