Publications

Degradation of matrix in normal glomeruli occurs through the action of neutral metalloproteinases which are in turn regulated by specific inhibitors. Both of these proteins are secreted by mesangial cells. Macrophages and IL-1 enhance the secretion of the proteinase. Decreased production of the metalloproteinase and for increased secretion of its inhibitor may lead to matrix accumulation. Neutrophil serine paternases degrade glomerular basement membrane (GBM) in vitro. In both animal and human disease urine excretion of these enzymes is accompanied by proteinuria and the presence of GBM-fragments. Further knowledge of the processes involved in matrix degradation may lead to improved therapy of glomerular disease.

Diverse neuropeptides are released by neuroendocrine and immune cells at the sites of allergic and inflammatory reactions. The neuropeptides and other neuromediators affect functions of smooth muscle, microvasculature and secretory cells, and are potent stimuli of mast cell, lymphocyte and other leucocyte contributions to such reactions. The distinctive immune sources, structures and cellular receptors for neuromediators suggest the possibility of novel pathogenetic mechanisms and levels of pharmacological intervention specific for neuroregulation of immunity and hypersensitivity.