Mechanism of acute fetal cardiovascular depression after maternal inflammatory challenge in mouse

Samuli Rounioja, Juha Rasanen, Marja Ojaniemi, Virpi Glumoff, Helena Autio-Harmainen, Mikko Hallman

Research output: Contribution to journalArticle

19 Citations (Scopus)

Abstract

Intra-amniotic lipopolysaccharide (LPS) causes an acute inflammatory response and cardiac dysfunction In fetal mice. We hypothesized that the placenta protects the fetus against maternally administered bacterial toxins, delaying the onset of a fetal inflammatory response and vascular compromise. At 14 to 15 days of gestation, DBA mice were randomized to receive LPS (2.4 mg/kg) or vehicle intraperitoneally. Doppler ultrasonography of fetal cardiovascular hemodynamics was performed before and 6 hours after maternal LPS. Six hours after the LPS, maternal serum concentrations of tumor necrosis factor-α and interleukin (IL)-6 (P <0.05) were increased. Placenta showed severe maternal vascular dilatation and congestion. The expressions of tumor necrosis factor-α, IL-1α, and IL-6 (P <0.05) were increased, and the expression of Toll-like receptor 4 was constitutive in placenta. The expression of Toll-like receptor 2 increased (P <0.05) and was detected in labyrinthine macrophages. No inflammatory activation was found in fetal tissues, and amniotic fluid revealed no significant increase in cytokines. The ultrasonographic examination demonstrated increased fetal cardiac afterload after LPS, with 65% of the fetuses exhibiting atrioventricular valve regurgitation. In conclusion, maternal inflammatory insult activates placental labyrinthine macrophages leading to an acute increase in placental vascular resistance and fetal cardiac dysfunction without an inflammatory response in fetus.

Original languageEnglish (US)
Pages (from-to)1585-1592
Number of pages8
JournalAmerican Journal of Pathology
Volume166
Issue number6
StatePublished - Jun 2005
Externally publishedYes

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Lipopolysaccharides
Mothers
Fetus
Placenta
Blood Vessels
Interleukin-6
Tumor Necrosis Factor-alpha
Macrophages
Bacterial Toxins
Toll-Like Receptor 2
Doppler Ultrasonography
Inbred DBA Mouse
Toll-Like Receptor 4
Amniotic Fluid
Interleukin-1
Vascular Resistance
Dilatation
Hemodynamics
Cytokines
Pregnancy

ASJC Scopus subject areas

  • Pathology and Forensic Medicine

Cite this

Rounioja, S., Rasanen, J., Ojaniemi, M., Glumoff, V., Autio-Harmainen, H., & Hallman, M. (2005). Mechanism of acute fetal cardiovascular depression after maternal inflammatory challenge in mouse. American Journal of Pathology, 166(6), 1585-1592.

Mechanism of acute fetal cardiovascular depression after maternal inflammatory challenge in mouse. / Rounioja, Samuli; Rasanen, Juha; Ojaniemi, Marja; Glumoff, Virpi; Autio-Harmainen, Helena; Hallman, Mikko.

In: American Journal of Pathology, Vol. 166, No. 6, 06.2005, p. 1585-1592.

Research output: Contribution to journalArticle

Rounioja, S, Rasanen, J, Ojaniemi, M, Glumoff, V, Autio-Harmainen, H & Hallman, M 2005, 'Mechanism of acute fetal cardiovascular depression after maternal inflammatory challenge in mouse', American Journal of Pathology, vol. 166, no. 6, pp. 1585-1592.
Rounioja S, Rasanen J, Ojaniemi M, Glumoff V, Autio-Harmainen H, Hallman M. Mechanism of acute fetal cardiovascular depression after maternal inflammatory challenge in mouse. American Journal of Pathology. 2005 Jun;166(6):1585-1592.
Rounioja, Samuli ; Rasanen, Juha ; Ojaniemi, Marja ; Glumoff, Virpi ; Autio-Harmainen, Helena ; Hallman, Mikko. / Mechanism of acute fetal cardiovascular depression after maternal inflammatory challenge in mouse. In: American Journal of Pathology. 2005 ; Vol. 166, No. 6. pp. 1585-1592.
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