Trypanosoma brucei brucei: a model for cerebral trypanosomiasis in mice--an immunological, histological and electronmicroscopic study
Poltera, A.A.; Hochmann, A.; Rudin, W.; Lambert, P.H.
Clinical and Experimental Immunology 40(3): 496-507
1980
ISSN/ISBN: 0009-9104 PMID: 6998617 Document Number: 159111
The successful induction of cerebral trypanosomiasis in ordinary laboratory mice using T. brucei brucei is reported. Sequential studies demonstrated the presence of trypanosomes in the interstitium of the choroid plexus at the 4th wk after infection which correlated with the appearance of anti-trypanosomal antibodies, a rise of Ig immunoglobulin M and IgG serum levels, a rise of Clq q fragment of complement component 1 binding activity and a decrease of C3 levels. EM studies showed that the parasites were flagellated and localized extracellularly mainly in the interstitium of the choroid plexus. Granular immunofluorescent deposits of Ig and C3 were most marked in the choroid plexus. Electron-dense deposits suggestive of immune complexes were seen in subendothelial, interstitial and subependymal areas of the choroid plexus. Since autoantibodies to the brain were found in the serum of some mice, possible involvement of autoimmune manifestations in the pathogenesis of cerebral lesions was considered. The pattern of inflammatory foci at the 8th wk after infection was very similar to that observed in cerebral African trypanosomiasis in man. After treatment with ethidium bromide, trypanosomes persisted in the tissues when circulating parasities could no longer be detected. A sequential involvement of brain structures during African trypanosomiasis was suggested. Trypanosomes may first migrate from the vascular compartment into the interstitium of the choroid plexus, possibly favored by increased vascular permeability. Circulating immune complexes and C activation may be involved at this stage. Trypanosomes localized in the choroid plexus may then trigger a local immunologically mediated inflammatory reaction favoring the migration of trypanosomes into the CSF and further invasion of other cerebral structures.