Efficient control of <i>Plasmodium yoelii</i> infection in BALB/c and C57BL/6 mice with pre‐existing <i>Strongyloides ratti</i> infection

Kolbaum, Julia; Eschbach, Marie‐Luise; Steeg, Christiane; Jacobs, Thomas; Fleischer, Bernhard; Breloer, Minka

doi:10.1111/j.1365-3024.2012.01369.x

Cited by 6 publications

(6 citation statements)

References 37 publications

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“…Some cases of human Malaria and VL co-infection were described in the past and recently in different parts of the world ( Yoeli, 1948 ; Ab Rahman and Abdullah, 2011 ; van den Bogaart et al, 2012 , 2014 ; Bin Mohanna, 2015 ), demonstrating that co-infection may occur more frequently than we would expect. An increasing amount of evidence shows that co-infections may affect the natural outcome and progression of diseases due to the modulation of immune response ( La Flamme et al, 2002 ; Kolbaum et al, 2012 ; Qi et al, 2013 ; van den Bogaart et al, 2014 ). In the present study, we established a co-infection model of American CL and a non-lethal murine Malaria and demonstrated that co-infection is able to affect the pathogenesis and outcome of both diseases.…”

Section: Discussionmentioning

confidence: 99%

“…Rodent Malaria parasites provide great models to investigate pathogenesis and immune mechanisms during infection ( Li et al, 2001 ; Zuzarte-Luis et al, 2014 ). The non-lethal strain 17XNL of P. yoelii generally causes a transient disease with moderate parasitaemia, weight loss, splenomegaly, hypothermia, and anemia ( Coleman et al, 1988b ; Kobayashi et al, 1996 ; Niikura et al, 2008 ; Kolbaum et al, 2012 ; Karadjian et al, 2014 ). In our study, BALB/c mice infected with blood-stage P. yoelii 17XNL develop a self-limiting infection with mild parasitaemia that resolve in 4 weeks.…”

Section: Discussionmentioning

confidence: 99%

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Malaria-Cutaneous Leishmaniasis Co-infection: Influence on Disease Outcomes and Immune Response

et al. 2016

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Malaria and Cutaneous Leishmaniasis (CL) are co-endemic throughout large regions in tropical countries and co-infection may impact the evolution of host-parasite interactions. In the present study, we evaluate Malaria/Leishmaniasis disease outcome, Th1/Th2 cytokine levels and the CD4 and CD8 T-cell profiles in a co-infection murine model (BALB/c) of Plasmodium yoelii 17XNL (Py) and Leishmania amazonensis (La) or L. braziliensis (Lb). Malaria parasitaemia was assessed through blood strains stained with Giemsa. Leishmania lesions were monitored with a digital caliper and parasite loads determined by limiting-dilution assay. Serum levels of IFN-γ, TNF, IL-2, IL-4, IL-6, IL-10, and IL-17 were determined using multiplexed bead assay and expression of CD3, CD4, and CD8 T-cells markers were determined by Flow Cytometry in the thymus, spleens and lymph nodes. Parasitaemia in Lb+Py co-infected group was lower than in Py single-infected group, suggesting a protective effect of Lb co-infection in Malaria progression. In contrast, La+Py co-infection increased parasitaemia, patent infection and induced mortality in non-lethal Malaria infection. Regarding Leishmaniasis, Lb+Py co-infected group presented smaller lesions and less ulceration than Lb single-infected animals. In contrast, La+Py co-infected group presented only a transitory delay on the development of lesions when compared to La single-infected mice. Decreased levels of IFN-γ, TNF, IL-6, and IL-10 were observed in the serum of co-infected groups, demonstrating a modulation of Malaria immune response by Leishmania co-infections. We observed an intense thymic atrophy in Py single-infected and co-infected groups, which recovered earlier in co-infected animals. The CD4 and CD8 T cell profiles in thymus, spleens and lymph nodes did not differ between Py single and co-infected groups, except for a decrease in CD4+CD8+ T cells which also increased faster in co-infected mice. Our results suggest that Py and Leishmania co-infection may change disease outcome. Interestingly Malaria outcome can be altered according to the Leishmania specie involved. Alternatively Malaria infection reduced the severity or delayed the onset of leishmanial lesions. These alterations in Malaria and CL development seem to be closely related with changes in the immune response as demonstrated by alteration in serum cytokine levels and thymus/spleens T cell phenotypes dynamics during infection.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Malaria-Cutaneous Leishmaniasis Co-infection: Influence on Disease Outcomes and Immune Response

et al. 2016

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“…In contrast, in C57BL/6 mice coinfected at day 6, parasitemia level and body weight were not altered. Interestingly, the Th2-type immune response induced by Sr was significantly reduced upon Py NXL coinfection [152]. In addition, Py NXL clearance was not affected by previous infection with Sr in either C57BL/6 or BALB/c mice.…”

Section: Experimental Models Of Coinfectionmentioning

confidence: 99%

Helminth Parasites Alter Protection againstPlasmodiumInfection

Salazar-Castañón

Legorreta-Herrera

Rodrı́guez-Sosa

2014

BioMed Research International

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More than one-third of the world's population is infected with one or more helminthic parasites. Helminth infections are prevalent throughout tropical and subtropical regions where malaria pathogens are transmitted. Malaria is the most widespread and deadliest parasitic disease. The severity of the disease is strongly related to parasite density and the host's immune responses. Furthermore, coinfections between both parasites occur frequently. However, little is known regarding how concomitant infection with helminths and Plasmodium affects the host's immune response. Helminthic infections are frequently massive, chronic, and strong inductors of a Th2-type response. This implies that infection by such parasites could alter the host's susceptibility to subsequent infections by Plasmodium. There are a number of reports on the interactions between helminths and Plasmodium; in some, the burden of Plasmodium parasites increased, but others reported a reduction in the parasite. This review focuses on explaining many of these discrepancies regarding helminth-Plasmodium coinfections in terms of the effects that helminths have on the immune system. In particular, it focuses on helminth-induced immunosuppression and the effects of cytokines controlling polarization toward the Th1 or Th2 arms of the immune response.

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“…Interestingly, IL-4 and IL-10 deficiency was necessary to reverse the obstructing effect of H. polygyrus infection on the CD8 + T cell response toward Toxoplasma (Marple et al, 2017). The majority of co-infection studies despite being protozoan, viral or bacterial infection, have focused on infections with helminth first due to their ability to downmodulate immune responses (Rousseau et al, 1997; Liesenfeld et al, 2004; Chen et al, 2005, 2006; Graham et al, 2005; Su et al, 2005, 2014a,b; Weng et al, 2007; Khan et al, 2008; Noland et al, 2008; Miller et al, 2009; Frantz et al, 2010; Dias et al, 2011; Potian et al, 2011; Kolbaum et al, 2012; du Plessis et al, 2013; Osborne et al, 2014; Budischak et al, 2015; Coomes et al, 2015; Gondorf et al, 2015; Rafi et al, 2015; Obieglo et al, 2016). In light of the fact, that Th2 immunity against helminths is an ongoing challenge in humans and livestock, we aimed to investigate how a previous protozoan infection affects the development of Th2 responses in CD4 + T cells and protection against helminths.…”

Section: Introductionmentioning

confidence: 99%

Toxoplasma Co-infection Prevents Th2 Differentiation and Leads to a Helminth-Specific Th1 Response

Ahmed

French

Kühl³

et al. 2017

Front. Cell. Infect. Microbiol.

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Nematode infections, in particular gastrointestinal nematodes, are widespread and co-infections with other parasites and pathogens are frequently encountered in humans and animals. To decipher the immunological effects of a widespread protozoan infection on the anti-helminth immune response we studied a co-infection with the enteric nematode Heligmosomoides polygyrus in mice previously infected with Toxoplasma gondii. Protective immune responses against nematodes are dependent on parasite-specific Th2 responses associated with IL-4, IL-5, IL-13, IgE, and IgG1 antibodies. In contrast, Toxoplasma gondii infection elicits a strong and protective Th1 immune response characterized by IFN-γ, IL-12, and IgG2a antibodies. Co-infected animals displayed significantly higher worm fecundity although worm burden remained unchanged. In line with this, the Th2 response to H. polygyrus in co-infected animals showed a profound reduction of IL-4, IL-5, IL-13, and GATA-3 expressing T cells. Co-infection also resulted in the lack of eosinophilia and reduced expression of the Th2 effector molecule RELM-β in intestinal tissue. In contrast, the Th1 response to the protozoan parasite was not diminished and parasitemia of T. gondii was unaffected by concurrent helminth infection. Importantly, H. polygyrus specific restimulation of splenocytes revealed H. polygyrus-reactive CD4+ T cells that produce a significant amount of IFN-γ in co-infected animals. This was not observed in animals infected with the nematode alone. Increased levels of H. polygyrus-specific IgG2a antibodies in co-infected mice mirrored this finding. This study suggests that polarization rather than priming of naive CD4+ T cells is disturbed in mice previously infected with T. gondii. In conclusion, a previous T. gondii infection limits a helminth-specific Th2 immune response while promoting a shift toward a Th1-type immune response.

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Efficient control of Plasmodium yoelii infection in BALB/c and C57BL/6 mice with pre‐existing Strongyloides ratti infection

Cited by 6 publications

References 37 publications

Malaria-Cutaneous Leishmaniasis Co-infection: Influence on Disease Outcomes and Immune Response

Malaria-Cutaneous Leishmaniasis Co-infection: Influence on Disease Outcomes and Immune Response

Helminth Parasites Alter Protection againstPlasmodiumInfection

Toxoplasma Co-infection Prevents Th2 Differentiation and Leads to a Helminth-Specific Th1 Response

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