Neutrophils are essential mediators of tissue damage in many forms of immune complex-induced injury. In vitro, they have been shown to release some of their content of injurious constituents upon reaction with immune complexes (Fig. 10). If the complexes are distributed along a nonphagocytosable surface, degranulation to the exterior of the cell is observed. When the complexes were phagocytized, however, degranulation into the phagocytic vacuole, and some loss of enzymes into the surrounding medium, occurred. This may have resulted from a momentary opening of the vacuole to allow ingestion of additional particles, as was demonstrated with the electron microscope. This phenomenon was particularly noticeable when the particles were relatively large. Far more immune complex is required to induce release when in a phagocytosable form than when on a nonphagocytosable membrane.
Neutrophils may be attracted to sites of immune complex deposition in many parts of the body (arteries, heart, skin, brain, kidney, joints) by complement-mediated processes. In some situations, e.g. in the joint fluid, they would encounter free immune complexes, phagocytose them, and release enzymes. In many others, in which immune complexes may be distributed along surfaces, such as in the glomerulus, adherence of neutrophils may also lead to release of injurious constituents (proteases, collagenase, elastase, permeability factors) capable of digesting and injuring the tissues.