Macrophage inflammatory protein-1α in amniotic and cervical fluids in spontaneous preterm labor with intact membranes with respect to intra-amniotic inflammation.

OBJECTIVE

Macrophage inflammatory protein 1α is a chemokine produced by various immune, epithelial, mesothelial, and fibroblast cells after exposure to bacterial lipopolysaccharide or pro-inflammatory molecules. The primary aim of this study was to determine MIP-1α concentrations in amniotic and cervical fluids from pregnancy with spontaneous preterm labor with intact membranes (PTL) with respect to the presence of intra-amniotic infection (both microbial invasion of the amniotic cavity and intra-amniotic inflammation) and sterile intra-amniotic inflammation (intra-amniotic inflammation alone). The secondary aim was to assess the diagnostic indices of MIP-1α in predicting intra-amniotic infection.

MATERIALS AND

METHODS

Seventy-four women with PTL were included in this study. Paired amniotic and cervical fluid samples were obtained using transabdominal amniocentesis and a Dacron polyester swab, respectively. Microbial invasion of the amniotic cavity was diagnosed based on a combination of culture and molecular biology methods. The concentration of IL-6 in the amniotic and cervical fluids was measured using an automated electrochemiluminescence immunoassay method. Intra-amniotic inflammation was defined as an amniotic fluid IL-6 concentration of ≥3000 pg/mL. The MIP-1α concentrations in the samples were assessed using an enzyme-linked immunosorbent assay.

RESULTS

A difference in amniotic fluid MIP-1α was observed among women with intra-amniotic infection, sterile intra-amniotic inflammation, and negative amniotic fluid (infection: median 1779.0 pg/mL; sterile, median 102.7 pg/mL; negative, median 19.9 pg/mL; p < .0001). No difference in the concentrations of MIP-1α was identified in cervical fluid after adjustment for gestational age at sampling (infection: median 77.7 pg/mL, sterile: median 152.7 pg/mL, negative: median 18.0 pg/mL; p = .30). The presence of intra-amniotic infection was associated with elevated MIP-1α concentrations in amniotic fluid (presence: 1779.0 pg/mL vs. absence: 26.3 pg/mL, p < .0001, area under receiver operating characteristic curve = 0.87).

CONCLUSIONS

In PTL pregnancies with the presence of intra-amniotic infection, the concentration of MIP-1α is elevated in amniotic fluid but not in cervical fluid. Amniotic fluid MIP-1α may provide a useful marker for intra-amniotic infection in women with PTL.