ArticleBrain, behavior, & immunity - health2026
Stem cells redirect the neuroinflammatory trajectory of primed microglia in an ovine chorioamnionitis model.
Article in Brain, behavior, & immunity - health, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Antenatal infection (e.g. chorioamnionitis), an important risk factor for preterm birth, can induce a fetal systemic inflammatory response (FIRS), initiating neuroinflammation. Microglia, as principal resident immune cells of the brain, are key targets for therapeutic interventions such as Multipotent adult progenitor cells (MAPC). We analyzed the effects of intravenous MAPC therapy on microglia and peripheral immune cells at the blood-brain barrier (BBB) in an ovine chorioamnionitis model. Ovine fetuses were intra-amniotic (i.a.) exposed to lipopolysaccharide (LPS) to induce FIRS, or saline (SAL) at 125 days gestational age (dGA), followed by intravenous MAPC therapy or SAL at 127 dGA. After sacrifice (132 dGA), isolated microglia were analyzed by qRT-PCR and RNA sequencing. Microglial function was assessed through efferocytosis of Jurkat cells. Additionally, immunohistochemistry of immune cells (CD45, IBA-1, MPO) and their ANXA1 co-expression were quantified in brain parenchyma and BBB. Antenatal inflammation resulted in an increased efferocytotic capacity following
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