Microglia and macrophages as innate producers of interferon-gamma in the brain following infection with Toxoplasma gondii

2005 ◽  
Vol 35 (1) ◽  
pp. 83-90 ◽  
Author(s):  
Yasuhiro Suzuki ◽  
Jennifer Claflin ◽  
Xisheng Wang ◽  
Andrea Lengi ◽  
Takane Kikuchi
2010 ◽  
Vol 107 (2) ◽  
pp. 424-424 ◽  
Author(s):  
David Lester

In a sample of 20 European nations, the prevalence of the brain parasite Toxoplasma gondii was positively associated with national suicide rates for men and women.


2017 ◽  
Vol 1 (6) ◽  
pp. 563-572 ◽  
Author(s):  
Pierre-Mehdi Hammoudi ◽  
Dominique Soldati-Favre

Typically illustrating the ‘manipulation hypothesis’, Toxoplasma gondii is widely known to trigger sustainable behavioural changes during chronic infection of intermediate hosts to enhance transmission to its feline definitive hosts, ensuring survival and dissemination. During the chronic stage of infection in rodents, a variety of neurological dysfunctions have been unravelled and correlated with the loss of cat fear, among other phenotypic impacts. However, the underlying neurological alteration(s) driving these behavioural modifications is only partially understood, which makes it difficult to draw more than a correlation between T. gondii infection and changes in brain homeostasis. Moreover, it is barely known which among the brain regions governing fear and stress responses are preferentially affected during T. gondii infection. Studies aiming at an in-depth dissection of underlying molecular mechanisms occurring at the host and parasite levels will be discussed in this review. Addressing this reminiscent topic in the light of recent technical progress and new discoveries regarding fear response, olfaction and neuromodulator mechanisms could contribute to a better understanding of this complex host–parasite interaction.


2021 ◽  
Author(s):  
Oscar A. Mendez ◽  
Emiliano Flores Machado ◽  
Jing Lu ◽  
Anita A. Koshy

AbstractToxoplasma gondii is an intracellular parasite that causes a long-term latent infection of neurons. Using a custom MATLAB-based mapping program in combination with a mouse model that allows us to permanently mark neurons injected with parasite proteins, we found that Toxoplasma-injected neurons (TINs) are heterogeneously distributed in the brain, primarily localizing to the cortex followed by the striatum. Using immunofluorescence co-localization assays, we determined that cortical TINs are commonly (>50%) excitatory neurons (FoxP2+) and that striatal TINs are often (>65%) medium spiny neurons (MSNs) (FoxP2+). As MSNs have highly characterized electrophysiology, we used ex vivo slices from infected mice to perform single neuron patch-clamping on striatal TINs and neighboring uninfected MSNs (bystander MSNs). These studies demonstrated that TINs have highly abnormal electrophysiology, while the electrophysiology of bystander MSNs was akin to that of MSNs from uninfected mice. Collectively, these data offer new neuroanatomic and electrophysiologic insights into CNS toxoplasmosis.


2014 ◽  
Vol 38 (1) ◽  
pp. 92-98
Author(s):  
Mohammed J. Alwan

The current study was performed an investigation in seropositive stray cats with Toxoplasma gondii and to correlate the results of pathological lesions with seropositive results of the cats. To achieve these goals, fifty blood samples and specimens from internal organs (liver, spleen, brain, kidney, intestine and lung) of stray cats were collected from different area of Baghdad Province during the period 1.10.2011-1.10.2012. Seropositive ELISA-IgG was demonstrated that 66 % of stray cats while female expressed (75 %) of seropositive ELISA-IgG were higher than male (30% ) and animals with average age 2months showed high percentage of seropositive ELISA-IgG (100%) as compared with age (adult cat) that expressed( 63.82 %) of seropositive. There was a significant difference (P≤0.01) among positive cases to anti-Toxoplasma ELISA-IgG. Severe pathological lesions were noticed in the lungs ,livers and intestines of animals that expressed high (optical density) (OD) of anti-Toxoplasma IgG ,in addition ,tachyzoits intracytoplasm of alveolar macrophages and hepatocytes as well as free zoites in alveolar space of the lung, were reported. Local necrosis with tachyzoites was seen in the brain of the cats, in addition to mineralization. On bases of the presence of pathological lesions in cats that expressed seropositive anti-Toxoplasma antibodies, it can be conclude that T.gondii is responsible for the appearance of inflammatory reaction in the internal organs of cats and there is a correlation between seropositive and pathological lesions of T.gondii infection and this parasite is highly distributed in Baghdad stray cats and it may be an important cause of abortion in the women.


2020 ◽  
Vol 88 (4) ◽  
Author(s):  
Rachel S. Coombs ◽  
Matthew L. Blank ◽  
Elizabeth D. English ◽  
Yaw Adomako-Ankomah ◽  
Ifeanyi-Chukwu Samuel Urama ◽  
...  

ABSTRACT Rodents are critical for the transmission of Toxoplasma gondii to the definitive feline host via predation, and this relationship has been extensively studied as a model for immune responses to parasites. Neospora caninum is a closely related coccidian parasite of ruminants and canines but is not naturally transmitted by rodents. We compared mouse innate immune responses to N. caninum and T. gondii and found marked differences in cytokine levels and parasite growth kinetics during the first 24 h postinfection (hpi). N. caninum-infected mice produced significantly higher levels of interleukin-12 (IL-12) and interferon gamma (IFN-γ) by as early as 4 hpi, but the level of IFN-γ was significantly lower or undetectable in T. gondii-infected mice during the first 24 hpi. “Immediate” IFN-γ and IL-12p40 production was not detected in MyD88−/− mice. However, unlike IL-12p40−/− and IFN-γ−/− mice, MyD88−/− mice survived N. caninum infections at the dose used in this study. Serial measures of parasite burden showed that MyD88−/− mice were more susceptible to N. caninum infections than wild-type (WT) mice, and control of parasite burdens correlated with a pulse of serum IFN-γ at 3 to 4 days postinfection in the absence of detectable IL-12. Immediate IFN-γ was partially dependent on the T. gondii mouse profilin receptor Toll-like receptor 11 (TLR11), but the ectopic expression of N. caninum profilin in T. gondii had no impact on early IFN-γ production or parasite proliferation. Our data indicate that T. gondii is capable of evading host detection during the first hours after infection, while N. caninum is not, and this is likely due to the early MyD88-dependent recognition of ligands other than profilin.


Parasitology ◽  
1997 ◽  
Vol 115 (1) ◽  
pp. 15-20 ◽  
Author(s):  
J. P. DUBEY

The persistence of Toxoplasma gondii tissue cysts in organs of cats (definitive host) and rodents (intermediate hosts) was studied. Nine cats, 12 rats, and 12 mice were fed T. gondii oocysts and their organs were digested in pepsin and then bioassayed for bradyzoites in mice. Of 9 cats killed 37 or 51 days after feeding 102 (2 cats), 103 (3 cats) or 104 (4 cats) oocysts of the VEG strain, tissue cysts were found in each cat; in the tongue of 9, in the heart of 5, in the brain of 4, and in the eyes of 1 cat. The dose had no effect on the distribution of tissue cysts in cats. Twelve rats were each fed 105 oocysts of the VEG strain of T. gondii and killed 21, 29, 64 or 237 days later. At each time-period, 11 tissues of 3 rats were pooled and bioassayed in mice. Tissue cysts were found in the brain, skeletal muscle, heart and kidneys of rats at each killing time; in the lungs, intestines, and mesenteric lymph nodes in 3 of 4 instances; in the tongue, liver, and eyes in 2 instances and in the spleen in 1 instance. Also, using the same procedures and sampling the same 11 tissues as used for rats, tissue cysts were seen in all organs except in the tongue and liver of 3 mice killed on day 82 after feeding the VEG strain. In 9 mice (3 with each strain) fed oocysts of the ME-49, GT-1, or P89 T. gondii strain and killed 62–130 days later, tissue cysts were found consistently only in the brain. Thus, in rats and mice, most tissue cysts were found in the brain and rarely in the tongue. This was in marked contrast to the distribution of tissue cysts in cats.


2014 ◽  
Vol 142 ◽  
pp. 51-58 ◽  
Author(s):  
Alexandre A. Tonin ◽  
Aleksandro S. Da Silva ◽  
Emerson A. Casali ◽  
Stephanie S. Silveira ◽  
Cesar E.J. Moritz ◽  
...  
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2020 ◽  
Vol 42 (6) ◽  
Author(s):  
Hae‐Ji Kang ◽  
Ki‐Back Chu ◽  
Su‐Hwa Lee ◽  
Min‐Ju Kim ◽  
Hyunwoo Park ◽  
...  

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