Using intravital microscopy, the research team visualized the immune response to Staphylococcus aureus bacteria in an animal model. The bacteria can catalyze abscesses or boils and lead to severe infections like pneumonia and endocarditis. For high-dose infections, monocytes surround the infection site, whereas neutrophils infiltrate it. Monocytes did not clear bacteria but converted to macrophages that persisted for weeks after infection. Doing so regulated hypodermal adipocyte expansion and production of the adipokine hormone leptin, the researchers found.

Also, the scientists learned for infected monocyte-deficient mice, there was an increased, persistent hypodermis thickening and an elevated leptin level, which drove overgrowth of dysfunctional blood vasculature and delayed healing. Ghrelin, which opposes leptin function, was produced locally by monocytes and reduced vascular overgrowth and improved healing post infection.

Next, the scientists plan to study the role of neutrophils more deeply, specifically how neutrophils become cleared from an infection and whether they take on different roles.

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