IMMUNOHISTOLOGICAL STUDIES ON MACROPHAGES IN LYMPH-NODES OF ONCHOCERCIASIS PATIENTS AFTER TREATMENT WITH IVERMECTIN

The role of macrophages in the killing and elimination of microfilaria e (mf) was studied immunohistologically in 14 lymph nodes from Io pati ents with generalized onchocerciasis 20-68 h after treatment with a si ngle oral dose of 150 mu g/kg ivermectin. Mf with signs of damage at l ight microscopical level were surrounded by a cellular infiltrate comp rising macrophages, eosinophils and neutrophils, whereas light microsc opically intact mf mostly showed no cellular reaction. Resident mature macrophages expressing the CD 68 epitope usually neither migrated nor attached to damaged mf, especially on the first and second day after ivermectin treatment. However, many young invading macrophages labelle d for the L1 protein (antibodies 27 E 10, MAC 387, S 3648 and 8.5C2) w ere found within the cellular infiltrate around damaged mf and in adhe rence to the mf in all lymph nodes after ivermectin treatment. Free L1 protein was observed on the cuticle of the mf. The attacking macropha ges contained increased amounts of the enzymes lysozyme, alpha-1-antic hymotrypsin and alpha-1-antitrypsin compared to resident macrophages. Free enzymes were found on the cuticle of the mf and around them, indi cating a role of these enzymes in the inflammatory reaction to the par asites. The attacking macrophages were strongly labelled for human HLA -DR and they showed further an increased expression of the complement receptors CR1 (CD 35) for C3b and CR3 (CD 11b) for C3 bi in comparison to resident macrophages and thus were considered as activated macroph ages. Rarely fragments of mf were seen within multinuclear macrophages . We conclude that young activated macrophages play a major role in th e elimination of mf transported to the regional lymph nodes after iver mectin treatment. The immunohistological findings are in accordance wi th the assumption that these activated macrophages together with granu locytes contribute to the killing of the damaged mf. They also help to limit the damage of the host tissue by release of alpha-1-antichymotr ypsin and alpha-1-antitrypsin.