Insulin-like growth factor I is a growth-promoting factor for<i>Leishmania</i>promastigotes and amastigotes

Goto, Hiro; Gomes, C. M. C.; Corbett, Carlos Eduardo Pereira; Monteiro, Hugo P.; Gidlund, Magnus

doi:10.1073/pnas.95.22.13211

Cited by 33 publications

(46 citation statements)

References 32 publications

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“…1B). One explanation for these results is that human insulin could enhance the growth of P. falciparum parasites directly in a manner analogous to human insulin=IGF-1 growth induction of Toxoplasma and Leishmania (10,45). To test this possibility, we examined the effects of increasing concentrations of human insulin on the growth of synchronized asexual-stage P. falciparum parasites in vitro.…”

mentioning

confidence: 95%

Reactive Oxygen Species-Dependent Cell Signaling Regulates the Mosquito Immune Response to Plasmodium falciparum

Surachetpong

Pakpour

Cheung

et al. 2011

Antioxidants & Redox Signaling

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Reactive oxygen species (ROS) have been implicated in direct killing of pathogens, increased tissue damage, and regulation of immune signaling pathways in mammalian cells. Available research suggests that analogous phenomena affect the establishment of Plasmodium infection in Anopheles mosquitoes. We have previously shown that provision of human insulin in a blood meal leads to increased ROS levels in Anopheles stephensi. Here, we demonstrate that provision of human insulin significantly increased parasite development in the same mosquito host in a manner that was not consistent with ROS-induced parasite killing or parasite escape through damaged tissue. Rather, our studies demonstrate that ROS are important mediators of both the mitogen-activated protein kinase and phosphatidylinositol 3-kinase/Akt signaling branches of the mosquito insulin signaling cascade. Further, ROS alone can directly activate these signaling pathways and this activation is growth factor specific. Our data, therefore, highlight a novel role for ROS as signaling mediators in the mosquito innate immune response to Plasmodium parasites.

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confidence: 95%

Reactive Oxygen Species-Dependent Cell Signaling Regulates the Mosquito Immune Response to Plasmodium falciparum

Surachetpong

Pakpour

Cheung

et al. 2011

Antioxidants & Redox Signaling

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“…TGF-ß produced by adherent antigen-presenting cells from infected hamsters was implicated in immunosuppression since a high level of TGF-ß was observed in the cell culture supernatant when the Leishmania antigen-induced lymphoproliferative response was inhibited (47). We have studied the effect of another growth factor, insulin-like growth factor-I, and we have shown its effect on in vitro Leishmania growth but also on enhancement of the lesion in cutaneous leishmaniasis (48). More recent data suggest that it is a suppressor factor of macrophages leading to the decreased production of nitric oxide in Leishmania-infected macrophages in vitro (49).…”

Section: Immunosuppression In Experimental Visceral Leishmaniasismentioning

confidence: 99%

Immunity and immunosuppression in experimental visceral leishmaniasis

Goto

Lindoso

2004

Braz J Med Biol Res

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Leishmaniasis is a disease caused by protozoa of the genus Leishmania, and visceral leishmaniasis is a form in which the inner organs are affected. Since knowledge about immunity in experimental visceral leishmaniasis is poor, we present here a review on immunity and immunosuppression in experimental visceral leishmaniasis in mouse and hamster models. We show the complexity of the mechanisms involved and differences when compared with the cutaneous form of leishmaniasis. Resistance in visceral leishmaniasis involves both CD4 + and CD8 + T cells, and interleukin (IL)-2, interferon (IFN)-γ, and IL-12, the latter in a mechanism independent of IFN-γ and linked to transforming growth factor (TGF)-ß production. Susceptibility involves IL-10 but not IL-4, and B cells. In immune animals, upon reinfection, the elements involved in resistance are different, i.e., CD8 + T cells and IL-2. Since one of the immunopathological consequences of active visceral leishmaniasis in humans is suppression of T-cell responses, many studies have been conducted using experimental models. Immunosuppression is mainly Leishmania antigen specific, and T cells, Th2 cells and adherent antigen-presenting cells have been shown to be involved. Interactions of the co-stimulatory molecule family B7-CTLA-4 leading to increased level of TGF-ß as well as apoptosis of CD4 + T cells and inhibition of macrophage apoptosis by Leishmania infection are other components participating in immunosuppression. A better understanding of this complex immune response and the mechanisms of immunosuppression in experimental visceral leishmaniasis will contribute to the study of human disease and to vaccine development.

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“…1992 ) and TNF‐α ( Bogdan et al . 1990 ) as well as factors constitutively present such as IGF‐I ( Goto et al . 1998 ).…”

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confidence: 99%

Insulin‐like Growth Factor (IGF)‐I affects parasite growth and host cell migration in experimental cutaneous leishmaniasis

Gomes¹,

Goto

Matta³

et al. 2000

Int J Experimental Path

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While the control or progression of leishmaniasis depends on host immune responses, the initial inflammatory process represents a key event. This process involves the participation of several cytokines and growth factors induced during inflammation as well as factors already present at the site of infection such as insulin-like growth factor (IGF)-I. We have previously demonstrated a potential role for IGF-I in experimental cutaneous leishmaniasis based on the significant increase in lesion size seen in mice injected with Leishmania promastigotes preactivated with IGF-I. In the present study we show that preactivation of Leishmania (Leishmania) amazonensis promastigotes with IGF-I induces an increase in the actual number of parasites at the lesion site from seven days postinfection, in addition to a more intense inflammatory infiltrate. There was a higher numerical density of polymorphonuclear neutrophils from 3 to 24 h, and of mononuclear cells from 48 h of infection onward. A higher density of polymorphonuclear neutrophils and mononuclear cells harboring parasites was also observed. The most important observation, however, was that more parasites per cell were present, revealing that IGF-I appears to favour parasite growth within the macrophages. These results strongly suggest an important role for IGF-I in the development of cutaneous leishmaniasis, where it influences both the inflammatory process and parasite growth.

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Insulin-like growth factor I is a growth-promoting factor forLeishmaniapromastigotes and amastigotes

Cited by 33 publications

References 32 publications

Reactive Oxygen Species-Dependent Cell Signaling Regulates the Mosquito Immune Response to Plasmodium falciparum

Reactive Oxygen Species-Dependent Cell Signaling Regulates the Mosquito Immune Response to Plasmodium falciparum

Immunity and immunosuppression in experimental visceral leishmaniasis

Insulin‐like Growth Factor (IGF)‐I affects parasite growth and host cell migration in experimental cutaneous leishmaniasis

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