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Rheumatoid factor accentuation of pulmonary lesions associated with experimental diffuse proliferative lung disease.

A rabbit model of diffuse proliferative lung disease induced by one intravenous injection of complete Freund's adjuvant was used to study the possible phlogistic effects of human anti-γ-globulins. When induction of proliferative lung disease was followed by intravenous administration of human γM anti-γ-globulins, considerable increment in perigranulomatous inflammation along with alveolar wall and arteriolar anti-γ-globulin deposition was noted. Four of 10 animals thus treated showed segmental hemorrhagic pulmonary infarctions. Control animals in which the induction of diffuse proliferative lung disease was followed by administration of serologically inactive normal human γM showed no accentuation of gross or microscopic pulmonary lesions and no specific pulmonary deposition of human γM globulins. These experiments suggest that human γM anti-γ-globulins fix in alveoli and arterioles near areas of active subacute or chronic pulmonary inflammation and are capable of accentuating inflammatory response and vascular injury.