Complement fragments, alveolar macrophages, and alveolitis.
Mechanisms of neutrophil infiltration into the rabbit alveolus have been investigated. Complement activation in the circulation induced pulmonary vascular margination but not a significant level of alveolar infiltration. Instillation of C5 fragments into the airways, however, attracted neutrophils into the alveolar airspaces. The anaphylatoxin-inactive fragment of C5, C5a des Arg, was found to be much more active in this regard than C5a. Furthermore, these fragments were shown to induce the production of a neutrophil-directed chemoctactic factor from pulmonary macrophages, raising the question of whether the C5a des Arg was acting directly to attract neutrophils or indirectly via the macrophage. To substantiate a possible role for C5 and C5 fragments in alveolitis, active C5 was demonstrated in lavage fluids, and macrophage-derived C5 cleaving enzymes have been described. Finally, a route of neutrophil infiltration via migration through the alveolar capillary wall into the interstitium is proposed, and subsequent penetration of the alveolar epithelium out into the airspace. (Am J Pathol 97:93--110, 1979).
D000542:Alveolitis, Extrinsic Allergic / Q000209:etiology / Q000276:immunology*; D000818:Animals; D002633:Chemotaxis; D003182:Complement C5 / Q000276:immunology* / Q000378:metabolism; D007249:Inflammation / Q000209:etiology; D008168:Lung / Q000378:metabolism; D008264:Macrophages / Q000276:immunology*; D009504:Neutrophils / Q000276:immunology*; D010587:Phagocytosis; D011650:Pulmonary Alveoli / Q000166:cytology / Q000276:immunology*; D011817:Rabbits
D003182:Complement C5