Enhancement of Leishmania amazonensis infection in BCG non-responder mice by BCG-antigen specific vaccine

Calabrese, Kátia da Silva; Costa, Salvatore

doi:10.1590/s0074-02761992000500010

Cited by 25 publications

(14 citation statements)

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“…This parasite, as well as the related organism Leishmania mexicana, induces a nonhealing infection in mouse strains that are resistant to L. major, such as C3H, C57BL/6, and C57BL/10 (13)(14)(15)(16)(17). Although these mice have a susceptible phenotype, the immune response cannot be readily defined as a Th2 response.…”

Section: Il-4-independent Inhibition Of Il-12 Responsiveness Duringmentioning

confidence: 99%

IL-4-Independent Inhibition of IL-12 Responsiveness DuringLeishmania amazonensisInfection

Jones

Buxbaum

Scott

2000

The Journal of Immunology

124

139

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Leishmania amazonensis induces a nonhealing infection in C3H mice, whereas infection with Leishmania major is self-healing. We found that C3H mice infected with L. amazonensis exhibited decreased IL-12 production, which could account for the susceptibility to this organism. However, exogenous IL-12 administration failed to induce a healing immune response. The failure of L. amazonensis-infected C3H mice to respond to IL-12 was associated with a specific defect in IL-12 receptor β2 (IL-12Rβ2) mRNA expression by CD4+ T cells. Furthermore, decreased IL-12Rβ2 mRNA expression correlated with a decrease in the IL-12-signaling capacity of the lymph node (LN) cells. IL-4 did not contribute to susceptibility or down-regulation of the IL-12Rβ2 subunit, because IL-4−/− mice remained susceptible to L. amazonensis infection, even after IL-12 administration, and CD4+ cells from infected IL-4−/− mice also had reduced expression of IL-12Rβ2 mRNA. These results demonstrate that regulation of the IL-12 receptor, independent of IL-4, is a point of control for the immune response to leishmaniasis. In contrast to experimental L. major infections, where host genetics control susceptibility, these studies demonstrate that the lack of IL-12 responsiveness may be dictated by the pathogen, rather than the host.

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Section: Il-4-independent Inhibition Of Il-12 Responsiveness Duringmentioning

confidence: 99%

IL-4-Independent Inhibition of IL-12 Responsiveness DuringLeishmania amazonensisInfection

Jones

Buxbaum

Scott

2000

The Journal of Immunology

124

139

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“…All strains of mice appear to be resistant to L. braziliensis; thus, a good murine model of infection with this species of parasite is not available [12][13][14][15]. In contrast, most strains of mice are susceptible to infection with Leishmania from the mexicana complex [13,[16][17][18][19]. Afonso et al [17] showed that the susceptibility of C57BL/10 mice to L. amazonensis was related to the absence of a Th1 immune response but not controlled exclusively by Th2 cells.…”

Section: Introductionmentioning

confidence: 99%

Different species determine distinct profiles of immune and histopathological responses in CBA mice

Souza

Silva

et al. 2000

Microbes and Infection

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Most experimental studies on leishmaniasis compare two different inbred strains of mice that are resistant or susceptible to one species of Leishmania. In the present study we characterized some cytokines and nitric oxide production as well as histological changes related to resistance and susceptibility in isogenic CBA mice infected with Leishmania major or Leishmania amazonensis. CBA mice are capable of controlling infection with L. major, but they succumb to infection with L. amazonensis. Cells from susceptible L. amazonensis-infected CBA mice produced interleukin (IL)-4 and IL-10 but no interferon (IFN)-gamma. On the other hand, resistant L. major-infected CBA mice produced IFN-gamma and IL-10, but IL-4 was detected only in the first week of infection. Histopathological studies showed patterns of tissue responses at the site of the infection and in the draining lymph nodes that correlated with resistance or susceptibility. Resistant mice showed a mixed inflammatory cell infiltration and granulomas in the lesions, whereas in susceptible mice only heavily parasitized macrophages were seen. Our results indicate an important role of the parasite species in determining the pattern of immune response. L. amazonensis induces a Th2-type immune response, whereas L. major induces a Th1-type response. These factors must be identified and taken into account in the strategies for the development of vaccines against leishmaniasis. The model presented here will be useful for the study of such factors.

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“…A more recent example is the finding that interleukin-4 (IL-4)-knockout (KO) and IL-4 receptor-KO mice have different susceptibilities to infection with different strains of L. major (27,32,33). Similarly, C3H and C57BL/6 mice are resistant to L. major but develop chronic lesions with persistent parasite loads when they are infected with L. amazonensis (2,5,7,39,45). These studies demonstrate that both host and parasite factors influence the outcome of an infection.…”

mentioning

confidence: 99%

Early Enhanced Th1 Response afterLeishmania amazonensisInfection of C57BL/6 Interleukin-10-Deficient Mice Does Not Lead to Resolution of Infection

et al. 2002

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C3H and C57BL/6 mice are resistant to Leishmania major but develop chronic lesions with persistent parasite loads when they are infected with Leishmania amazonensis. These lesions develop in the absence of interleukin-4 (IL-4), indicating that susceptibility to this parasite is not a result of development of a Th2 response. Expression of the cytokine IL-10 during infection could account for the lack of IL-12 expression and poor cell-mediated immunity towards the parasite. Therefore, we tested the hypothesis that IL-10 plays a central role in downmodulating the Th1 response after L. amazonensis infection. Infection of C57BL/6 IL-10-deficient mice indicated that in the absence of IL-10 there was early enhancement of a Th1 response, which was downregulated during the more chronic stage of infection. In addition, although there were 1-to 2-log reductions in the parasite loads within the lesions, the parasites continued to persist, and they were associated with chronic lesions whose size was similar to that of the control lesions. These experiments indicated that L. amazonensis resistance to killing in vivo is only partially dependent on expression of host IL-10. However, IL-10-deficient mice had an enhanced delayed-type hypersensitivity response during the chronic phase of infection, indicating that there were Th1 type effector cells in vivo at this late stage of infection. These results indicate that although IL-10 plays a role in limiting the Th1 response during the acute infection phase, other immunomodulatory factors are responsible for limiting the Th1 response during the chronic phase.

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Enhancement of Leishmania amazonensis infection in BCG non-responder mice by BCG-antigen specific vaccine

Cited by 25 publications

References 0 publications

IL-4-Independent Inhibition of IL-12 Responsiveness DuringLeishmania amazonensisInfection

IL-4-Independent Inhibition of IL-12 Responsiveness DuringLeishmania amazonensisInfection

Different species determine distinct profiles of immune and histopathological responses in CBA mice

Early Enhanced Th1 Response afterLeishmania amazonensisInfection of C57BL/6 Interleukin-10-Deficient Mice Does Not Lead to Resolution of Infection

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