MgSO4 increases intracellular magnesium, reducing inflammatory cytokine production and release, potentially elucidating the mechanism by which MgSO4 prevents cerebral palsy, eclampsia, and preterm birth.

Histological assessment demonstrated that this model of NOG mice repeatedly exhibited regular menstrual cycles, and this model mimicked not 'ectopic endometrium', but 'eutopic endometrium' in humans. Change in number of NK cells suggested that NK cell might be derived from the endometrium.

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MgSO 4 exposure before preterm birth is neuroprotective, reducing the risk of cerebral palsy and major motor dysfunction. Neonatal inflammatory cytokine levels correlate with neurologic outcome, leading us to assess the effect of MgSO 4 on cytokine production in humans. We found reduced maternal TNF-α and IL-6 production following in vivo MgSO 4 treatment. Short-term exposure to a clinically effective MgSO 4 concentration in vitro substantially reduced the frequency of neonatal monocytes producing TNF-α and IL-6 under constitutive and TLRstimulated conditions, decreasing cytokine gene and protein expression, without influencing cell viability or phagocytic function. In summary, MgSO 4 reduced cytokine production in intrapartum women, term and preterm neonates, demonstrating effectiveness in those at risk for inflammationassociated adverse perinatal outcomes. By probing the mechanism of decreased cytokine production, we found that the immunomodulatory effect was mediated by magnesium and not the sulfate moiety, and it was reversible. Cellular magnesium content increased rapidly upon MgSO 4 exposure, and reduced cytokine production occurred following stimulation with different TLR ligands as well as when magnesium was added after TLR stimulation, strongly suggesting that magnesium acts intracellularly. Magnesium increased basal IκBα levels, and upon TLR stimulation was associated with reduced NF-κB activation and nuclear localization. These findings establish a new paradigm for innate immunoregulation, whereby magnesium plays a critical regulatory role in NF-κB activation, cytokine production, and disease pathogenesis.