Secreted Toxoplasma gondii molecules interfere with expression of MHC-II in interferon gamma-activated macrophages

Leroux, Louis‐Philippe; Dasanayake, Dayal; Rommereim, Leah M.; Fox, Barbara A.; Bzik, David J.; Jardim, Armando; Dzierszinski, Florence

doi:10.1016/j.ijpara.2015.01.003

Cited by 30 publications

(24 citation statements)

References 125 publications

(166 reference statements)

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“…Unfortunately, the mechanisms and the net fitness effects remain to be investigated for virtually all described cases of host manipulation. Multiple parasites of insects have been speculated to secrete chemical compounds for host manipulation (Libersat et al, 2009), T. gondii secretes peptides that interact in multiple ways with the host immune system (Leroux et al, 2015), and even the release of small RNAcontaining vesicles has been reported for the filarial parasite Brugia malayi (Zamanian et al, 2015). However, the detailed nature of these molecules and their modes of action in the host remain to be identified.…”

Section: Physiological Mechanismsmentioning

confidence: 99%

Host Manipulation by Parasites: Cases, Patterns, and Remaining Doubts

Heil

2016

Front. Ecol. Evol.

106

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Parasites must overcome host immunity and change hosts for dispersal. Therefore, seemingly odd behaviors of parasitized animals, like those exhibited by "Zombie ants" or the "fatal attraction" of mammals to their predators, have been explained as the extended phenotype of parasites that manipulate their hosts for transmission enhancement. Manipulation has evolved in all major phylogenetic lineages of parasites but is not ubiquitous. In fact, the real frequency and relevance of manipulation is still matter of debate. Here, I highlight some of the most pertinent questions that arise if we aim at a broader understanding of the ecological relevance and evolutionary trajectory of manipulating parasites. Why are more parasites with a trophic mode of transmission manipulating their host than horizontally transmitted parasites? Why are the causal agents of sexually transmitted diseases (STDs) so rarely reported to manipulate their host? Why do parasites of animals usually manipulate their intermediate host, whereas many pathogens of plants manipulate their final host and then cause a "fatal attraction" of herbivores to the already infected plant? How can we distinguish manipulation effects from adaptive host responses to parasitization? Does manipulation cause a cost to certain parasites that can select against the evolution of manipulation? More emphasis should be put on direct comparisons among parasites of animals, plants, and humans. Manipulation for transmission enhancement should be studied in concert with manipulation for host immunity suppression, the molecular mechanisms that control the manipulation effect need to be deciphered, and we should test for alternative explanations for the observed phenotypic changes. Finally, we should quantify transmission rates and net fitness for manipulating and non-manipulating parasites, in ecologically realistic setups, to identify the forces that select against the evolution of manipulation. Ultimately, parasite net fitness represents the relevant outcome of any manipulation effect.Keywords: immunity, malaria, partner manipulation, pathogen, plant-enemy interaction, STDs, toxoplasmosis "FATAL ATTRACTION" AND MANIPULATING PARASITES Parasites represent a ubiquitous aspect in the life of multicellular organisms (Wood and Johnson, 2015) and most, if not all, of us have experienced how strongly an infection can interfere with our normal activities and well-being. Therefore, it might not appear to be too surprising when parasitized hosts exhibit behavioral alterations (see Glossary) as compared to healthy conspecifics.

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Section: Physiological Mechanismsmentioning

confidence: 99%

Host Manipulation by Parasites: Cases, Patterns, and Remaining Doubts

Heil

2016

Front. Ecol. Evol.

106

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“…Based on all this, we searched existing excreted secreted antigen lists (15) for proteins predicted to have: 1) a signal sequence for export; 2) no transmembrane domain that might prevent translocation across the PVM; 3) a nuclear localization signal to mediate import into the host nucleus; and 4) either no orthologue in Neospora caninum or a very low level of similarity with such a gene. For the first two criteria, we used the predictions in ToxoDB (version 27, released Feb 19, 2016) and then confirmed these with the publically available prediction software Phobius (http://phobius.sbc.su.se/), a combined transmembrane topology and signal peptide predictor.…”

Section: Resultsmentioning

confidence: 99%

Toxoplasmacontrols host cyclin E expression through the use of a novel MYR1-dependent effector protein, HCE1

Panas

Naor

Cygan

et al. 2019

Preprint

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“…101211 and phycoerythrin (PE)-antimouse F4/80 antibody no. 123109 (BioLegend), as previously described (53).…”

Section: Discussionmentioning

confidence: 99%

Leishmania donovani Lipophosphoglycan Increases Macrophage-Dependent Chemotaxis of CXCR6-Expressing Cells via CXCL16 Induction

et al. 2019

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CXCL16 is a multifunctional chemokine that is highly expressed by macrophages and other immune cells in response to bacterial and viral pathogens; however, little is known regarding the role of CXCL16 during parasitic infections. The protozoan parasite Leishmania donovani is the causative agent of visceral leishmaniasis. Even though chemokine production is a host defense mechanism during infection, subversion of the host chemokine system constitutes a survival strategy adopted by the parasite. Here, we report that L. donovani promastigotes upregulate CXCL16 synthesis and secretion by bone marrow-derived macrophages (BMDM). In contrast to wild-type parasites, a strain deficient in the virulence factor lipophosphoglycan (LPG) failed to induce CXCL16 production. Consistent with this, cell treatment with purified L. donovani LPG augmented CXCL16 expression and secretion. Notably, the ability of BMDM to promote migration of cells expressing CXCR6, the cognate receptor of CXCL16, was augmented upon L. donovani infection in a CXCL16-and LPG-dependent manner. Mechanistically, CXCL16 induction by L. donovani required the activity of AKT and the mechanistic target of rapamycin (mTOR) but was independent of Toll-like receptor signaling. Collectively, these data provide evidence that CXCL16 is part of the inflammatory response elicited by L. donovani LPG in vitro. Further investigation using CXCL16 knockout mice is required to determine whether this chemokine contributes to the pathogenesis of visceral leishmaniasis and to elucidate the underlying molecular mechanisms.

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Secreted Toxoplasma gondii molecules interfere with expression of MHC-II in interferon gamma-activated macrophages

Cited by 30 publications

References 125 publications

Host Manipulation by Parasites: Cases, Patterns, and Remaining Doubts

Host Manipulation by Parasites: Cases, Patterns, and Remaining Doubts

Toxoplasmacontrols host cyclin E expression through the use of a novel MYR1-dependent effector protein, HCE1

Leishmania donovani Lipophosphoglycan Increases Macrophage-Dependent Chemotaxis of CXCR6-Expressing Cells via CXCL16 Induction

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