Parasitic load and histopathology of cutaneous lesions, lymph node, spleen, and liver from BALB/c and C57BL/6 mice infected with Leishmania mexicana.

Torrentera, Fabiola Aguilar; Lambot, Marie-Alexandra; Laman, Jon D.; Meurs, Marjan van; Kiss, Róbert; Noël, Jean‐Christophe; Carlier, Yves

doi:10.4269/ajtmh.2002.66.273

Cited by 34 publications

(20 citation statements)

References 30 publications

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“…Fig. 1A shows that lesions in WT mice never healed during the 97-day period of infection, compatible with previous reports on the incapacity of these animals to cure L. amazonensis infection (Song et al 1997, Aguilar Torrentera et al 2002a, Maioli et al 2004). IFN-γ deficiency did not lead to more progressive disease at least during the first two months of infection, as seen by the comparable lesion sizes of IFN-γ KO mice and WT mice.…”

Section: Role Of Ifn-γ During L Amazonensis Infection -The Course Ofsupporting

confidence: 89%

Interferon-gamma is required for the late but not early control of Leishmania amazonensis infection in C57Bl/6 mice

Pinheiro

Rossi-Bergmann

2007

Mem. Inst. Oswaldo Cruz

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The critical role of interferon-gamma (IFN-γ) in the resistance of C57Bl/6 mice to Leishmania major is widely established but its role in the relative resistance of these animals to L. amazonensis infection is still not clear. In this work we use C57Bl/6 mice congenitally deficient in the IFN-γ gene (IFN-γ KO) Leishmaniasis is a complex of diseases caused by the obligate intracellular protozoan parasites of the genus Leishmania. The various clinical forms of human leishmaniasis have been partially reproduced in different strains of mice. For example, C57Bl/6 mice infected with L. major develop cutaneous lesions that spontaneously heal, whereas BALB/c mice harbor non-healing cutaneous lesions. Such experimental models have earlier allowed definition of some of the immunological factors involved in resistance and susceptibility to L. major infection (Reiner & Locksley 1995). During L. major infection of mice, a polarized differentiation of Th1/Th2 CD4 + T cells occurs in resistant and susceptible mice and the Th1 cytokine interferon-γ (IFN-γ) plays an essential role in controlling parasite growth and disease progression (Scott 1991, Liew et al. 1997. Evidence for the critical role for IFN-γ in the control of L. major infection comes from the demonstration that IFN-γ knockout (KO) mice fail to cure infection (Wang et al. 1994).In contrast to L. major, the immunological mechanisms determining susceptibility and resistance to L. amazonensis have been less studied. This is of relevance since the pathogenesis caused by L. amazonensis in humans follows a pattern different from that described for L. major and has been associated not only with localized cutaneous lesions but also with diffuse cutaneous leishmaniasis and more rarely, fatal visceral leishmaniasis (Convit et al. 1993, Almeida et al. 1996. Notably, in IFN-γ production by CD8 + T cells has been associated with immunoregulatory responses induced by leishmanial antigens that elicit significant protection against L. amazonensis (Champsi & McMahon-Pratt 1988, Soong et al. 1997) and an overproduction of IFN-γ seems necessary for development of a resistant phenotype (Afonso & Scott 1993). The protective role of IFN-γ in L. amazonensis infection is further questioned in a more recent report showing that IFN-γ promotes the replication of L. amazonensis amastigotes in macrophages, as opposed to its inhibitory effect on L. major infected macrophages (Qi et al. 2004). In vivo, adoptive transfer of naïve splenocytes devoid of CD4 + CD25 + Treg cells into RAG1-/-mice before infection markedly exacerbated disease progression, and this effect was associated with a marked production of IFN-γ by the effector T cells (Ji et al. 2005). Since the role of IFN-γ during L. amazonensis infection is not a resolved issue, in the present work we proposed to evaluate the course of L. amazonensis infection in IFN-γ KO mice. MATERIALS AND METHODSMice -C57Bl/6-background IFN-γ KO mice were a kind gift of Dr Leda Quércia Vieira (Gnotobiology Laboratory, Federal University of Minas Gerais,...

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Section: Role Of Ifn-γ During L Amazonensis Infection -The Course Ofsupporting

confidence: 89%

Interferon-gamma is required for the late but not early control of Leishmania amazonensis infection in C57Bl/6 mice

Pinheiro

Rossi-Bergmann

2007

Mem. Inst. Oswaldo Cruz

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“…Various studies have reported a resistance of C57BL/6 mice and a susceptibility of BALB/c mice to parasitic infections (12,13), including trypanosomiasis (14). In addition, it was previously shown that NO production by macrophages from infected C57BL/6 mice is greater than that from BALB/c mice (15,16), and a correlation between the level of NO production and the susceptibility of mouse strains to parasitic infections has been suggested.…”

mentioning

confidence: 99%

Mouse Strain Susceptibility to Trypanosome Infection: An Arginase-Dependent Effect

Duleu¹,

Vincendeau²,

Courtois³

et al. 2004

The Journal of Immunology

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We previously reported that macrophage arginase inhibits NO-dependent trypanosome killing in vitro and in vivo. BALB/c and C57BL/6 mice are known to be susceptible and resistant to trypanosome infection, respectively. Hence, we assessed the expression and the role of inducible NO synthase (iNOS) and arginase in these two mouse strains infected with Trypanosoma brucei brucei. Arginase I and arginase II mRNA expression was higher in macrophages from infected BALB/c compared with those from C57BL/6 mice, whereas iNOS mRNA was up-regulated at the same level in both phenotypes. Similarly, arginase activity was more important in macrophages from infected BALB/c vs infected C57BL/6 mice. Moreover, increase of arginase I and arginase II mRNA levels and of macrophage arginase activity was directly induced by trypanosomes, with a higher level in BALB/c compared with C57BL/6 mice. Neither iNOS expression nor NO production was stimulated by trypanosomes in vitro. The high level of arginase activity in T. brucei brucei-infected BALB/c macrophages strongly inhibited macrophage NO production, which in turn resulted in less trypanosome killing compared with C57BL/6 macrophages. NO generation and parasite killing were restored to the same level in BALB/c and C57BL/6 macrophages when arginase was specifically inhibited with Nω-hydroxy-nor-l-arginine. In conclusion, host arginase represents a marker of resistance/susceptibility to trypanosome infections.

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“…It remains to be elucidated whether the infiltration of lymph nodes and spleen, the key organs controlling the parasite dissemination by Leishmania infected macrophages during an experimental infection in animals is the cause or the consequence of the final breakdown of the microarchitecture of T-and B-cell areas (Saito et al, 1996). Bloodstream dissemination of the parasite to internal organs and probably t o other cutaneous tissues was reported to be due to the destruction of the lymphoid tissue and the lymph node capsule leading to the invasion of capillaries by the infected macrophages, as well as parasites in the red pulp of spleen and portal space of the liver (Aguilar-Torrentera et al, 2002). Donnelly et al (1998) studied the histological characterization of cutaneous leishmaniosis in BALB/c mice experimentally infected with L. major and C3H mice with L. braziliensis.…”

Section: Resultsmentioning

confidence: 99%

Morphologic Changes due to Cutaneous Leishmaniosis in BALB/c Mice Experimentally Infected withLeishmania major

Oryan

Mehrabani

Owji

et al. 2008

Journal of Applied Animal Research

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Parasitic load and histopathology of cutaneous lesions, lymph node, spleen, and liver from BALB/c and C57BL/6 mice infected with Leishmania mexicana.

Cited by 34 publications

References 30 publications

Interferon-gamma is required for the late but not early control of Leishmania amazonensis infection in C57Bl/6 mice

Interferon-gamma is required for the late but not early control of Leishmania amazonensis infection in C57Bl/6 mice

Mouse Strain Susceptibility to Trypanosome Infection: An Arginase-Dependent Effect

Morphologic Changes due to Cutaneous Leishmaniosis in BALB/c Mice Experimentally Infected withLeishmania major

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