Abstract

Monocyte-chemotactic-protein-1 (MCP-1) plays vital roles in immune response, angiogenesis, and pregnancy outcome. We investigated plasma MCP-1 concentrations in 40 mothers and their 20 intrauterine-growth-restricted (IUGR) and 20 appropriate-for-gestational-age (AGA) fetuses and neonates on postnatal days 1 (N1) and 4 (N4). Maternal and fetal MCP-1 concentrations were decreased ( and = .018, resp.), whereas N1 MCP-1 concentrations were elevated in IUGR group ( = .012). In both groups, fetal MCP-1 concentrations were lower compared to N1 and N4 ones ( = .045, = .012, resp., for AGA, .001 in each case for IUGR). Reduced maternal and fetal MCP-1 concentrations in IUGR may reflect failure of trophoblast invasion, suggesting that down-regulation of MCP-1 may be involved in the pathogenesis of IUGR. Increased MCP-1 concentrations in IUGR neonates and higher postnatal ones in all infants may be attributed to gradual initiation of ex utero angiogenesis, which is possibly enhanced in IUGR.

Highlights

  • Evidence is accumulating that maintenance of a normal pregnancy is dependent on a delicate interaction between the endocrine and immune systems [1]

  • Maternal and fetal Monocyte chemotactic protein (MCP)-1 concentrations were significantly decreased in the intrauterine growth restriction (IUGR) compared to the AGA group after adjusting for multiple comparisons (b: 167.018, 95% CI: 114.511–219.525, P < .001 and b: 216.322, 95% CI: 40.423– 392.221, P = .018, resp.)

  • N1 MCP-1 concentrations were significantly elevated in the IUGR compared to the AGA group after adjusting for multiple comparisons ((b: −467.934, 95% CI: −824.383−(−111.484), P = .012)

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Summary

Introduction

Evidence is accumulating that maintenance of a normal pregnancy is dependent on a delicate interaction between the endocrine and immune systems [1] Disturbance of this balance can result in a wide range of abnormalities including intrauterine growth restriction (IUGR) [2]. Chemokines, a subset of cytokines, specific in their ability to attract and activate immune cells, are thought to play pivotal roles in the immune recognition, maintenance of pregnancy, and parturition [4]. In this respect, unbalanced chemokine expression may contribute to defective placentation and pregnancy failures [3]. The perinatal expression of MCP-1 has not been, up to the present, investigated in IUGR pregnancies

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