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pubmed-article:7643744pubmed:abstractTextIt is now generally agreed that several cytokines released by immunocompetent cells such as macrophages play a crucial role in the outcome of infections caused by protozoa belonging to the genus Leishmania. In particular, tumor necrosis factor (TNF) induction during the course of cutaneous leishmaniasis has been related to resistance to L. major infection in mice. However, the role played by interleukin 1 (IL-1) in the host response to leishmaniasis has yet to be completely elucidated. The aim of this work was to study whether different species and strains of Leishmania could induce IL-1 alpha in murine macrophages in vitro. Resident peritoneal macrophages of BALB/c and C3H/HeN mice were infected with L. donovani, L. major, or different strains of L. infantum. It was found that L. donovani did not induce IL-1 alpha in macrophages from either mice strain. Infection with L. major or with three out of six strains of L. infantum induced consistent amounts of IL-1 alpha, but only in macrophages from genetically resistant C3H/HeN mice. No relationship was found between the rate of infection of macrophages and the amount of IL-1 alpha detected in the supernatants of infected macrophages. Data obtained confirm that the release of IL-1 alpha by murine macrophages infected in vitro with Leishmania is influenced by the genetic background of the cells as well as by the parasite species.lld:pubmed
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pubmed-article:7643744pubmed:pagination73-80lld:pubmed
pubmed-article:7643744pubmed:dateRevised2006-11-15lld:pubmed
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pubmed-article:7643744pubmed:year1995lld:pubmed
pubmed-article:7643744pubmed:articleTitleInduction of interleukin 1 alpha in murine macrophages infected in vitro with different species and strains of Leishmania.lld:pubmed
pubmed-article:7643744pubmed:affiliationIstituto di Microbiologia, Università di Messina, Italy.lld:pubmed
pubmed-article:7643744pubmed:publicationTypeJournal Articlelld:pubmed
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pubmed-article:7643744pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed