Analysis of CD86 and CD69 expression on blood lymphocytes in inflammation-induced premature mice

Abstract

Objective To investigate the role of Toll-like receptor 4 ( TLR4) in lipopolysaccharide ( LPS)-induced preterm delivery by analyzing the CD86 and CD69 expression in lymphocyte subgroups of mice. Methods LPS was administered intraperitoneally to establish a mouse model of preterm delivery,with or without TLR4 blockade. The incidences of preterm delivery and fetal death were calculated in each group ( LPS group,TLR4 blockade group,and control group). The percentages of blood CD45 + CD86 + ,CD3 + CD69 + ,CD19 + CD69 + and CD49b + CD69 + subsets were measured by flow cytometry. Results The incidences of preterm delivery and fetal death in LPS group were significantly higher than those in the control group ( 50. 0% [8/16]vs 0[0/16]; 11. 0%[9/82]vs 3. 1% [5/163],P 0. 01 or 0. 05). The incidences of preterm delivery( 6. 3%[1/16]) and fetal death ( 3. 9%[6/154]) in the TLR4 blockade group were significantly lower than those in the LPS group ( P 0. 01 or 0. 05). TLR4 blockade almost completely abrogated LPS -induced increase of CD45 + CD86 + ,CD3 + CD69 + and CD49b + CD69 + cell proportions ( P 0. 01). Conclusion Interaction between LPS and its receptor TLR4 triggers the mobilization of CD86 + dendritic cells,which subsequently activates blood T cells and NK cells and plays an important role in preterm delivery.