The role of macrophages in the killing and elimination of microfilariae (mf) was studied immunohistologically in 14 lymph nodes from 10 patients with generalized
onchocerciasis 20-68 h
after treatment with a single oral dose of 150 microg/kg
ivermectin. Mf with signs of damage at light microscopical level were surrounded by a cellular infiltrate comprising macrophages, eosinophils and neutrophils, whereas light microscopically 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 labelled for the L1
protein (
antibodies 27
E 10, MAC 387, S 36.48 and 8.5C2) were found within the cellular infiltrate around damaged mf and in adherence to the mf in all lymph nodes after
ivermectin treatment. Free L1
protein was observed on the cuticle of the mf. The attacking macrophages contained increased amounts of the
enzymes lysozyme, alpha-1-antichymotrypsin and alpha-1-antitrypsin compared to resident macrophages. Free
enzymes were found on the cuticle of the mf and around them, indicating a role of these
enzymes in the inflammatory reaction to the parasites. 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 macrophages. Rarely fragments of mf were seen within multinuclear macrophages. We conclude that young activated macrophages play a major role in the elimination of mf transported to the regional lymph nodes after
ivermectin treatment. The immunohistological findings are in accordance with the assumption that these activated macrophages together with granulocytes contribute to the killing of the damaged mf. They also help to limit the damage of the host tissue by release of alpha-1-antichymotrypsin and alpha-1-antitrypsin.