Infection withTrypanosoma lewisiorTrypanosoma musculimay promote the spread ofToxoplasma gondii

Gao, Jianhong; Yi, Siqi; Geng, Guo-Qing; Xu, Zhi-Shen; Hide, Geoff; Lun, Zhao‐Rong; Lai, De‐Hua

doi:10.1017/s0031182021000196

Cited by 4 publications

(6 citation statements)

References 30 publications

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Section: Discussionmentioning

confidence: 92%

“…If this was to be true co-infection rates observed in natural small mammal populations would be very reduced. At the same time, Gao and colleagues, [31] found that laboratory Norway rats infected with T. lewisi were more susceptible to T. gondii infections. Although this does not necessarily remain true for wild rodents, a fortiori for wild black rats, a T. lewisi -induced increased susceptibility to T. gondii would be expected to an increase in the proportions of co-infected animals [27–31].…”

Section: Discussionmentioning

confidence: 99%

“…At the same time, Gao and colleagues, [31] found that laboratory Norway rats infected with T. lewisi were more susceptible to T. gondii infections. Although this does not necessarily remain true for wild rodents, a fortiori for wild black rats, a T. lewisi -induced increased susceptibility to T. gondii would be expected to an increase in the proportions of co-infected animals [27–31]. Yet, this was not observed, thus rather suggesting very high mortality in co-infected animals, or no co-infection.…”

Section: Discussionmentioning

confidence: 99%

“…and Trypanosoma spp. For example T. lewisi can have immunosuppressive effects in rats and reduce their immune defenses against co-infectious parasites such as Toxoplasma gondii [27][28][29][30][31] whereas in mice, the immune response to T. gondii is enhanced following primary infection by Trypanosoma musculi [31]. If true in the wild, this would have important consequences for parasite ecology.…”

Section: Indeed Experimental Studies Have Shown Complex Co-infection ...mentioning

confidence: 99%

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Toxoplasma gondiiandTrypanosoma lewisiinfection in urban small mammals from Cotonou, Benin, with special emphasis on co-infection patterns

Etougbétché,

Houéménou,

Missihoun

et al. 2023

Preprint

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A growing number of studies has highlighted the importance of co-infections in eco-evolutionary processes underlying host-parasite interactions and the resulting epidemiology of zoonotic agents. Small mammals, and particularly rodents, are known to be important reservoirs of many zoonotic pathogens, such as Toxoplasma gondii and Trypanosoma lewisi that are responsible for toxoplasmosis and atypical trypanosomiasis in human, respectively. Laboratory experiments on rodent models have shown that primary infection with T. lewisi increases the host susceptibility to other co-infectious parasites, including T. gondii, following an alteration of the immune system. However, data on potential interactions between these parasites in wild small mammals remain scarce. In this study, we estimate the T. lewisi prevalence in 553 small mammals from four localities of Cotonou city, Benin. They were then combined with T. gondii data previously collected on the same individuals in order to investigate the influence of T. lewisi on T. gondii infection, and vice-versa, using cooccurrence tests and Generalized Linear Mixed Models. Despite quite high overall prevalence (32.5% and 15.2% for T. gondii and T. lewisi, respectively), we observed a clear and significant segregation between the two parasites. This may be explained by (i) differences in the species-specific susceptibility of small mammal host species to infection by these two parasites, with R. rattus and M. natalensis being the main reservoirs of T. lewisi while C. olivieri and M. m. domesticus are the main hosts for T. gondii; and/or by (ii) a possibly high mortality in co-infected animal in the wild. Although dedicated experimental studies are required to confirm this pattern, as they stand, our data fail to support that infection of small mammals by one of these two parasites favours widespread infection by the second one in nature.

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Section: Discussionmentioning

confidence: 92%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Indeed Experimental Studies Have Shown Complex Co-infection ...mentioning

confidence: 99%

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Toxoplasma gondiiandTrypanosoma lewisiinfection in urban small mammals from Cotonou, Benin, with special emphasis on co-infection patterns

Etougbétché,

Houéménou,

Missihoun

et al. 2023

Preprint

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“…By contrast, natural coinfection by T. gondii and T. cruzi has already been reported in a female red-necked wallaby that had sudden death but did not present clinical signs but microscopic and molecular analysis confirmed T. gondii cysts and T. cruzi genotype I ( 27 ). In an experimental study, T. lewisi infection increased the susceptibility of Sprague–Dawley rats to T. gondii infection, and this phenomenon was associated with the reduction in the production of nitric oxide (NO) and inducible nitric oxide synthase (iNOS) in peritoneal macrophages ( 28 ), important molecules for the control of T. gondii infection ( 29 ), favoring its dissemination in the host, showing that in situations of coinfection, the presence of a pathogen can favor infection by another pathogen.…”

Section: Introductionmentioning

confidence: 99%

Trypanosoma cruzi P21 recombinant protein modulates Toxoplasma gondii infection in different experimental models of the human maternal–fetal interface

de Souza,

Teixeira,

Fajardo Martínez

et al. 2023

Front. Immunol.

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IntroductionToxoplasma gondii is the etiologic agent of toxoplasmosis, a disease that affects about one-third of the human population. Most infected individuals are asymptomatic, but severe cases can occur such as in congenital transmission, which can be aggravated in individuals infected with other pathogens, such as HIV-positive pregnant women. However, it is unknown whether infection by other pathogens, such as Trypanosoma cruzi, the etiologic agent of Chagas disease, as well as one of its proteins, P21, could aggravate T. gondii infection.MethodsIn this sense, we aimed to investigate the impact of T. cruzi and recombinant P21 (rP21) on T. gondii infection in BeWo cells and human placental explants.ResultsOur results showed that T. cruzi infection, as well as rP21, increases invasion and decreases intracellular proliferation of T. gondii in BeWo cells. The increase in invasion promoted by rP21 is dependent on its binding to CXCR4 and the actin cytoskeleton polymerization, while the decrease in proliferation is due to an arrest in the S/M phase in the parasite cell cycle, as well as interleukin (IL)-6 upregulation and IL-8 downmodulation. On the other hand, in human placental villi, rP21 can either increase or decrease T. gondii proliferation, whereas T. cruzi infection increases T. gondii proliferation. This increase can be explained by the induction of an anti-inflammatory environment through an increase in IL-4 and a decrease in IL-6, IL-8, macrophage migration inhibitory factor (MIF), and tumor necrosis factor (TNF)-α production.DiscussionIn conclusion, in situations of coinfection, the presence of T. cruzi may favor the congenital transmission of T. gondii, highlighting the importance of neonatal screening for both diseases, as well as the importance of studies with P21 as a future therapeutic target for the treatment of Chagas disease, since it can also favor T. gondii infection.

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Novel insertions in the mitochondrial maxicircle of Trypanosoma musculi, a mouse trypanosome

et al. 2022

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Trypanosoma musculi is a, globally distributed, mouse-specific haemoflagellate, of the family Trypanosomatidae, which shares similar characteristics in morphology with Trypanosoma lewisi. The kinetoplast (mitochondrial) DNA of Trypanosomatidae flagellates is comprised of catenated maxicircles and minicircles. However, genetic information on the T. musculi kinetoplast remains largely unknown. In this study, the T. musculi maxicircle genome was completely assembled, with PacBio and Illumina sequencing, and the size was confirmed at 34 606 bp. It consisted of 2 distinct parts: the coding region and the divergent regions (DRs, DRI and II). In comparison with other trypanosome maxicircles (Trypanosoma brucei, Trypanosoma cruzi and T. lewisi), the T. musculi maxicircle has a syntenic distribution of genes and shares 73.9, 78.0 and 92.7% sequence identity, respectively, over the whole coding region. Moreover, novel insertions in MURF2 (630 bp) and in ND5 (1278 bp) were found, respectively, which are homologous to minicircles. These findings support an evolutionary scenario similar to the one proposed for insertions in Trypanosoma cruzi, the pathogen of American trypanosomiasis. These novel insertions, together with a deletion (281 bp) in ND4, question the role of Complex I in T. musculi. A detailed analysis of DRII indicated that it contains numerous repeat motifs and palindromes, the latter of which are highly conservative and contain A5C elements. The comprehensively annotated kinetoplast maxicircle of T. musculi reveals a high degree of similarity between this parasite and the maxicircle of T. lewisi and suggests that the DRII could be a valuable marker for distinguishing these evolutionarily related species.

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Infection withTrypanosoma lewisiorTrypanosoma musculimay promote the spread ofToxoplasma gondii

Abstract: Abstract

Cited by 4 publications

References 30 publications

Toxoplasma gondiiandTrypanosoma lewisiinfection in urban small mammals from Cotonou, Benin, with special emphasis on co-infection patterns

Toxoplasma gondiiandTrypanosoma lewisiinfection in urban small mammals from Cotonou, Benin, with special emphasis on co-infection patterns

Trypanosoma cruzi P21 recombinant protein modulates Toxoplasma gondii infection in different experimental models of the human maternal–fetal interface

Novel insertions in the mitochondrial maxicircle of Trypanosoma musculi, a mouse trypanosome

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