Depression of monocyte chemotaxis in intravenous drug abusers (IDA): cell alteration

Intravenous drug abusers (IDA) show an important immunological dysfunction that plays a key role in pathogenesis of infections found in these patients. A defective adherence and chemotaxis has been described at the level of mononuclear phagocytic system (MPS). In this paper, we center on defective chemotaxis. In the face of a chemotactic alteration, the first step is trying to locate the alteration as humoral or cellular; we have used the work sheme proposed by Yousif-Kadaru. Serum of IDA and controls, E. Coli endotoxin-activated and non-activated were used as attractants. Chemotaxis was studied by the morphologic method of Snyderman. Attractant capacity of E. Coli endotoxin activated serum was 55.93 +/- 10.88, similar to that of controls, 59 +/- 10.58. The same was true for non-activated serum, 42.5 +/- 16.8 compared to 44.67 +/- 19.54. That means, according with the scheme proposed, that the alteration is localized in the cell. Some factors that could participate in the pathogenesis of the motor defect are commented in the discussion. The elevation in immunocomplexes titer observed in IDA could depress monocyte chemotaxis, but the defect would be humoral. A deficit in chemotactic factor could be discarded because its production capacity is preserved in IDA. Liver disease, both acute and chronic, is one of the most frequent medical complications in these patients. The cellular localization of depression eliminates any participation in the pathogenesis of chemotactic alteration.