Abstract: Objective　To explore the effect of in utero exposure to inflammation on innate immune response in preterm infants. Methods Forty-seven premature infants with gestational age < 35 weeks were recruited in this study. According to histological evidence of placental infection, all neonates were divided into intrauterine inflammation positive group and negative group. Mononuclear cells and monocytes were isolated from umbilical cord blood, and were cultured in vitro in the presence or absence of LPS (100 ng/ml). The levels of interleukin 1β (IL-1β), interleukin 6 (IL-6), tumor necrosis factor alpha (TNF-α) and interleukin 10 (IL-10) in cord blood plasma and monocyte cultural supernatants were measured by ELISA respectively. The level of IL-1β, TNF-α, IL-6 and IL-10 mRNA were detected by Real-time PCR. Expression of HLA-DR on surface of CD14+ monocytes and ratio of CD3+CD4+ / CD3+CD8+ T was analyzed by flow cytometry. Results (1) The level of cord plasma IL-6 in intrauterine inflammation positive group was significantly higher than in negative group. (p=0.02). (2) After stimulation of LPS, levels of IL-1β, IL-6, TNF-α, IL-10 in supernatants were increased significantly, in consistence with their mRNA expression (p<0.05) in both groups. (3) Expression of HLA-DR on surface of monocytes was significantly decreased after stimulation with LPS in intrauterine inflammation positive group (p=0.012), but was significantly increased in negative group (p=0.0305). Conclusions In utero exposure to inflammation does not suppress the response of monocytes to LPS in preterm neonates, but impairs the antigen presenting function in monocytes.