Intraperitoneal injection of bone marrow-derived mast cells (BMMCs) has therapeutic efficacy against acute bacterial peritonitis. For this role, BMMCs need to settle down the mesentery from the peritoneal cavity. Interaction between BMMCs and the mesentery was examined by using mast cell deficient WBB6F(1)(F-1)- W/W-G [c-kit receptor tyrosine kinase (KIT) mutant], F-1-Sl/Sl(d) [KIT ligand stem cell factor mutant], and F-1-tg/tg [a practically microphthalmia transcription factor (MITF)-null mutant] mice. Three parameters were measured: the number of BMMCs: (1) developed in the mesentery 5 weeks after intraperitoneal injection into mast cell deficient mice, (2) adhered to mesenteric mesothelial cells, and (3) transmigrated across the mesenteric mesothelial cell monolayer when coculturing both cells for 3 and 18 h, respectively. After intraperitoneal injection, F-1-wild type (+/+) BMMCs developed in the mesentery of F-1-W/W-u mice but not in that of F-1-Sl/Sl(d) mice, while F-1-tg/tg BMMCs did not develop, even in the mesentery of WBB6F(1)-W/W-u mice. In the coculture, WB-W/W BMMCs normally adhered to but poorly transmigrated across F-1-+/+ mesothelial cells, and in accordance, F-1-+/+ BMMCs normally adhered to but poorly transmigrated across F-1-Sl/Sl(d) mesothelial cells. F(1-)tg/tg BMMCs showed poor adhesion and transmigration, but both parameters were partially but significantly improved by ectopic expression of spermatogenic immunoglobulin superfamily (SgIGSF), a mast-cell adhesion molecule critically regulated by MITF. Since F-1-tg/tg BMMCs expressed reduced levels of KIT, these results suggested that SgIGSF and KIT independently played a significant role in the transmigration. Among three parameters, development of mast cells in the mesentery well correlated with the transmigration. This process seemed important for mast cells to settle down from the peritoneal cavity to the mesentery. (C) 2004 Elsevier Inc. All rights reserved.