Newborn immune cells called monocytes responded differently to platelets from adults than to platelets from newborns, according to a study recently published in the journal Platelets. The authors suggested this may stem partly from a “developmental mismatch” between adult donor platelets and a newborn’s own blood cells.
This research helps scientists understand what may happen when a baby with a low platelet countPlatelet count A measure of how many platelets are in the blood. FNAIT is characterized by severely reduced counts in a fetus or newborn. receives a transfusion of platelets donated by adults, whose platelets are more mature than a baby’s own.
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Newborns in intensive care, especially those born early, often have low platelet counts and are at risk of serious bleeding. Low platelet counts can also be a result of neonatal disorders such as fetal and neonatal alloimmune thrombocytopenia (FNAIT), a condition in which a mother’s antibodies attack her baby’s platelets.
Platelet transfusions are a common treatment for those newborns, and the donated platelets always come from adults. However, earlier research suggests that giving premature babies platelet transfusions at higher platelet counts may cause more harm than benefit.
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To explore this, the researchers collected monocytes, a type of white blood cell that helps fight infection and travels to areas of inflammation, from the umbilical cord blood of healthy, full-term babies. They then mixed these cells in the lab with platelets taken either from cord blood or from healthy adult volunteers.
The researchers found that adult platelets differed from newborn platelets in two key ways. After being activated, adult platelets carried about twice as much of a protein called P-selectin, which appears on the platelet surface and allows platelets to attach to immune cells such as monocytes. Adult platelets also released more of beta-2-microglobulin, a protein involved in immune signaling, both before and after activation.
When mixed with the monocytes, both adult and newborn platelets led the cells to release more inflammation-related proteins than monocytes left on their own, and the amounts did not differ significantly between the two types of platelets. Both types also raised the levels of two receptors on the monocytes that help these cells leave the bloodstream and move into body tissues, but adult platelets raised them substantially more.
When they blocked P-selectin, adult platelets no longer increased the receptors that help monocytes move into tissues, though the cells still released inflammation-related proteins. Beta-2-microglobulin on its own had no effect. According to the authors, this suggests that P-selectin plays a key role in preparing newborn immune cells to move into tissues. This matters because once monocytes enter tissues, they can add to inflammation there. The authors suggested this could help explain why platelet transfusions have been linked to worsening lung disease and necrotizing enterocolitis, a serious bowel condition, in sick newborns.
The authors noted that the study used cord blood from full-term babies, so the results may not fully reflect how premature babies, who receive transfusions most often, would respond.
