Resveratrol inhibits Staphylococcus aureus-induced TLR2/MyD88/NF-{kappa}B-dependent VCAM-1 expression in human lung epithelial cells

Staphylococcus aureus (S. aureus) is the most commonly found Gram-positive bacterium in patients admitted in 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 signaling pathways involved in the lung diseases. Here, we reported that resveratrol reduced S. aureus-mediated vascular cell adhesion molecule-1 (VCAM-1) expression in human lung epithelial cells (HPAEpiCs) and the lungs of mice. In an in vivo study, we showed that resveratrolinhibited S. aureus-induced pulmonary hematoma and leukocytecount in BAL fluid in mice. In an in vitro study, we observed that resveratrolattenuated S. aureus-induced TLR2, MyD88, and PI3K complex formation. S. aureus stimulated Akt, JNK1/2, and p42/p44 MAPK phosphorylation, which were inhibited by resveratrol. In addition, S. aureus induced IkBa and NF-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 signalings, not only by inhibiting VCAM-1 expression but also by diminishing TLR2/MyD88/PI3K complex formation and Akt, JNK1/2, p42/p44 MAPK, p300, and NF-κB activation in HPAEpiCs.
Source: Clinical Science - Category: Biomedical Science Authors: Source Type: research