| Title | Weigela florida inhibits the expression of inflammatory mediators induced by Pseudomonas aeruginosa and Staphylococcus aureus infection |
|---|---|
| Author | Hyo Bin Kim1, Soomin Cho1, Yeji Lee1, Weihui Wu2, and Un-Hwan Ha1,3* |
| Address | 1Department of Biotechnology and Bioinformatics, Korea University, Sejong 30019, Republic of Korea, 2State Key Laboratory of Medicinal Chemical Biology, Key Laboratory of Molecular Microbiology and Technology of the Ministry of Education, Department of Microbiology, Nankai University, Tianjin 300071, P. R. China, 3Interdisciplinary Graduate Program for Artificial Intelligence Smart Convergence Technology, Korea University, Sejong 30019, Republic of Korea |
| Bibliography | Journal of Microbiology, 60(6),649-656, 2022, |
| DOI | 10.1007/s12275-022-1638-6 |
| Key Words | anti-inflammation, Pseudomonas aeruginosa, Staphylococcus aureus, Weigela florida |
| Abstract | Inflammatory responses involve the action of inflammatory mediators that are necessary for the clearance of invading bacterial pathogens. However, excessive production of inflammatory mediators can damage tissues, thereby impairing bacterial clearance. Here, we examined the effects of Weigela florida on the expression of inflammatory cytokines induced by Pseudomonas aeruginosa or Staphylococcus aureus infection in macrophages. The results showed that pre-treatment with W. florida markedly downregulated the bacterial infectionmediated expression of cytokines. Additionally, post-treatment also triggered anti-inflammatory effects in cells infected with S. aureus to a greater extent than in those infected with P. aeruginosa. Bacterial infection activated inflammation-associated AKT (Thr308 and Ser473)/NF-κB and MAPK (p38, JNK, and ERK) signaling pathways, whereas W. florida treatment typically inhibited the phosphorylation of AKT/NF‐κB and p38/JNK, supporting the anti‐inflammatory effects of W. florida. The present results suggest that W. florida decreases the infection-mediated expression of inflammatory mediators by inhibiting the AKT/NF-κB and MAPK signaling pathways, implying that it may have potential use as an inhibitory agent of excessive inflammatory responses. |