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Kinetics of an experimental inflammatory reaction induced by Leishmania major during the implantation of paraffin tablets in mice.

  • Tafuri, W L
  • Melo, M N
  • Paiva, M C
  • Mosser, D M
  • Tafuri, W L
Published Article
Virchows Archiv : an international journal of pathology
Publication Date
Oct 01, 2000
PMID: 11097369


In leishmaniasis, macrophages play important but potentially divergent roles. They act as the host cell in which the parasite may reside and replicate, and, at the same time, they act as an effector cell with the potential to eliminate the parasite. In this work, we experimentally induced an inflammatory model that provokes a continued recruitment of the monocytes to the site of inflammation. This model was carried out by means of implanting paraffin tablets under the skin of Balb/c or C57BL/6 mice. Mice were then infected with Leishmania major to determine how the monocyte inflammatory response to paraffin could influence the course of infection with L. major. Mice were sacrificed 15, 21, 30, and 45 days after infection, and skin and inflammatory capsule were collected for histopathology. At 15 days and 21 days, the lesions induced by L. major in combination with paraffin contained markedly increased numbers of parasites relative to lesions in parallel control animals infected with L. major (without paraffin). Both Balb/c and C57BL/6 mice exhibited high parasite numbers in their lesions. The intense parasite burden observed following paraffin implantation would suggest that the monocytes-macrophages that are recruited to the lesion are acting more as a host cell permitting parasite growth than as an effector cell capable of eliminating L. major. At later times, the two strains of mice stratified according to their genetic susceptibility/resistance profiles. Susceptible Balb/c mice continue to have large parasite burdens, whereas the resistant C56BL/6 mice begin to control parasite numbers. This later observation indicates that the genetic difference between susceptible and resistant strains is not due to differences in monocyte recruitment and cannot be reversed through the altering of monocyte inflammation.


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