title: Cryptoporus volvatus polysaccharides attenuate LPS-induced expression of pro-inflammatory factors via the TLR2 signaling pathway in human alveolar epithelial cells.
abstract: BACKGROUND
  Cryptoporus volvatus (Peck) Hubb grows wild in China, and its fruiting bodies have been used traditionally to treat asthma and bronchitis.
  
  
  OBJECTIVE
  This study evaluates the anti-inflammatory effect of Cryptoporus polysaccharides (CP) extracted from fruiting bodies of C. volvatus on lipopolysaccharide (LPS)-induced pro-inflammatory factors and the signaling pathways involved in human alveolar epithelial cells.
  
  
  METHODS
  To evaluate the effects of CP on LPS-induced pro-inflammatory factors, A549 cells were pre-incubated with CP 1, 10, and 100 μg/ml for 1 h and then stimulated with LPS 10 μg/ml for 24 h. The expression of pro-inflammatory factors monocyte chemoattractant protein-1 (MCP-1), tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), Toll-like receptor 2 (TLR2), and phosphorylation of ERK1/2, p38, and NF-κB p65 were measured by q-PCR, ELISA, and western blotting.
  
  
  RESULTS
  CP decreased LPS-induced mRNA expression of MCP-1, TNF-α, and IL-1β (IC50 = 83.3, 85.2, and 91.6 μg/ml, respectively) and their correspondent protein expression (IC50 = 88.6, 76.4, and 81.6 μg/ml, respectively). Investigation of potential mechanisms indicated that CP 100 μg/ml reduced LPS-induced expression of TLR2 mRNA (66.9%, p < 0.01) and protein (63.2%, p < 0.01) that was a result of the decreased pro-inflammatory factors. LPS induction increased the expression of TLR2 and the phosphorylation of p38 and ERK1/2, NF-kB p65 concomitantly. CP 100 μg/ml inhibited the LPS-induced phosphorylation of the signaling proteins (p < 0.05).
  
  
  CONCLUSIONS
  This suggests that CP pretreatment down-regulates LPS-mediated inflammation in lung epithelial cells. This study further confirmed that CP is a potential anti-inflammatory drug for the treatment of airway inflammatory diseases.
authors.affiliation: a Affiliated Sir Run Run Shaw Hospital, Zhejiang University School of Medicine , Hangzhou , China .
authors.forename: Jian-Ping
authors.initials: JP
authors.lastname: Zhu
authors.affiliation: b Zhejiang Respiratory Drugs Research Laboratory of State Food and Drug Administration of China, Zhejiang University School of Medicine , Hangzhou , China , and.|c Animal Laboratoy Center of Zhejiang , Hangzhou , China.
authors.forename: Kai
authors.initials: K
authors.lastname: Wu
authors.affiliation: b Zhejiang Respiratory Drugs Research Laboratory of State Food and Drug Administration of China, Zhejiang University School of Medicine , Hangzhou , China , and.
authors.forename: Jin-You
authors.initials: JY
authors.lastname: Li
authors.affiliation: a Affiliated Sir Run Run Shaw Hospital, Zhejiang University School of Medicine , Hangzhou , China .|b Zhejiang Respiratory Drugs Research Laboratory of State Food and Drug Administration of China, Zhejiang University School of Medicine , Hangzhou , China , and.
authors.forename: Yan
authors.initials: Y
authors.lastname: Guan
authors.affiliation: b Zhejiang Respiratory Drugs Research Laboratory of State Food and Drug Administration of China, Zhejiang University School of Medicine , Hangzhou , China , and.
authors.forename: Yan-Hong
authors.initials: YH
authors.lastname: Sun
authors.affiliation: b Zhejiang Respiratory Drugs Research Laboratory of State Food and Drug Administration of China, Zhejiang University School of Medicine , Hangzhou , China , and.
authors.forename: Wen-Jiang
authors.initials: WJ
authors.lastname: Ma
authors.affiliation: b Zhejiang Respiratory Drugs Research Laboratory of State Food and Drug Administration of China, Zhejiang University School of Medicine , Hangzhou , China , and.|c Animal Laboratoy Center of Zhejiang , Hangzhou , China.
authors.forename: Qiang-Min
authors.initials: QM
authors.lastname: Xie
mesh_terms: D000893:Anti-Inflammatory Agents / Q000302:isolation & purification / Q000494:pharmacology*; D015153:Blotting, Western; D018929:Cell Culture Techniques; D002460:Cell Line; D002470:Cell Survival / Q000187:drug effects; D055453:Coriolaceae / Q000737:chemistry*; D016207:Cytokines / Q000235:genetics* / Q000276:immunology; D004305:Dose-Response Relationship, Drug; D004847:Epithelial Cells / Q000187:drug effects* / Q000276:immunology; D062610:Fungal Polysaccharides / Q000302:isolation & purification / Q000494:pharmacology*; D006801:Humans; D008070:Lipopolysaccharides / Q000494:pharmacology; D011650:Pulmonary Alveoli / Q000166:cytology / Q000187:drug effects* / Q000276:immunology; D015398:Signal Transduction; D013997:Time Factors; D051195:Toll-Like Receptor 2 / Q000378:metabolism*
chemical_list: D000893:Anti-Inflammatory Agents; D016207:Cytokines; D062610:Fungal Polysaccharides; D008070:Lipopolysaccharides; C495342:TLR2 protein, human; D051195:Toll-Like Receptor 2
keywords: Anti-inflammatory drug; asthma; bronchitis; interleukin-1β; monocyte chemoattractant protein-1; tumor necrosis factor-α