rM mediates postresolution homeostasis. Mice were injected intravenously with clodronate-filled liposomes followed by zymosan (0.1 mg). Inflammation was first determined 4 hours later showing a significant increase over controls of (A) PMNs at onset followed by a confirmed reduction in (B) macrophages during resolution (48 hours) concomitant with a surprising reduction in (C) PMN numbers during this phase, suggesting that when phagocytosing macrophage are limited in numbers, PMNs may be efficiently cleared by parenchymal/stromal cells. However, (D) T- and B-lymphocyte numbers were also significantly reduced, revealing that rM cells are central to recruiting postresolution innate-type lymphocytes, which we have shown to be critical for postinflammation susceptibility to superinfection and restoration of tissue homeostasis.¹¹  (E) We identified that an rM COX 2–derived prostanoid mediated these effects as NS-398 at 10 mg/kg dosed orally during resolution (48 and 60 hours) impaired CD3 cell repopulation at 72 hours. Moreover, (F) adoptively transferring PKH26-PCL^red rM along with equal numbers of PKH2-PCL^green M1 cells to a murine peritoneal cavity revealed that after 24 hours rM cells remained in the peritoneum, whereas M1 displayed a greater clearance rate, suggesting that rM cells possess a greater propensity to remain in the peritoneum to elicit their prohomeostatic functions, with the dotted line denoting the original numbers of MΦs injected. (G) FACS dot plot to prove the successful transfer of differentially labeled MΦs and illustrating the greater number of PKH26-PCL^red MΦs (bottom right quadrant) compared with fewer PKH2-PCL^green MΦs (top left quadrant). *P ≤ .05 and **, P ≤ .01, determined by Bonferroni t test with data expressed as mean plus or minus SEM.