Abstract
Recent studies demonstrate significant neuroimmune changes in postpartum females, a period that also carries an increased risk of stroke. Oxytocin, a major hormone upregulated in the brains of nursing mothers, has been shown to both modulate neuroinflammation and protect against stroke. In the present study we assessed whether and how nursing modulates the neuroimmune response and injury after stroke. We observed that postpartum nursing mice were markedly protected from 1 h of transient middle cerebral artery occlusion (MCAO) relative to either non-pregnant/non-postpartum or non-nursing (pups removed) postpartum females. Nursing mice also expressed reduced levels of pro-inflammatory cytokines, had decreased migration of blood leukocytes into the brain following MCAO, and displayed peripheral neuroimmune changes characterized by increased spleen weight and increased fraction of spleen monocytes. Intranasal oxytocin treatment in non-pregnant females in part recapitulated the protective and anti-inflammatory effects associated with nursing. In summary, the results of the present study demonstrate that nursing in the postpartum period provides relative protection against transient ischemic stroke associated with decreased brain leukocytes and increased splenic monocytes. These effects appear to be regulated, at least in part, by oxytocin.
Highlights
Over the past decades significant progress has been achieved in understanding the complex cellular and molecular mechanisms of stroke pathology
This study is the first to assess the effects of nursing and exogenous oxytocin treatment in stroke outcomes in female mice
Our study demonstrates for the first time strong nursing-associated neuroprotection against experimental stroke, along with observed oxytocin-associated anti-inflammatory mechanisms
Summary
Over the past decades significant progress has been achieved in understanding the complex cellular and molecular mechanisms of stroke pathology. While stroke is uncommon in young women, the peripartum period is associated with a significantly increased risk of stroke (Kittner et al, 1996; James et al, 2005). Approximately 15% of pregnant women who experience a stroke die as a result, making it the 8th leading cause of pregnancy-associated. Stroke-induced release of pro-inflammatory mediators and cytokines leads to brain cell damage and apoptosis (Choe et al, 2011; Vogelgesang et al, 2014), tied to increased levels of pro-inflammatory cytokines IL-6 and TNFα (Campbell et al, 1993; Rothwell and Relton, 1993; Meistrell et al, 1997; Lavine et al, 1998). Induction of stroke results in brain damage and local neuroinflammation, and has profound effects on peripheral immune responses, promoting peripheral immune suppression, splenic atrophy and changes in circulating leukocytes (Offner et al, 2006; Lafargue et al, 2012)
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