Ocular toxoplasmosis: the role of retinal pigment epithelium migration in infection

Tedesco, Roberto; Smith, Ricardo Luiz; Cortê-Real, Suzana; Calabrese, Kátia da Silva

doi:10.1007/s00436-003-1031-2

Cited by 25 publications

(31 citation statements)

References 12 publications

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“…These cells become hypertrophic, migrate to the retina, and appear to contain parasites (45,68,69). It has been suggested that this may represent an attempt at parasite eradication by retinal pigment epithelial cells (45). Our studies raise the possibility that the autophagy proteindependent antimicrobial activity induced by CD40 ligation in endothelial cells and retinal pigment epithelial cells may play a role in protection against T. gondii.…”

Section: Discussionmentioning

confidence: 58%

“…Retinal pigment epithelial cells (RPE) are another type of nonhematopoietic cell that is relevant to toxoplasmosis since RPE are thought to be effectors of resistance against ocular toxoplasmosis (45). We used primary mouse RPE and a human RPE (HRPE) cell line (ARPE-19) to examine the effects of CD40 ligation on the induction of anti-T. gondii activity.…”

Section: Resultsmentioning

confidence: 99%

“…Retinal pigment epithelial cells are thought to play an important role in ocular toxoplasmosis. These cells become hypertrophic, migrate to the retina, and appear to contain parasites (45,68,69). It has been suggested that this may represent an attempt at parasite eradication by retinal pigment epithelial cells (45).…”

Section: Discussionmentioning

confidence: 99%

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CD40 Induces Anti-Toxoplasma gondii Activity in Nonhematopoietic Cells Dependent on Autophagy Proteins

et al. 2013

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Section: Discussionmentioning

confidence: 58%

Section: Resultsmentioning

confidence: 99%

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CD40 Induces Anti-Toxoplasma gondii Activity in Nonhematopoietic Cells Dependent on Autophagy Proteins

et al. 2013

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“…In evidence, toxoplasmic retinochorioiditis affects straight the retina as a structure, but most damaged layers are nuclear plexiform and ganglion layers, as well as the segments of photoreceptor, once RPE presents a migration, causing a discontinuity forming great interstitial lacunae. Also is observed inflammatory cells in the inner plexiform layers, also responsible for none well function of retina tissue [11].…”

Section: Ocular Toxoplasmosismentioning

confidence: 98%

Experimental Models of Ocular Toxoplasmosis

Násare¹,

Tedesco²

2017

Toxoplasmosis

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First described in Ctenodactylus gundi and simultaneously in rabbit, Toxoplasma gondii, an etiological agent of toxoplasmosis, affects different species of vertebrates and invertebrates, presenting different manifestations depending on the host. Ocular toxoplasmosis is one of the mean manifestations of toxoplasmosis in humans, affecting 2% of infected individuals in Europe and North America. Otherwise many aspects of ocular toxoplasmosis still await answer. One of the major factors limiting this process is the difficulty to obtain human samples, doing necessary the use of experimental models. By the way, animal models do not express reality of human disease. The present study defines a compilation of report cases and results that supports the choice of an ideal experimental animal model of ocular toxoplasmosis. Actual literature bears new researches contributing in the choice of a specific experimental animal model. Moreover, the choice must consider behavior, period of life, and maintenance in captivity and ocular toxoplasmosis manifestation. Previous studies contribute for a best-chosen experimental animal model, by the way fragmented information makes difficult to compare mostly animal models picked that do not present efficiency enough. In conclusion, experimental animal models are able to bring relevant information about the course of ocular toxoplasmosis.

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“…a state characteristic for autistic patients) also have been demonstrated to cause parasite encystment in vitro [581,582] [595]; with own modification). important finding because retinopathy and other abnormalities were frequent complications reported in individuals with ocular toxoplasmosis [605][606][607], and cataracts have been demonstrated also in both streptozotocin-induced diabetic rats [608] and T1DM pediatric population [609]. Tedesco et al [607] demonstrated free parasites in the retinal vasculature, the presence of mononuclear inflammatory infiltrate and parasites in the vasculature of choroids in infected eyes.…”

Section: Vitamin D Deficiency Is Linked With Development Of Diabetes mentioning

confidence: 99%

T. gondii Infection Acquired during Pregnancy and/or after Birth may be Responsible for Development of both Type 1 and 2 Diabetes Mellitus

Pr¹,

ota²

2013

J Diabetes Metab

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Recently, it was suggested that maternal T and potentially B cells transferred during pregnancy and/or the breast milk feeding and their encounter with the antigen in mesenteric lymph nodes might play a role in development of type 1 diabetes mellitus (T1DM). T. gondii infection during gestation and/or after birth may be responsible for development of both T1DM and T2DM in children, adolescents and adults because: a) maternal microchimerism in peripheral blood was demonstrated to be significantly higher in patients with T1DM compared to unaffected siblings and healthy subjects, b) transmission of T. gondii as a Trojan horse in various types of eukaryotic cells, including T and B lymphocytes, c) swallowing by the fetus of amniotic fluid containing infected leukocytes and other cells, d) elimination of T. gondii in the breast milk during lactation, e) involvement of mesenteric lymph nodes after oral infection with the parasite, and f) damage of the myenteric neurons during infection with the parasite in both the animals with streptozotocin-induced diabetes and diabetic patients. Moreover, a significantly lower occurrence of antibodies against T. gondii found in the sera of patients with T1DM compared with their first-degree family members or healthy controls may be due to their T and/or B cell exhaustion perspective caused by chronic infection with the parasite. This suggestion may be supported by the finding that latent toxoplasmosis was associated with markedly reduced lymphocyte B-cell counts responsible for production of antibodies, markedly lower serum IgG, IgM, and IgA levels, and a significant suppression of IL-2. On the other hand, patients with T2DM had increased anti-T. gondii antibodies significantly more frequently than respective controls. Impaired vascular endothelial function characteristic for the patients with diabetes mellitus may be at least in part due to the preferential T. gondii infection of endothelial cells. Vitamin D and minocycline exerted beneficial effects on development and clinical course of diabetes mellitus probably because of their immunomodulatory and antitoxoplasmatic activities. These data strongly suggest that the parasite play an important role in development of both types of diabetes mellitus.

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Ocular toxoplasmosis: the role of retinal pigment epithelium migration in infection

Cited by 25 publications

References 12 publications

CD40 Induces Anti-Toxoplasma gondii Activity in Nonhematopoietic Cells Dependent on Autophagy Proteins

CD40 Induces Anti-Toxoplasma gondii Activity in Nonhematopoietic Cells Dependent on Autophagy Proteins

Experimental Models of Ocular Toxoplasmosis

T. gondii Infection Acquired during Pregnancy and/or after Birth may be Responsible for Development of both Type 1 and 2 Diabetes Mellitus

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