Abstract
Untreated 30 patients with pulmonary sarcoidosis and 14 healthy subjects were studied with respect to serum chemotactic inhibitor of macrophage. Tuberculin skin test was determined in 27/30 patients from whom sample serum was obtained. Macrophages were obtained from rabbit peritoneal exudate 4 days after intraperitoneal injection of 0.4% glycogen. The chemotactic assay was performed with modified Boyden chambers. Fresh human serum activated with E. coli. endotoxin was used as a chemotactic attractant. Macrophages were preincubated with sample serum for 30 minutes at 37°C and then washed before being introduced into the Boyden chamber.
Macrophage chemotaxis was significantly suppressed by sera from patients who had tuberculin anergy compared with those from healthy subjects and patients who exhibited positive tuberculin reaction. This is probably due to the serum chemotactic inhibitor rather than to the chemotactic deactivation of the cells. This inhibitor exhibited a direct inhibitory effect both on the macrophages and on the polymorphonuclear leukocytes. In addition, the inhibitory effect remained even after serum was removed from the cells by washing. The inhibitor was heat-stable for 30 minutes at 56°C. The features of the inhibitor obtained in this study were close to those of the cell-directed inhibitor (CDI) as described by Ward et al. In this study, it is concluded that CDI is present in sarcoid patients and that suppression of macrophage chemotaxis has highly significant association with tuberculin anergy. CDI may play a role in the pathogenesis of tuberculin anergy in sarcoidosis.
