Anionic Sites, Fucose Residues and Class I Human Leukocyte Antigen Fate During Interaction of Toxoplasma gondii with Endothelial Cells

Stumbo, Ana Carolina; Barbosa, Helene Santos; Carvalho, Técia Maria Ulisses de; Pôrto, Luís Cristóvão; Carvalho, Laís de

doi:10.1590/s0074-02762002000400012

Cited by 6 publications

(5 citation statements)

References 22 publications

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“…In congenital toxoplasmosis, infection of endothelial cells lining the umbilical cord and the placental blood vessels by the parasite is potentially the major transmission route to the fetus [767]. T. gondii invades and proliferates in HUVEC where it resides in parasitophorous vacuoles (PV), and at the time of PV formation, the cell surface anionic sites and fucose residues (human endothelial cells contain exposed fucose residues) are excluded, while HLA class I molecules are present only on a minority of the parasite-containing vacuoles.…”

Section: T Gondii Infectionmentioning

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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Section: T Gondii Infectionmentioning

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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“…T. gondii binds and infects retinal‐brain endothelial cells, bovine umbilical vein endothelial cells (BUVEC) and human endothelium in vitro , leading to BBB activation. In retinal EC and BUVEC, T. gondii induces increases in transcripts for E‐, P‐selectin, VCAM‐1 and ICAM‐1 within 1–4 h and inflammatory mediators including GRO1, MCP‐1, Fractalkine, RANTES, IL8, IP10, MCP‐1, GM‐CSF, COX2 and iNOS persist at least up to 72 h post infection (Daubener et al ., 2001; Stumbo et al ., 2002; Smith et al ., 2004; Knight et al ., 2005; Taubert et al ., 2006a,b). Once T. gondii crosses the BBB, subsequent microglial infection and astrocyte activation can then have a negative effect on the BBB leading to activation and loss of integrity (Silva et al ., 2010; Dellacasa‐Lindberg et al ., 2011).…”

Section: Bbb Activation By Other Pathogensmentioning

confidence: 99%

How can microbial interactions with the blood-brain barrier modulate astroglial and neuronal function?

Grab

Chakravorty

Heyde

et al. 2011

Cellular Microbiology

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SummaryThe vascular endothelium of the blood-brain barrier (BBB) is regarded as a part of the neurovascular unit (NVU). This emerging NVU concept emphasizes the need for homeostatic signalling among the neuronal, glial and vascular endothelial cellular compartments in maintaining normal brain function. Conversely, dysfunction in any component of the NVU affects another, thus contributing to disease. Brain endothelial activation and dysfunction is observed in various neurological diseases, such as (ischemic) stroke, seizure, brain inflammation and infectious diseases and likely contributes to or exacerbates neurological conditions. The role and impact of brain endothelial factors on astroglial and neuronal activation is unclear. Similarly, it is not clear which stages of BBB endothelial activation can be considered beneficial versus detrimental. Although the BBB plays an important role in context of encephalopathies caused by neurotropic microbes that must first penetrate into the brain, a crucial role of the BBB in contributing to neurological dysfunction may be seen in cerebral malaria (CM), where the Plasmodium parasite remains sequestered in the brain vasculature, does not enter the brain parenchyma, and yet causes coma and seizures. In this minireview some of the scenarios and factors that may play a role in BBB as a relay station to modulate astroneuronal functioning are discussed

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“…During congenital toxoplasmosis, infection of the endothelial cells lining the umbilical cord blood vessels is probably the main transmission route to the fetus (Woodman et al, 1991). T. gondii is an obligate intracellular pathogen, replicating within a specialized membrane-bounded cytoplasmic vacuole designated as parasitophorous vacuole (PV) formed in the cytoplasm of nearly all cell types (Carruthers and Boothroyd, 2007;Morisaki et al, 1995;Stumbo et al, 2002).…”

Section: Introductionmentioning

confidence: 99%

“…Once inside the host cell, the parasite avoids host cell defenses in order to meet its requirements for feeding and reproduction (Carruthers, 2002;Martin et al, 2007). The PV membrane (PVM) incorporates components from both the host cell and the parasite, thus establishing a hybrid membrane (Carvalho and de Souza, 1989;Pacheco-Soares and De Souza, 1998;Stumbo et al, 2002). T. gondii PVM exhibits a high affinity interaction with host cell endoplasmic reticulum and mitochondria in a process termed PVM-organelle association (de Melo et al, 1992;Sinai et al, 1997), once the NH 2 -terminal domain of ROP2, a parasite protein localized in PVM, is also suggested as having characteristics of a mitochondrial target signal (Sinai and Joiner, 2001).…”

Section: Introductionmentioning

confidence: 99%

Mitochondrial localization of non‐histone protein HMGB1 during human endothelial cell–Toxoplasma gondii infection

Stumbo

Cortez

Rodrigues

et al. 2008

Cell Biology International

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Toxoplasma gondii is an obligate intracellular pathogen, replicating only within a specialized membrane-bounded cytoplasmic vacuole, the parasitophorous vacuole (PV), which interacts with host cell mitochondria. High mobility group box 1 (HMGB1), a known nuclear transcription factor, also may be involved in pathological conditions, whose function is to signal tissue damage. Using confocal microscopy, we have investigated the localization of HMGB1 and the mitochondria performance during interaction between human umbilical vein endothelial cells (HUVEC) and Toxoplasma. Immunofluorescence showed HMGB1 localization in HUVEC tubular mitochondria stained with Mito Tracker (MT). At 2h post-infection, MT labeled spherical structures scattered throughout the cytoplasm and HMGB1 were still present. After 24h of infection, long and tubular structures were localized around PVs and were double labeled by MT and HMGB1, suggesting a structural reorganization of the mitochondria over a long period of infection. For the first time, these results show there is HMGB1 in HUVEC mitochondria and that this protein could be playing a part in mitochondrial DNA events which are important for fission and fusion processes reported here during HUVEC-T. gondii infection.

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Anionic Sites, Fucose Residues and Class I Human Leukocyte Antigen Fate During Interaction of Toxoplasma gondii with Endothelial Cells

Cited by 6 publications

References 22 publications

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

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

How can microbial interactions with the blood-brain barrier modulate astroglial and neuronal function?

Mitochondrial localization of non‐histone protein HMGB1 during human endothelial cell–Toxoplasma gondii infection

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