Objective:To investigate the effect of PMN migration between myeloid cells TLR4 and LSEC TLR4 in hepatic ischemia/reperfusion(I/R) injury in mice. 
Methods:TLR4 wild-type mice (C3H/HeN) and TLR4 mutant mice(C3H/HeJ) were the research subjects, bone marrow cells of the donor mice were injected into the irradiated recipient ones, and  four chimeric models were established as follows:class A, myeloid cells TLR4+/+ ［recipient (R) HeN］and  LSECTLR4+/+［donor (D) HeN］; class B,myeloid cells TLR4+/+ (R, HeN) and LSECTLR4-/- (D, HeN); class C,myeloid cellsTLR4-/- (R, HeN) and LSECTLR4+/+ (D, HeN); class D,myeloid cellsTLR4-/- (R, HeN) and LSECTLR4-/- (D, HeN). Each mouse of the four chimeric models underwent hepatic I/R injury.Finally,inflammatory protein extracted from liver tissue and PMN isolated from peripheral blood were placed into separate wells of Transwell,and PMN migration was recorded by calculating the numbers of PMN.C3a was used as a positive control and buffer as a negative control.
Results:Compared with class C(67.10±6.89), there was statistical increase of PMN migrating numbers in class A(148.95±11.04)(P＜0.05). Compared with class D(63.15±8.86), class B (142.65±8.67)had statistical increase of PMN migrating numbers(P＜0.05).While there was no significant difference between class A and class B(P＞0.05), and class C and class D had no significant difference (P＞0.05)as well.
Conclusions:Myeloid cells TLR4,not endothelial cell TLR4,play a leading role of PMN migration in hepatic I/R injury.