Oliveira, Marcia Rosa deTafuri, Wagner LuizAfonso, Luís Carlos CroccoOliveira, Milton Adriano Pelli deNicoli, Jacques RobertVieira, Etel RochaScott, PhillipMelo, Maria NormaVieira, Leda Quercia2017-06-132017-06-132005OLIVEIRA, M. R. de. Germ-free mice produce high levels of interferon-gamma in response to infection with Leishmania major but fail to heal lesions. Parasitology, Reino Unido, v. 131, p. 477-488, 2005. Disponível em: <https://goo.gl/IaLWv7>. Acesso em: 19 fev. 2017.1469-8161http://www.repositorio.ufop.br/handle/123456789/7961In order to investigate the importance of the host microbiota on differentiation of T cell subsets in response to infection, Swiss/NIH germ-free mice and conventional (microbiota-bearing) mice were infected with Leishmania major, and lesion development, parasite loads, and cytokine production were assessed. Germ-free mice failed to heal lesions and presented a higher number of parasites at the site of infection than their conventional counterparts. In addition, histopathological analysis indicated a higher density of parasitized macrophages in lesions from germ-free mice than in conventional mice. The initial production of interleukin (IL)-12 and interferon-gamma (IFN-c) in germ-free mice was comparable to the conventional controls. Also, germ-free mice produced elevated levels of IFN-c and lower levels of IL-4 throughout the course of infection, suggesting the development of a Th1 response. Macrophages from germ-free mice exposed to IFN-c and infected with amastigotes in vitro were not as efficient at killing parasites as macrophages from conventional animals. These observations indicate that the microbiota is not essential for the development of Th1 immune responses, but seems to be important for macrophage activation.en-USrestritoLeishmaniasisMicrobiotaGnotobioticGnotobiologyArtigo publicado em periodicohttps://goo.gl/IaLWv7https://doi.org/10.1017/S0031182005008073