Monocytes and macrophages are professional phagocytic cells and are the major differentiated mediators of immune responses. These cells are widely distributed in many tissues and organs. Under normal (steady state) conditions, large number of these phagocytic cells (called resident macrophages) reside in the peritoneal cavity and in the ldquomilky spotsrdquo of the mesentery. As a result of inflammatory stimulus (i.e. intraperitoneal Freundrsquos adjuvant injection) these resident peritoneal macrophages become activated, and their number and endocytic activity is significantly increase. The origin and plasticity of these chronic, heterogeneous inflammatory macrophages are not entirely known. Tissue-resident macrophages as well as infiltrating monocyte-derived macrophages play a distinct role in the progression of inflammation, but the large number of these inflammatory macrophages suggests that cells originating from other, non-hematopoietic sources can also contribute to this subset of macrophages. Our morphological and biochemical results provided evidence that under the effect of inflammatory cytokines mesenteric mesothelial cells undergo epithelial-mesenchymal transition (EMT) and transdifferentiate into macrophages, thus these transformed mesenteric mesothelial cells can contribute to the large increase of peritoneal macrophages during inflammation. In this paper, we summarize our morphological and biochemical data supporting this transition and we describe how cavolae and caveolar endocytosis can regulate both epithelial-mesenchymal transition (EMT) and mesenchymal-epithelial transition (MET).