کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
2541818 | 1122676 | 2006 | 8 صفحه PDF | دانلود رایگان |

The activation of phospholipases is one of the earliest key events in receptor-mediated cellular responses to a number of extracellular signaling molecules. Lipopolysaccharide (LPS) is a principle component of the outer membrane of Gram-negative bacteria and a prime target for recognition by the innate immune system. In the present study, we evaluated the role of specific phospholipase in the activation of a chicken macrophage cell line HD11 by LPS. Activation of HD11 cells by LPS results in induction of nitric oxide (NO). Using selective inhibitors, we have identified that phosphatidylinositol (PI)-phospholipase C (PI-PLC), but not phosphatidylcholine (PC)-phospholipase C (PC-PLC) nor PC-phospholipase D (PC-PLD), was required for LPS-induced NO production. Preincubation with PI-PLC selective inhibitors (U-73122 and ET-18-OCH3) abrogated LPS-induced NO production in HD11 cells, whereas PC-PLC inhibitor (D609), phosphatide phosphohydrolase inhibitor (propranolol), and PC-PLD inhibitor (n-butanol) had no inhibitory effects. We also showed that inhibition of protein kinase C (PKC) by selective inhibitors Ro 31-8220 and calphostin C and chelating intracellular Ca2+ by BAPTA-AM significantly reduced NO production in LPS-stimulated HD11 cells. Our results demonstrate that PI-PLC plays a critical role, most likely through activation of PKC pathway, in TLR4 mediated immune responses of avian macrophage cells to LPS.
Journal: International Immunopharmacology - Volume 6, Issue 12, 5 December 2006, Pages 1780–1787