The Cytokine Network Controlling Peritoneal Inflammation

p eritoneal dialysis is being used increasingly as a treatment for end-stage renal failure. This has focused attention on the importance of preserving the functional integrity of the peritoneal membrane as a dialyzing organ. This membrane forms the permeability barrier across which ultrafiltration and diffusion occur. Damage to this membrane as a result of repeated infection or possibly as a result of the long-term exposure to nonphysiological dialysis solutions can in some patients result in the long-term loss of ultrafiltration. Such patients may develop interstitial thickening and sclerosis with complete and irreparable damage to the peritoneal membrane (1). The end result of this process may force the cessation of this form of dialysis procedure (2). A large amount of evidence suggests that the principal cell type involved in peritoneal inflammation is the peritoneal macrophage (PMΦ) (3). It is assumed that resident PMΦs form the first line of defense against invading microorganisms and that their secretion of chemotactic and inflammatory cytokines and eicosanoids are important in the host's response to infection. More recently, however, it has become apparent that the mesothelial cell, which lines the peritoneal cavity, is also capable of contributing to intraperitoneal inflammatory processes. This review will examine inflammation in the peritoneum and the roles of the resident peritoneal cell populations (PMΦ, mesothelial cell) in this process. It will discuss their potential to contribute to the peritoneal "cytokine network," both in terms of secretion of proinflammatory and anti