Micheliolide provides protection of mice against Staphylococcus aureus and MRSA infection by down-regulating inflammatory response View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2017-12

AUTHORS

Xinru Jiang, Yuli Wang, Yifei Qin, Weigang He, Adel Benlahrech, Qingwen Zhang, Xin Jiang, Zhenhui Lu, Guang Ji, Yuejuan Zheng

ABSTRACT

A major obstacle to therapy in intensive care units is sepsis caused by severe infection. In recent years gram-positive (G+) bacteria, most commonly staphylococci, are thought to be the main pathogens. Micheliolide (MCL) was demonstrated to provide a therapeutic role in rheumatoid arthritis, inflammatory intestinal disease, colitis-associated cancer, and lipopolysaccharide (LPS, the main component of G- bacterial cell wall) induced septic shock. We proved here that MCL played an anti-inflammatory role in Staphylococcus aureus (S. aureus) and methicillin-resistant S. aureus (MRSA) induced peritonitis. It inhibited the expression of inflammatory cytokines and chemokines in macrophages and dendritic cells upon stimulation with peptidoglycan (PGN, the main cell wall composition of G+ bacteria). PI3K/Akt and NF-κB pathways account for the anti-inflammatory role of MCL after PGN stimulation. MCL reduced IL-6 secretion through down-regulating NF-κB activation and improved the survival status in mice challenged with a lethal dose of S. aureus. In MRSA infection mouse model, MCL down-regulated the expression of IL-6, TNF-α, MCP-1/CCL2 and IFN-γ in sera, and ameliorated the organ damage of liver and kidney. In conclusion, MCL can help maintain immune equilibrium and decrease PGN, S. aureus and MRSA-triggered inflammatory response. These provide the rationality for the potential usage of MCL in sepsis caused by G+ bacteria (e.g., S. aureus) and antibiotic-resistant bacteria (e.g., MRSA). More... »

PAGES

41964

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/srep41964

DOI

http://dx.doi.org/10.1038/srep41964

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1083685794

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/28165033


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