Vaginal Acinetobacter infection as a cause of cervical collagenolysis

The vaginal microbiota demonstrates considerable heterogeneity and is shaped by factors such as race, geographic location, and individual variation. Although its central role in maintaining host health is well established, the precise mechanisms through which it contributes to the onset and progression of preterm birth remain incompletely understood and continue to be debated.

This study aimed to characterize the vaginal microbiota of pregnant women who experienced preterm birth compared with those with full-term pregnancies. Through both in vivo and in vitro experiments, the study investigated whether vaginal pathogenic bacteria associated with preterm birth can trigger cervical collagen fiber degradation and induce the expression of MMP-1.

High-throughput sequencing was used to analyze the vaginal microbial communities of women with preterm and full-term pregnancies. On gestational days (GD) 14 and 15, pregnant C57BL/6 mice received intravaginal inoculations of 50 μL containing either 5 × 10⁸ CFU/mL Acinetobacter, 5 × 10⁸ CFU/mL Lactobacillus gasseri, or sterile phosphate-buffered saline (PBS). Cervical tissues were collected on GD16. Collagen fiber degradation was evaluated using Sirius red staining, and MMP-1 expression was assessed by immunohistochemistry. Hcer Epic cells were co-cultured with Acinetobacter or Lactobacillus gasseri, after which MMP-1 expression was measured using ELISA, qPCR, Western blotting, and immunofluorescence staining. The transcriptional regulatory role of Snai2 in controlling MMP-1 expression was examined using chromatin immunoprecipitation (ChIP), dual-luciferase reporter assays, and Western blot analysis.

Acinetobacter was identified as a characteristic bacterium in the vaginal microbiota of women with preterm birth. Experimental results showed that this bacterium induced cervical collagen fiber degradation in pregnant mice and increased MMP-1 expression in both the mouse model and Hcer Epic cells. Mechanistic analyses revealed that Snai2 binds to the GCACCTGT motif in the MMP-1 promoter. Furthermore, Acinetobacter might enhance MMP-1 expression through the activation of Snai2. These findings are limited to the specific strains examined and warrant further investigation across additional isolates.

These findings indicate that Acinetobacter promotes cervical collagen fiber degradation and elevates MMP-1 expression in both animal and cellular models, suggesting that this bacterium may contribute to cervical collagen remodeling and potentially play a pathogenic role in the development of preterm birth.