Email updates

Keep up to date with the latest news and content from BMC Cell Biology and BioMed Central.

Open Access Research article

Upregulation of Toll-like receptor (TLR) expression and release of cytokines from P815 mast cells by GM-CSF

Haiwei Yang1, Jifu Wei1, Huiyun Zhang2, Liyan Lin2, Wei Zhang1 and Shaoheng He12*

Author affiliations

1 Clinical Research Center, the First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu 210029, PR China

2 Allergy and Inflammation Research Institute, Shantou University Medical College, Shantou, PR China

For all author emails, please log on.

Citation and License

BMC Cell Biology 2009, 10:37  doi:10.1186/1471-2121-10-37

Published: 9 May 2009

Abstract

Backgroud

Recently, mast cells have been recognized to express several Toll-like receptors (TLRs) on their membrane surfaces, and granulocyte-macrophage colony-stimulating factor (GM-CSF) was reported to be able to alter expression of TLRs and cytokine production in neutrophils. However, whether GM-CSF modulates the expression of TLR and cytokine production in mast cells is not clear.

Results

Using flow cytometry and real time PCR techniques, we found that GM-CSF upregulated expression of TLR3 and TLR7 in P815 cells in a concentration dependent manner. GM-CSF also provoked approximately up to 2.4 and 2.3 fold increase in IL-13 and IL-6 release from P815 cells, respectively following 16 h incubation. GM-CSF induced IL-13 secretion, TLR3 and TLR7 expression appeared to be through activation of mitogen-activated protein kinase (MAPK) and phosphotidylinositol 3-kinase (PI3K)/Akt signaling pathways, whereas GM-CSF elicited IL-6 release seemed via Akt signaling pathway. At 10 ng/ml, GM-CSF significantly enhanced R-848-induced IL-6 release from P815 cells.

Conclusion

The ability of GM-CSF in modulation of expression of TLR3 and TLR7 in P815 mast cells and in stimulation of IL-13 and IL-6 release from P815 mast cells in vitro suggests that GM-CSF might play an important role in enhancing the innate immune responses of mast cell to viral infection