Resveratrol inhibitsStaphylococcus aureus-induced TLR2/MyD88/NF-κB-dependent VCAM-1 expression in human lung epithelial cells

Abstract

Staphylococcus aureus is the most commonly found Gram-positive bacterium in patients admitted to intensive-care units, causing septicaemia or pneumonia. S. aureus is considered to play an important role in the induction of cell adhesion molecules. Resveratrol, a compound found in the skins of red fruits, may inhibit the inflammatory signalling pathways involved in lung diseases. In the present paper, we have shown that resveratrol reduced S. aureus-mediated VCAM-1 (vascular cell adhesion molecule-1) expression in HPAEpiCs (human lung epithelial cells) and lungs of mice. In an in vivo study, we have shown that resveratrol inhibited S. aureus-induced pulmonary haematoma and leucocyte count in BAL (bronchoalveolar lavage) fluid in mice. In an in vitro study, we observed that resveratrol attenuated S. aureus-induced TLR2 (Toll-like receptor 2), MyD88 (myeloid differentiation factor 88) and PI3K (phosphoinositide 3-kinase) complex formation. S. aureus stimulated Akt, JNK1/2 (c-Jun N-terminal kinase 1/2) and p42/p44 MAPK (mitogen-activated protein kinase) phosphorylation, which were inhibited by resveratrol. In addition, S. aureus induced IκB (inhibitor of nuclear factor κB) α and NF-κB (nuclear factor κB) p65 phosphorylation and NF-κB p65 translocation, which were reduced by resveratrol. Finally, we found that S. aureus induced NF-κB and p300 complex formation and p300 phosphorylation, which were inhibited by resveratrol. Thus resveratrol functions as a suppressor of S. aureus-induced inflammatory signalling not only by inhibiting VCAM-1 expression, but also by reducing TLR2-MyD88-PI3K complex formation and Akt, JNK1/2, p42/p44 MAPK, p300 and NF-κB activation in HPAEpiCs.

Endothelial NOD1 directs myeloid cell recruitment in atherosclerosis through VCAM‐1

“…Endothelial cell injury during atherogenesis triggers leukocyte infiltration through up-regulation of ECAMs (31). In this regard, VCAM-1 expression has been shown to be stimulated in response to bacterial components in human ECs through the TLR2/4 signaling pathway (32)(33)(34), as well as through NOD1/2 in periodontal fibroblasts (35). In agreement with these observations, our findings provide evidence for endothelial NOD1 in directing the expression of VCAM-1 in the inflamed vessel wall.…”

Surfactin from Bacillus subtilis induces apoptosis in human oral squamous cell carcinoma through ROS-regulated mitochondrial pathway

“…SCC4 and SCC25 cells were grown to confluence in 6-well plates and then treated with surfactin for the indicated time intervals. The cells were washed, scraped, collected, and centrifuged at 45000 × g at 4°C for 1 h to yield the whole cell extract, as previously described 18 . Samples were denatured, subjected to SDS-PAGE using a 12% running gel, and transferred to nitrocellulose membrane.…”

Extracts of Artocarpus communis Induce Mitochondria-Associated Apoptosis via Pro-oxidative Activity in Human Glioblastoma Cells

“…The cells were then collected and placed in ice-cold lysis buffer containing 25 mM Tris-HCl (pH 7.4), 25 mM NaCl, 25 mMNaF, 25 mM sodium pyrophosphate, 1 mM sodium vanadate, 2.5 mM EDTA, 0.05% (w/v) Triton X-100, 0.5% (w/v) sodium dodecyl sulfate (SDS), 0.5% (w/v) deoxycholate, 0.5% (w/v) NP-40, 5 μ g/ml leupeptin, 5 μ g/ml aprotinin, and 1 mM phenylmethylsulfonyl fluoride (PMF). Lysates were centrifuged at 45,000 × g for 1 h at 4°C and whole cell extracts were obtained according to methods described in previous studies ( Lee et al, 2014 ). Samples were denatured, subjected to SDS-PAGE on a 12% running gel, and transferred to a nitrocellulose membrane.…”