Feldmeier Hermann, Witt Lars-Henrik, Schwalfenberg Stefan, Albuquerque Ribeiro Ronaldo, Queiroz Cunha Fernando, Harms Gundel, Mehlhorn Heinz, Liesenfeld Oliver, Heukelbach Jörg
Department of Medical Microbiology and Immunology of Infection, Institute of Infection Medicine, Charité University Medicine Berlin, Campus Benjamin Franklin, 12203 Berlin, Germany.
Parasitol Res. 2004 Nov;94(5):371-6. doi: 10.1007/s00436-004-1219-0. Epub 2004 Oct 2.
Tungiasis is caused by the penetration of the female sand flea Tunga penetrans into the skin of its host. This parasitic skin disease is almost invariably associated with an intense inflammation around embedded fleas, the underlying mechanisms being unknown. A study was undertaken to determine whether Wistar rats can be used as an animal model to assess cytokine kinetics during the natural course of the infection. Laboratory-raised Wistar rats were exposed in cages put on the soil in an area with high human attack rates. Rats were examined daily and blood samples were taken before exposure and at 2, 6, 10, 13, 16 and 20 days after flea penetration. TNF-alpha, IL-1 beta, IFN-gamma, IL-4, IL-10 and CINC (a rat cytokine- induced neutrophil chemoattractant and member of the IL-8 family) were determined by enzyme immunoassay. The results showed an increasing serum concentration of TNF-alpha and IL-1 beta 10-13 days after penetration and a rapid increase in IL-4 2 days after fleas became embedded. During the natural course of the infection, the ratio of the serum concentration of TNF-alpha to that of IL-10 decreased, indicating a relative increase in the secretion of the anti-inflammatory cytokine. The treatment of lesions with silicone oil abrogated the natural disease course and changed the pattern of cytokine secretion. We conclude that the Wistar rat is an appropriate model to study immune responses in tungiasis.
