Phagocytic cell function in response to immunosuppressive therapy
D. B. Drath and B. D. Kahan
The increased incidence of pulmonary infection in human renal allograft
recipients is presumably related to antirejection immunosuppressive
therapy. To assess immunosuppressive-related disturbances of the immune
responses of the lung, we evaluated the functional abilities of the
pulmonary alveolar macrophage (PAM) and polymorphonuclear leukocyte (PMN)
of rats in chemotaxis, phagocytosis, and superoxide-release assays
following 30 days of intraperitoneal administration of cyclosporine,
azathioprine, and/or prednisolone sodium succinate. None of these drugs
affected superoxide release by stimulated PAMs or PMNs. Except for a
transient inhibition by azathioprine, the drugs had no effect on
phagocytosis of Staphylococcus aureus by either cell type. On the other
hand, cyclosporine inhibited formyl-methionyl-leucyl-phenylalanine
(FMLP)-directed chemotaxis by PAMs, and both FMLP and C5a stimulated
chemotaxis by PMNs. Azathioprine had more dramatic effects on PAMs than on
PMNs and prednisolone at 2 mg/kg inhibited PAMs. The results indicated
that, with the exception of chemotaxis, the immunosuppressive agents
largely spare nonspecific elements of host defense.
