NEUROGENIC AMPLIFICATION OF IMMUNE-COMPLEX INFLAMMATION

The formation of intrapulmonary immune complexes in mice generates a v igorous inflammatory response characterized by microvascular permeabil ity and polymorphonuclear neutrophil influx. Gene-targeted disruption of the substance P receptor (NK-1R) protected the lung from immune com plex injury, as did disruption of the C5a anaphylatoxin receptor. Immu noreactive substance P was measurable in fluids lining the lung at tim e points before neutrophil influx and may thus be involved in an early step in the inflammatory response to immune complexes in the lung.