Abstract
Idiopathic pulmonary fibrosis is a destructive inflammatory disease with unknown etiology and limited therapeutic options. Inflammation and damage due to deregulated cytokine expression are definitely involved. 17(R)-ResolvinD1(RvD1) has potent anti-inflammatory pro-resolving activity. Recently, the specific receptors that bind RvD1 were identified on human macrophages. Monocyte chemotactic and activating factor (MCP-1) is one of the key chemokine by regulating migration of inflammatory cells. It is produced by macrophages and plays an integral role in the development of some pulmonary diseases. We examined the effect of 17(R)-RvD1 by assessment of MCP-1 and any other cytokines mRNA. We used 8-10-weeks old female C57BL/6J mice and administerd BLM subcutaneouly via micro-osmotic pump. 17(R)-RvD1 was injected intraperitoneally for 5 days consecutively from day1. We measured cell differentiation and total number in bronchoaveloar fluid(BALF) and sacrificed mice at day7, 14 and 28. At day 7, MCP-1 mRNA was significantly lower in BLM/RvD1 group than BLM/Vehicle(veh) group. However, macrophages in BALF in BLM/RvD1 group resulted in no statistical difference compared with BLM/veh group. At day 14, the level of TGF- b1 mRNA after 17(R)-RvD1 treatment were decreased. The significant decreases of macrophages were observed in BALF from BLM/RvD1 group vs. from BLM/veh group. At day 28, the histology of the lung sections in the BLM/RvD1 group exhibited less collagen deposition. These results suggest that 17(R)-RvD1 ameliorates pulmonary fibrosis partly through the reduction of MCP-1 production during onset of the acute inflammatory phase leading to attenuate infiltration of inflammatory cells.
- Copyright ©ERS 2015
