Cryptoporus volvatus polysaccharides attenuate LPS-induced expression of pro-inflammatory factors via the TLR2 signaling pathway in human alveolar epithelial cells

Pharm Biol. 2016;54(2):347-53. doi: 10.3109/13880209.2015.1042981. Epub 2015 May 12.

Abstract

Context: Cryptoporus volvatus (Peck) Hubb grows wild in China, and its fruiting bodies have been used traditionally to treat asthma and bronchitis.

Objectives: 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.

Materials and 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.

Keywords: Anti-inflammatory drug; asthma; bronchitis; interleukin-1β; monocyte chemoattractant protein-1; tumor necrosis factor-α.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Anti-Inflammatory Agents / isolation & purification
  • Anti-Inflammatory Agents / pharmacology*
  • Blotting, Western
  • Cell Culture Techniques
  • Cell Line
  • Cell Survival / drug effects
  • Coriolaceae / chemistry*
  • Cytokines / genetics*
  • Cytokines / immunology
  • Dose-Response Relationship, Drug
  • Epithelial Cells / drug effects*
  • Epithelial Cells / immunology
  • Fungal Polysaccharides / isolation & purification
  • Fungal Polysaccharides / pharmacology*
  • Humans
  • Lipopolysaccharides / pharmacology
  • Pulmonary Alveoli / cytology
  • Pulmonary Alveoli / drug effects*
  • Pulmonary Alveoli / immunology
  • Signal Transduction
  • Time Factors
  • Toll-Like Receptor 2 / metabolism*

Substances

  • Anti-Inflammatory Agents
  • Cytokines
  • Fungal Polysaccharides
  • Lipopolysaccharides
  • TLR2 protein, human
  • Toll-Like Receptor 2