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Abstract: Body cavities are an evolutionarily conserved architectural feature of metazoans: fluid-filled spaces in which organs are suspended, allowed to move, and mechanically interact to fulfill their function. These same spaces harbor a primordial, highly specialized immune ecosystem. Among its most striking components are cavity-resident macrophages, which exist in suspension within the serous fluid. Positioned for constant surveillance, they sense deviations from homeostasis within minutes and initiate broad, pleiotropic responses that shape the ensuing inflammatory trajectory.

Using intravital microscopy, we have uncovered new principles of the biology of these cavity macrophages—how they patrol, how they respond to micro-injury, and how rapidly they can be depleted. Their depletion, classically observed as “macrophage disappearance” from the peritoneal fluid, marks a critical threshold: once resident macrophages are spent, secondary waves of immune cells such as neutrophils and monocytes are recruited. These monocytes, in turn, differentiate into non-resident macrophages with distinct phenotypes and functions.

I will discuss how these macrophage populations and mesenchymal cells cooperate during inflammation and resolution, and how their division of labor ultimately influences tissue repair within serous environments.