Eicosanoids and the modulation of glomerular immune injury View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

1989-04

AUTHORS

E A Lianos

ABSTRACT

For the purposes of this review, glomerular immune injury is viewed as a process initiated at the level of glomerular structures following deposition and interaction of defined immunologic reactants which may activate the synthesis of proinflammatory mediators. Renal hemodynamic perturbations and glomerular capillary wall injury resulting in proteinuria are the most frequent sequelae. When glomerular injury is initiated by deposition of antibody with specificity against glomerular antigens (structural or trapped) or against non-renal soluble antigens, the ensuing reaction can be of an inflammatory or noninflammatory type. The former is frequently associated with intraglomerular complement activation, recruitment of neutrophils and platelets and recruitment or enhanced expression of sensitized monocytes-macrophages. In noninflammatory forms, capillary wall injury can be mediated by antibody deposition alone or it may require complement activation. Regardless the type of injury, activation of a number of proinflammatory mediator systems has been documented following glomerular deposition of immunologic reactants. The metabolic products formed following activation of these systems may mediate perturbations in renal hemodynamics and in the permeability of the glomerular capillary wall. Moreover, they may play a regulatory role on the function of endogenous glomerular or blood borne cells recruited in glomerular structures following initiation of injury. Table 1 summarizes the mediator systems which have been studied in various forms of experimental glomerulonephritis. More... »

PAGES

985-992

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/ki.1989.82

DOI

http://dx.doi.org/10.1038/ki.1989.82

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1001025620

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/2651775


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