Oxygen radicals, cytokines, adhesion molecules, and lung injury.
Inflammatory injury in the lung or dermis occurring after systemic activation of complement or after local deposition of immune complexes is related to local activation of tissue macrophages and/or recruitment of blood neutrophils. While requirements for cytokines (IL-1, TNF alpha, MCP-1) vary with the model of injury, requirements for adhesion molecules (beta 2 integrins, selectins, ICAM-1) differ. In most cases the immediate events related to tissue injury can be linked to toxic products from oxygen and L-arginine. Whether there is a single toxic product or a variety of toxic products remains to be determined. These data emphasize similarities and differences in the mechanisms of inflammatory injury, as a function of the inciting inflammatory agent and the organ system involved.
Ward
P A
PA
Department of Pathology, University of Michigan Medical School, Ann Arbor 48109-0602.
D000818:Animals; D000936:Antigen-Antibody Complex / Q000502:physiology; D015815:Cell Adhesion Molecules / Q000502:physiology*; D003167:Complement Activation; D016207:Cytokines / Q000502:physiology*; D006801:Humans; D007074:Immunoglobulin G / Q000276:immunology; D008171:Lung Diseases / Q000209:etiology*; D017382:Reactive Oxygen Species; D012867:Skin / Q000098:blood supply; D014652:Vascular Diseases / Q000209:etiology
D000936:Antigen-Antibody Complex; D015815:Cell Adhesion Molecules; D016207:Cytokines; D007074:Immunoglobulin G; D017382:Reactive Oxygen Species