Neutrophil Adhesion to Glomerular Mesangial Cells: Regulation by Lipoxygenase-Derived Eicosanoids

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Abstract
Glomerulonephritis (GN) is the leading cause of end-stage renal failure (1). While the pathophysiology of this condition is incompletely understood, polymorphonuclear leukocyte (PMN) and monocyte infiltration of the glomerulus is a characteristic early pathologic finding in many forms of human and experimental GN (reviewed in refs.1–4). For example, an intense PMN infiltrate is a prominant feature of several primary glomerular diseases in man, such as acute diffuse proliferative and crescentic GN (1–5, e.g. Fig.1), and also characterizes proliferative GN complicating systemic diseases, such as systemic lupus erythematosus (9). In addition, PMN infiltration is a common finding during the heterologous phase of experimental nephrotoxic serum nephritis, and glomerular hypercellularity and proteinuria can be abrogated in this model by prior depletion of phagocytes (6). Monocytic infiltration of the glomerulus has also been identified by morphologic and immunohistochemical techniques in clinical forms of postinfectious and crescentic GN (1–4), and the accelerated model of experimental nephrotoxic serum nephritis (1–4, 7, 8). In the latter condition, glomerular monocyte infiltration parallels the development of proteinuria, and, here also, prior depletion of monocytes by irradiation abrogates the development of proteinuria and glomerular hypercellularity (7). The mechanism(s) involved in leukocyte entrapment within the glomerulus in acute GN have not been fully established.