Magnesium sulfate reduces bacterial LPS-induced inflammation at the maternal-fetal interface

O. Dowling, P. K. Chatterjee, M. Gupta, H. B. Tam Tam, X. Xue, D. Lewis, B. Rochelson, C. N. Metz

Research output: Contribution to journalArticlepeer-review

55 Scopus citations


Objectives: Maternal magnesium sulfate (MgSO 4) administration exerts anti-inflammatory and fetal neuroprotective effects. Based on the link between placental inflammation and fetal immune responses, we examined the effect of MgSO 4 on LPS-induced inflammation at the maternal-fetal interface. Study design: In vivo model: Pregnant rats (GD19) were injected intraperitoneally with saline, LPS, or MgSO 4 plus LPS (n = 6 per group). Rats were euthanized; placentas were assayed for CCL2, IL6, and TNFα and placentas were screened for gene expression. Ex vivo model: Human placental cultures were treated with vehicle, LPS, or MgSO 4 plus LPS. Supernatants were assayed for CCL2, IL6, and TNFα. In addition, placental cultures were analyzed for inflammation-related gene expression and NFκ B activation. Results: In vivo model: Maternal LPS administration resulted in pro-inflammatory mediator production within the placenta; maternal MgSO 4 treatment significantly attenuated LPS-induced inflammation. Several placental transcripts (APOE, CCL4, CXCL1, and NFκBIZ) differentially expressed following maternal LPS challenge were counter-regulated by MgSO 4 treatment. Ex vivo model: LPS promoted human placental inflammation and MgSO 4 significantly reduced inflammation induced by LPS. MgSO 4 treatment of human placental explants significantly reversed the expression of numerous genes sensitive to LPS regulation and suppressed LPS-induced NFκB activation. Conclusions: MgSO 4 administration inhibited placental inflammation during LPS-mediated maternal infection. Several placental inflammatory genes whose expression was regulated by LPS were reversed by MgSO 4 treatment. Our data support the hypothesis that MgSO 4 attenuates excessive inflammation at the maternal-fetal interface, which when uncontrolled may compromise neonatal health, including neurologic outcomes.

Original languageEnglish
Pages (from-to)392-398
Number of pages7
Issue number5
StatePublished - May 2012
Externally publishedYes


  • Apolipoprotein E (APOE)
  • CCL4
  • CXCL1
  • Chemokines
  • Cytokines
  • Inflammation
  • Maternal infection
  • Nuclear factor kappa B
  • Placenta


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