Differential Regulation of the Immune Response in the Spleen and Liver of Mice Infected with<i>Leishmania donovani</i>

Bankoti, Rashmi; Stäger, Simona

doi:10.1155/2012/639304

Cited by 44 publications

(52 citation statements)

References 72 publications

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“…Accordingly, immune responses develop differently in the two organs which may in part explain the different gene expression patterns that we observed in liver and spleen. Spleen immunity to L donovani is less well understood compared to that of the liver, but splenomegaly and L donovani parasite persistence and propagation have been intimately associated with elevated IL‐10 in both humans and animals . The regulatory cytokines IL‐10 and TGF‐β are known to be induced by helminths and facilitate establishment of chronic infection .…”

Section: Discussionmentioning

confidence: 86%

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Intestinal nematode infection exacerbates experimental visceral leishmaniasis

Classon

Feng

Eidsmo

et al. 2019

Parasite Immunology

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Summary Leishmania donovani exposure often results in subclinical infection in immunocompetent individuals, and the factors dictating development of visceral leishmaniasis (VL) are not known. Infection with intestinal worms skew immunity towards type 2 and regulatory responses, thereby theoretically increases susceptibility to intracellular infections controlled by type 1 responses. Here we have tested how chronic infection with the intestinal nematode Heligmosomoides polygyrus affected immunity to a secondary infection with L donovani. We found that mice infected with H polygyrus displayed higher Leishmania burden in liver and spleen compared to worm‐free animals. This increased infectious load was accompanied by reduced leucocyte infiltration and nos2 transcription in livers and increased il4 and il10 transcription in spleens. Collectively, these data show that chronic infection with intestinal nematodes skew immune responses in a way that may favour development of VL.

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Section: Discussionmentioning

confidence: 86%

“…Leishmania donovani infection of mice causes an acute and subsequently controlled infection in the liver which results in hepatic resistance against further infection . In the spleen on the other hand, parasites slowly continue to proliferate and can persist throughout the lifespan of the mouse .…”

Section: Discussionmentioning

confidence: 99%

Intestinal nematode infection exacerbates experimental visceral leishmaniasis

Classon

Feng

Eidsmo

et al. 2019

Parasite Immunology

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“…Once in the liver, the development of cell-mediated immune responses is essential for the clearance of L. infantum parasites. In contrast, the spleen ultimately becomes the site of parasite persistence [63], [81], [82], suggesting that it is more susceptible to L. infantum infection than the liver [83]. Interestingly, the leishmanicidal efficacy of hepatic granulomas is dependent on their degree of maturation [63], [84], [85].…”

Section: Discussionmentioning

confidence: 99%

Development of Novel Prime-Boost Strategies Based on a Tri-Gene Fusion Recombinant L. tarentolae Vaccine against Experimental Murine Visceral Leishmaniasis

et al. 2013

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Visceral leishmaniasis (VL) is a vector-borne disease affecting humans and domestic animals that constitutes a serious public health problem in many countries. Although many antigens have been examined so far as protein- or DNA-based vaccines, none of them conferred complete long-term protection. The use of the lizard non-pathogenic to humans Leishmania (L.) tarentolae species as a live vaccine vector to deliver specific Leishmania antigens is a recent approach that needs to be explored further. In this study, we evaluated the effectiveness of live vaccination in protecting BALB/c mice against L. infantum infection using prime-boost regimens, namely Live/Live and DNA/Live. As a live vaccine, we used recombinant L. tarentolae expressing the L. donovani A2 antigen along with cysteine proteinases (CPA and CPB without its unusual C-terminal extension (CPB-CTE)) as a tri-fusion gene. For DNA priming, the tri-fusion gene was encoded in pcDNA formulated with cationic solid lipid nanoparticles (cSLN) acting as an adjuvant. At different time points post-challenge, parasite burden and histopathological changes as well as humoral and cellular immune responses were assessed. Our results showed that immunization with both prime-boost A2-CPA-CPB-CTE-recombinant L. tarentolae protects BALB/c mice against L. infantum challenge. This protective immunity is associated with a Th1-type immune response due to high levels of IFN-γ production prior and after challenge and with lower levels of IL-10 production after challenge, leading to a significantly higher IFN-γ/IL-10 ratio compared to the control groups. Moreover, this immunization elicited high IgG1 and IgG2a humoral immune responses. Protection in mice was also correlated with a high nitric oxide production and low parasite burden. Altogether, these results indicate the promise of the A2-CPA-CPB-CTE-recombinant L. tarentolae as a safe live vaccine candidate against VL.

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“…In experimental models, control of infection is mediated by a polarized Th1 response, induced by an initial production of IL-12 by DCs (75). IFN-γ secreting CD4 and CD8 T cells contribute to parasite control by enhancing the ability of phagocytic cells to kill intracellular Leishmania (74, 76). …”

Section: Protozoan Parasites and Ifn-imentioning

confidence: 99%

Protozoan Parasites and Type I IFNs

Silva‐Barrios¹,

Stäger²

2017

Front. Immunol.

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For many years, the role of interferon (IFN)-I has been characterized primarily in the context of viral infections. However, regulatory functions mediated by IFN-I have also been described against bacterial infections and in tumor immunology. Only recently, the interest in understanding the immune functions mediated by IFN-I has dramatically increased in the field of protozoan infections. In this review, we discuss the discrete role of IFN-I in the immune response against major protozoan infections: Plasmodium, Leishmania, Trypanosoma, and Toxoplasma.

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Differential Regulation of the Immune Response in the Spleen and Liver of Mice Infected withLeishmania donovani

Cited by 44 publications

References 72 publications

Intestinal nematode infection exacerbates experimental visceral leishmaniasis

Intestinal nematode infection exacerbates experimental visceral leishmaniasis

Development of Novel Prime-Boost Strategies Based on a Tri-Gene Fusion Recombinant L. tarentolae Vaccine against Experimental Murine Visceral Leishmaniasis

Protozoan Parasites and Type I IFNs

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