In a rat intrauterine infection model, KLF4 knockdown decreased LPS-induced preterm birth rates from 65% to 20%, accompanied by significantly reduced fetal stillbirth rates.<h4>Conclusion</h4>This study reveals that the fibroblast subpopulation Ccl2+fib contributes to preterm birth through a KLF4-dependent inflammatory regulatory network. This evidence concerns the gene CCL2 and Stillbirth.