Prevention of lipopolysaccharide-induced preterm labor by the lack of CX3CL1-CX3CR1 interaction in mice.

Abstract

Preterm labor (PTL) is the most common cause of neonatal death and long-term adverse outcome. The pharmacological agents for PTL prevention are palliative and frequently fail to prevent PTL and improve neonatal outcome. It is essential to fully understand the molecular mechanisms of PTL in order to develop novel therapeutic methods against PTL. Several lines of evidence indicate some chemokines are expressed in gestational tissues during labor or PTL. To reveal the pathophysiological roles of the CX3CL1-CX3CR1 axis in PTL, we performed present study using LPS-induced PTL mice model in CX3CR1-deficient (Cx3cr1-/-) mice. We indicated that PTL was suppressed in Cx3cr1-/- mice and immunoneutralization of CX3CL1 in WT mice. From immunohistochemical and the gene expression analyses, the CX3CL1-CX3CR1 axis has detrimental roles in PTL through intrauterine recruitment of macrophages and the enhancement of macrophage-derived inflammatory mediators. Thus, the CX3CL1-CX3CR1 axis may be a good molecular target for preventing PTL.

• Authors: Mika Mizoguchi, Yuko Ishida, Mizuho Nosaka, Akihiko Kimura, Yumi Kuninaka, Tamaki Yahata, Sakiko Nanjo, Saori Toujima, Sawako Minami, Kazuhiko Ino, Naofumi Mukaida, Toshikazu Kondo
• Journal: PloS one (PLoS One) Vol. 13 Issue 11 Pg. e0207085 ( 2018) ISSN: 1932-6203 [Electronic] United States
• PMID: 30399192 (Publication Type: Journal Article)

Chemical References

• CX3C Chemokine Receptor 1
• CX3CL1 protein, human
• CX3CR1 protein, human
• Chemokine CX3CL1
• Cx3cl1 protein, mouse
• Cx3cr1 protein, mouse
• Lipopolysaccharides
• Recombinant Proteins

Topics

• Adult
• Animals
• CX3C Chemokine Receptor 1 (deficiency, genetics, metabolism)
• Chemokine CX3CL1 (deficiency, genetics, metabolism)
• Disease Models, Animal
• Escherichia coli
• Female
• Gene Expression
• Humans
• Inflammation (metabolism, pathology)
• Lipopolysaccharides
• Macrophages (metabolism, pathology)
• Mice, Inbred C57BL
• Mice, Knockout
• Obstetric Labor, Premature (metabolism, pathology)
• Placenta (metabolism, pathology)
• Pregnancy
• Recombinant Proteins (metabolism)