INFECTION OF C57BL/6 MICE BY<i>TRYPANOSOMA MUSCULI</i>MODULATES HOST IMMUNE RESPONSES DURING<i>BRUCELLA ABORTUS</i>COCOLONIZATION

Lowry, Jake E.; Leonhardt, Jack A.; Yao, Chaoqun; Belden, E. L.; Andrews, Gerard P.

doi:10.7589/2013-03-080

Cited by 5 publications

(7 citation statements)

References 28 publications

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“…Were an effective vaccine available, feedgrounds could facilitate an annual ‘doctor's visit’ to reduce contagion and risk. Unfortunately, the tools developed for use in cattle have yet to overcome either the immunological differences of elk, or some other unknown element such as co-infection [ 39 ]. Vaccine-development efforts are further constrained by the Select Agent status designated to B. abortus in the USA, which increases the regulations associated with handling live Brucella cultures.…”

Section: Adaptive Managementmentioning

confidence: 99%

“…Cytokines, which are cell-signalling proteins that mediate a host's anti-parasitic response, can be modulated by parasites themselves, and thus have been proposed as a useful way to gauge interactions like competition or synergism between co-infecting parasites [37]. Some evidence for synergism between B. abortus and the weakly pathogenic Trypanosoma cervi, with which Wyoming elk are chronically infected [38], has recently emerged [39]. Both appear to share a strategy in which they upregulate host production of the cytokine interleukin-10 (IL-10), which can impair immune response and facilitate chronic infections [40][41][42][43].…”

Section: (B) Intraspecific Transmission In Elkmentioning

confidence: 99%

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Winter feeding of elk in the Greater Yellowstone Ecosystem and its effects on disease dynamics

Cotterill

Cross

Cole

et al. 2018

Phil. Trans. R. Soc. B

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Providing food to wildlife during periods when natural food is limited results in aggregations that may facilitate disease transmission. This is exemplified in western Wyoming where institutional feeding over the past century has aimed to mitigate wildlife–livestock conflict and minimize winter mortality of elk (Cervus canadensis). Here we review research across 23 winter feedgrounds where the most studied disease is brucellosis, caused by the bacterium Brucella abortus. Traditional veterinary practices (vaccination, test-and-slaughter) have thus far been unable to control this disease in elk, which can spill over to cattle. Current disease-reduction efforts are being guided by ecological research on elk movement and density, reproduction, stress, co-infections and scavengers. Given the right tools, feedgrounds could provide opportunities for adaptive management of brucellosis through regular animal testing and population-level manipulations. Our analyses of several such manipulations highlight the value of a research–management partnership guided by hypothesis testing, despite the constraints of the sociopolitical environment. However, brucellosis is now spreading in unfed elk herds, while other diseases (e.g. chronic wasting disease) are of increasing concern at feedgrounds. Therefore experimental closures of feedgrounds, reduced feeding and lower elk populations merit consideration.This article is part of the theme issue ‘Anthropogenic resource subsidies and host–parasite dynamics in wildlife’.

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Section: Adaptive Managementmentioning

confidence: 99%

Section: (B) Intraspecific Transmission In Elkmentioning

confidence: 99%

Winter feeding of elk in the Greater Yellowstone Ecosystem and its effects on disease dynamics

Cotterill

Cross

Cole

et al. 2018

Phil. Trans. R. Soc. B

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“…Blood parasites are not eliminated in T cell-deprived mice, blood parasite evolution is modified by nutrition and, curiously, previously infected pregnant mothers quickly became parasitemic (13,17,18). T. musculi modulates the host immune response in coinfection with various infectious agents (19). T. musculi can be considered an appropriate model of a hostparasite relationship.…”

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confidence: 99%

Trypanosoma musculi Infection in Mice Critically Relies on Mannose Receptor–Mediated Arginase Induction by a TbKHC1 Kinesin H Chain Homolog

Nzoumbou‐Boko

Muylder

Semballa

et al. 2017

The Journal of Immunology

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Arginase activity induction in macrophages is an escape mechanism developed by parasites to cope with the host's immune defense and benefit from increased host-derived growth factor production. We report that arginase expression and activity were induced in macrophages during mouse infection by , a natural parasite of this host. This induction was reproduced in vitro by excreted/secreted factors of the parasite. A mAb directed toKHC1, an orphan kinesin H chain from , inhibited excreted/secreted factor-mediated arginase induction. Anti-KHC1 Ab also inhibited growth, both in vitro and in vivo. Induction of arginase activity and parasite growth involved C-type lectin receptors, because mannose injection decreased arginase activity induction and parasite load in vitro and in vivo. Accordingly, the parasite load was reduced in mice lacking mannose receptor C-type 1. The KHC1 homolog showed high similarity with KHC1. Bioinformatics analysis revealed the presence of homologs of this gene in other trypanosomes, including pathogens for humans and animals. Host metabolism dysregulation represents an effective parasite mechanism to hamper the host immune response and modify host molecule production to favor parasite invasion and growth. Thus, this orphan kinesin plays an important role in promoting trypanosome infection, and its neutralization or the lock of its partner host molecules offers promising approaches to increasing resistance to infection and new developments in vaccination against trypanosomiasis.

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“…To the best of our knowledge, neither T. brucei nor T. cruzi infection has been previously associated with an increased response to unrelated pathogens. A study by Lowry et al (42) compared the course of B. abortus S19 in control and Trypanosoma musculi -infected mice. In striking contrast with our results, Lowry et al showed that T. musculi favor B. abortus infection by suppressing the IFNγ response.…”

Section: Discussionmentioning

confidence: 99%

Trypanosoma Infection Favors Brucella Elimination via IL-12/IFNγ-Dependent Pathways

et al. 2017

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This study develops an original co-infection model in mice using Brucella melitensis, the most frequent cause of human brucellosis, and Trypanosoma brucei, the agent of African trypanosomiasis. Although the immunosuppressive effects of T. brucei in natural hosts and mice models are well established, we observed that the injection of T. brucei in mice chronically infected with B. melitensis induces a drastic reduction in the number of B. melitensis in the spleen, the main reservoir of the infection. Similar results are obtained with Brucella abortus- and Brucella suis-infected mice and B. melitensis-infected mice co-infected with Trypanosoma cruzi, demonstrating that this phenomenon is not due to antigenic cross-reactivity. Comparison of co-infected wild-type and genetically deficient mice showed that Brucella elimination required functional IL-12p35/IFNγ signaling pathways and the presence of CD4+ T cells. However, the impact of wild type and an attenuated mutant of T. brucei on B. melitensis were similar, suggesting that a chronic intense inflammatory reaction is not required to eliminate B. melitensis. Finally, we also tested the impact of T. brucei infection on the course of Mycobacterium tuberculosis infection. Although T. brucei strongly increases the frequency of IFNγ+CD4+ T cells, it does not ameliorate the control of M. tuberculosis infection, suggesting that it is not controlled by the same effector mechanisms as Brucella. Thus, whereas T. brucei infections are commonly viewed as immunosuppressive and pathogenic, our data suggest that these parasites can specifically affect the immune control of Brucella infection, with benefits for the host.

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INFECTION OF C57BL/6 MICE BYTRYPANOSOMA MUSCULIMODULATES HOST IMMUNE RESPONSES DURINGBRUCELLA ABORTUSCOCOLONIZATION

Cited by 5 publications

References 28 publications

Winter feeding of elk in the Greater Yellowstone Ecosystem and its effects on disease dynamics

Winter feeding of elk in the Greater Yellowstone Ecosystem and its effects on disease dynamics

Trypanosoma musculi Infection in Mice Critically Relies on Mannose Receptor–Mediated Arginase Induction by a TbKHC1 Kinesin H Chain Homolog

Trypanosoma Infection Favors Brucella Elimination via IL-12/IFNγ-Dependent Pathways

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