Association between Toxoplasma gondii types and outcomes of human infection: A meta-analysis

Xia, Jing; Cheng, Xinyu; Wang, Xiaojun; Peng, Hong‐Juan

doi:10.1556/030.64.2017.016

Cited by 12 publications

(9 citation statements)

References 44 publications

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“…Although there was no relationship between T. gondii infection and AD determined in the present study, we believe that reproduction of the study with other genotypes of T. gondii would be a positive contribution to the literature. Xia et al [31] observed in the study they conducted in 2017 that different T. gondii species demonstrate different virulence levels and cause different results in humans. Studies with a larger sample size investigating various species of T. gondii are required to extend the findings of the current study.…”

Section: Resultsmentioning

confidence: 99%

S100B and Latent Toxoplasmosis in Alzheimer’s disease

Ayyıldız¹

2019

Int J Med Biochem

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A lzheimer's disease (AD) is a fatal neurodegenerative disorder characterized by progressive neuronal loss and loss of cognitive function. AD is the most common type of dementia and its prevalence is approximately 10% after 90 years of age [1]. The number of cases worldwide in 2005 was 47 million and it is expected to be 131 million in the year 2050 [2]. Although neuronal loss and brain dysfunction is well known in AD, its pathogenic mechanism is not fully clear. Studies in the literature have focused on 3 pathological conditions in patients with AD: amyloid plaques, neurofibrillary tangles, and astrogliosis [3-5]. The development of amyloid plaques is related to the pathologies of astrocytes [6], and this condition may be induced by neurotoxic molecules, cytokine secretion, or the activation of the complement system [7]. Toxoplasma gondii is a protozoan parasite that infects both animals and humans. In humans it is usually transmitted through the ingestion of the oocyst, which can be found in cat feces, or undercooked meat containing tissue cysts [8]. Due to the high neurotrophic effects of the parasite, the most affected body tissue in a case of chronic infection is the brain [9]. This infection causes neurodegenerative changes related to neuronal inflammation in the central nervous system (CNS) [10]. Neural degeneration caused by neuroinflammation is known to be the basis of the pathogenesis in chronic neurodegenerative Objectives: Alzheimer's disease (AD) is a fatal, multifactorial neurodegenerative disorder characterized by progressive neuronal loss and the loss of cognitive function. The etiology has not yet been fully elucidated. It has been suggested in some studies that central nervous system infections may play a role in the development of Alzheimer's disease. The aim of the present study was to investigate a possible relationship with a latent Toxoplasma gondii (T. gondii) infection in astrocytes and S100 proteins released as a result of astrocyte damage. Methods: A total of 33 patients with AD and 32 healthy individuals were included in this study. There were 16 Toxoplasma-negative and 17 Toxoplasma-positive patients in the AD group, and 15 Toxoplasma-negative and 17 Toxoplasmapositive individuals in the control group. Results: There were no statistically significant differences between the groups in terms of mean age or gender. An inter-group comparison of the subjects revealed that the S100B level was higher in patients with AD than in the control group (p<0.05). There was no statistically significant difference between the groups in terms of the T. gondii immunoglobulin G test (p>0.05). Conclusion: In our study, although there was no relationship between T. gondii infection and AD, significantly higher levels of S100B in patients with AD suggest that this protein may be important both in diagnosis and in possible treatment processes. The authors suggest that reproduction of the current study using different genotypes of T. gondii would further contribute to knowledge of the etiology of AD.

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Section: Resultsmentioning

confidence: 99%

S100B and Latent Toxoplasmosis in Alzheimer’s disease

Ayyıldız¹

2019

Int J Med Biochem

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“…T. gondii exists as many strains, which belong to clonal lineages or present atypical or recombinant genetics; these strains are often distinguished on virulence, defined by rates of migration, invasion, and replication in vitro, and lethal dose 100 in vivo in mice [31]. Both virulent and avirulent strains commonly cause human ocular toxoplasmosis [32]. In keeping, we observed the proliferating phenotype in human retinal pigment epithelial cells exposed to virulent (GT-1) or avirulent (DEG) T. gondii strains.…”

Section: Discussionmentioning

confidence: 99%

Molecular Basis of The Retinal Pigment Epithelial Changes That Characterize The Ocular Lesion in Toxoplasmosis

et al. 2019

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When a person becomes infected with Toxoplasma gondii, ocular toxoplasmosis is the most common clinical presentation. The medical literature describes retinitis with surrounding hyperpigmentation secondary to proliferative changes in the retinal pigment epithelium, which is sufficiently characteristic that investigation often is not needed to make the diagnosis. We aimed to establish the frequency of “typical” ocular toxoplasmosis and delineate its molecular basis. Among 263 patients presenting consecutively with ocular toxoplasmosis to Ribeirão Preto General Hospital in Brazil, where T. gondii infection is endemic, 94.2% of 345 eyes had retinal hyperpigmentation. In ARPE-19 and primary human retinal pigment epithelial cell monolayers exposed to minimal numbers of T. gondii tachyzoites, the proliferation marker–KI-67–was increased in uninfected cells, which also were rendered more susceptible to infection. RT-qPCR and ELISA detected increased expression of vascular endothelial growth factor A (VEGF) and insulin-like growth factor (IGF)1, and decreased expression of thrombospondin (TSP)1 by infected cells. Blockade of VEGF and IGF1—or supplementation of TSP1—reversed the proliferation phenotype in uninfected cells. Our findings confirm that hyperpigmentation is a characteristic feature of retinitis in ocular toxoplasmosis, and demonstrate that T. gondii-infected human retinal pigment epithelial cells secrete VEGF and IGF1, and reduce production of TSP1, to promote proliferation of adjacent uninfected cells and create this disease-specific appearance.

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“…This reflects not only the ability of T. gondii to evade the immune system and establish a latent infection but also the heterogeneity of T. gondii strains in the clinical population [138]. Strains noticeably differ in virulence, clinical outcomes, and prevalence between regions [139,140]. In North America and Europe, approximately 90% of reported samples can be classified into one of three intercontinental clonal lineages (types I, II, and III) which exhibit approximately 1-2% differences at the nucleotide level [141,142].…”

Section: Toxoplasma Gondiimentioning

confidence: 99%

“…Moreover, a great deal of diversity has arisen in South America as a result of atypical and recombinant strains, and as such clonal lineage prevalence is low [140]. In humans, type II strains (e.g., typified by the isolates Prugniaud and ME49) are strongly associated with infection irrespective of clinical presentation; however, differences in virulence have been suggested due to associations of type I and type III strains with cerebral and pulmonary toxoplasmosis, respectively [139]. The vast diversity between strains exemplifies the need to study T. gondii virulence effectors, how clinical outcomes vary between strains, and increase awareness of prevention strategies in regions with high T. gondii seroprevalence.…”

Section: Toxoplasma Gondiimentioning

confidence: 99%

Catastrophic consequences: can the feline parasite Toxoplasma gondii prompt the purrfect neuroinflammatory storm following traumatic brain injury?

Baker

Sun

Semple

et al. 2020

J Neuroinflammation

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Traumatic brain injury (TBI) is one of the leading causes of morbidity and mortality worldwide; however, treatment development is hindered by the heterogenous nature of TBI presentation and pathophysiology. In particular, the degree of neuroinflammation after TBI varies between individuals and may be modified by other factors such as infection. Toxoplasma gondii, a parasite that infects approximately one-third of the world's population, has a tropism for brain tissue and can persist as a lifelong infection. Importantly, there is notable overlap in the pathophysiology between TBI and T. gondii infection, including neuroinflammation. This paper will review current understandings of the clinical problems, pathophysiological mechanisms, and functional outcomes of TBI and T. gondii, before considering the potential synergy between the two conditions. In particular, the discussion will focus on neuroinflammatory processes such as microglial activation, inflammatory cytokines, and peripheral immune cell recruitment that occur during T. gondii infection and after TBI. We will present the notion that these overlapping pathologies in TBI individuals with a chronic T. gondii infection have the strong potential to exacerbate neuroinflammation and related brain damage, leading to amplified functional deficits. The impact of chronic T. gondii infection on TBI should therefore be investigated in both preclinical and clinical studies as the possible interplay could influence treatment strategies.

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Association between Toxoplasma gondii types and outcomes of human infection: A meta-analysis

Cited by 12 publications

References 44 publications

S100B and Latent Toxoplasmosis in Alzheimer’s disease

S100B and Latent Toxoplasmosis in Alzheimer’s disease

Molecular Basis of The Retinal Pigment Epithelial Changes That Characterize The Ocular Lesion in Toxoplasmosis

Catastrophic consequences: can the feline parasite Toxoplasma gondii prompt the purrfect neuroinflammatory storm following traumatic brain injury?

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