Immune Cells Trigger Labour via Mitochondria Transfer — SkimNews
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- Stephen Lye and colleagues at Mount Sinai Hospital in Toronto found macrophages form tube-like structures that attach to uterine muscle cells and transfer mitochondria into them, boosting ATP levels to power contractions.
- The team previously showed that near term the uterus releases cytokines and chemokines that recruit monocytes from the blood, which then accumulate in uterine muscle tissue and convert into macrophages.
- Mitochondrial transfer also raised levels of an enzyme that breaks down progesterone locally inside uterine muscle cells — addressing the puzzle of why human labor begins despite circulating progesterone levels remaining steady.
- The researchers previously tested a broad-spectrum chemokine inhibitor that blocked preterm birth in four macaques, but it has not yet been tested in humans.
- Current tocolytics for preterm labor only delay delivery by a few days, and the team is separately studying blood immune cells to identify which patients showing early labor signs are truly at risk of delivering.
- Lye envisions a future blood test that detects monocyte activation to predict whether a full-term person is about to go into labor.
- Preterm birth, defined as delivery before 37 weeks, increases the risk of cerebral palsy, learning difficulties, asthma, and vision and hearing problems.
Why it matters: Preterm birth before 37 weeks raises the risk of cerebral palsy, learning difficulties, asthma, and vision and hearing problems, yet current tocolytics only delay labor by a few days. By targeting the immune-cell trigger itself, the chemokine inhibitor already proven in four macaques offers the first mechanistic pathway to actually prevent preterm delivery rather than briefly postpone it.
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