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

作者：Yang, Haiwei; Wei, Jifu; Zhang, Huiyun; Lin, Liyan; Zhang, Wei; He, Shaoheng^*

来源：BMC Cell Biology, 2009, 10(1): 37.

DOI：10.1186/1471-2121-10-37

• COLONY-STIMULATING FACTOR
• PROINFLAMMATORY CYTOKINES
• NEUTROPHIL ACTIVATION
• INNATE IMMUNITY
• ASTHMA
• RESPONSES
• IGE
• TOLL-LIKE-RECEPTOR-4
• LEUKOCYTES
• IL-13

Backgroud: Recently, mast cells have been recognized to express several Toll-like receptors (TLRs) on their membrane surfaces, and granulocyte-macrophage colony-stimulating factor (GMCSF) 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 GMCSF might play an important role in enhancing the innate immune responses of mast cell to viral infection

• 出版日期2009-5-9
• 单位汕头大学; 南京医科大学