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

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...

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Bibliographic Details
Published in:PloS one 2018-11, Vol.13 (11), p.e0207085-e0207085
Main Authors: Mizoguchi, Mika, Ishida, Yuko, Nosaka, Mizuho, Kimura, Akihiko, Kuninaka, Yumi, Yahata, Tamaki, Nanjo, Sakiko, Toujima, Saori, Minami, Sawako, Ino, Kazuhiko, Mukaida, Naofumi, Kondo, Toshikazu
Format: Article
Language:English
Subjects:
Biology and Life Sciences
Chemokines
CX3CR1 protein
Cytokines
Fetuses
Forensic medicine
Gene expression
Gynecology
Inflammation
Kinases
Labor
Laboratories
Lipopolysaccharides
Macrophages
Medicine and Health Sciences
Membranes
Mice
Molecular modelling
Neonates
Obstetrics
Pharmacology
Pregnancy
Prevention
Research and Analysis Methods
Rodents
Tumor necrosis factor-TNF
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Summary: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.
ISSN:1932-6203
1932-6203
DOI:10.1371/journal.pone.0207085