Toxoplasma gondii: The severity of toxoplasmic encephalitis in C57BL/6 mice is associated with increased ALCAM and VCAM-1 expression in the central nervous system and higher blood–brain barrier permeability

Silva, Neide Maria da; Manzan, Roberto Martins; Carneiro, Wesley Pereira; Milanezi, Cristiane M.; Silva, João; Ferro, Eloísa Amália Vieira; Mineo, José Roberto

doi:10.1016/j.exppara.2010.04.019

Cited by 51 publications

(45 citation statements)

References 60 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…T. gondii -infected DXM-treated C57BL/6 mice presented similar symptoms as do untreated mice in the same period of infection. As demonstrated previously C57BL/6 mice presented higher parasite load in the brain than BALB/c mice, on days 32 [33] and 56 p.i., despite not statistically significant. DXM treatment induced an increase in brain tissue parasitism in C57BL/6 mice in parallel with a decreasing in tissue inflammation.…”

Section: Discussionsupporting

confidence: 83%

Toxoplasma gondii 70 kDa Heat Shock Protein: Systemic Detection Is Associated with the Death of the Parasites by the Immune Response and Its Increased Expression in the Brain Is Associated with Parasite Replication

et al. 2014

Self Cite

View full text Add to dashboard Cite

The heat shock protein of Toxoplasma gondii (TgHSP70) is a parasite virulence factor that is expressed during T. gondii stage conversion. To verify the effect of dexamethasone (DXM)-induced infection reactivation in the TgHSP70-specific humoral immune response and the presence of the protein in the mouse brain, we produced recombinant TgHSP70 and anti-TgHSP70 IgY antibodies to detect the protein, the specific antibody and levels of immune complexes (ICs) systemically, as well as the protein in the brain of resistant (BALB/c) and susceptible (C57BL/6) mice. It was observed higher TgHSP70-specific antibody titers in serum samples of BALB/c compared with C57BL/6 mice. However, the susceptible mice presented the highest levels of TgHSP70 systemically and no detection of specific ICs. The DXM treatment induced increased parasitism and lower inflammatory changes in the brain of C57BL/6, but did not interfere with the cerebral parasitism in BALB/c mice. Additionally, DXM treatment decreased the serological TgHSP70 concentration in both mouse lineages. C57BL/6 mice presented high expression of TgHSP70 in the brain with the progression of infection and under DXM treatment. Taken together, these data indicate that the TgHSP70 release into the bloodstream depends on the death of the parasites mediated by the host immune response, whereas the increased TgHSP70 expression in the brain depends on the multiplication rate of the parasite.

show abstract

Section: Discussionsupporting

confidence: 83%

Toxoplasma gondii 70 kDa Heat Shock Protein: Systemic Detection Is Associated with the Death of the Parasites by the Immune Response and Its Increased Expression in the Brain Is Associated with Parasite Replication

et al. 2014

Self Cite

View full text Add to dashboard Cite

show abstract

“…Plasmodium species incapable of forming knobs in infected erythrocytes (knobless Plasmodium) show a passive adhesion of infected RBCs to activated endothelial cells [75]. Thus, knobless Plasmodium activates endothelial cells to the same extent as knob-forming Plasmodium [66,73], which suggests that ECM may also be induced by parasitized erythrocytes.…”

Section: Inflammatory Components In the Development Of Cerebral Malariamentioning

confidence: 99%

“…A main characteristic of brain anatomy is the presence of the BBB, which confers protection against circulating cell diapedesis into brain tissue. Nevertheless, the BBB composition of postcapillary venules allows leukocyte diapedesis during non-malarial brain injury [65,66]. However, leukocytes are not observed within brain tissue during CM2 [62,67], suggesting an indirect contribution of these cells to the development of cerebral malaria.…”

Section: Inflammatory Components In the Development Of Cerebral Malariamentioning

confidence: 99%

Multiple Organ Dysfunction During Severe Malaria: The Role of the Inflammatory Response

Souza¹,

Pádua²,

Henriques³

2016

Current Topics in Malaria

View full text Add to dashboard Cite

Severe malaria is a systemic illness characterized by the dysfunction of one or more peripheral organs, such as the lungs [acute respiratory distress syndrome (ARDS)] and kidneys [acute kidney injury (AKI)]. Several clinical and experimental studies suggest that features of the inflammatory response are related to the multi-organ dysfunction observed in severe malaria. Our group has been dedicated to studying the roles of proand anti-inflammatory mediators in the multi-organ dysfunction observed in experimental severe malaria, especially in the lungs, kidneys, and brain. Herein, we explore severe malaria as a pathology derived from intense inflammatory responses in different organs and further distinguish and compare these organ-specific inflammatory responses. The pathophysiological mechanism of severe malaria is not fully elucidated; however, it is important to study it as a complex inflammatory response assembled by different actors, each one orchestrating a different mechanism.

show abstract

“…The extracellular parasite can also migrate through multiple tissue layers of the human retina [11]. Infection enhances the expression of the host adhesion molecules ICAM-1, VCAM-1, and ALCAM in the CNS [6,12]. In particular, ICAM-1 interacts with MIC2 to facilitate the migration of extracellular tachyzoites across epithelium [13] and retinal endothelium [8] without disrupting monolayer integrity.…”

Section: Introductionmentioning

confidence: 98%

“…Within days after oral infection of mice with tissue cysts, T. gondii can be detected both inside monocytes and as extracellular parasites in the blood [5]. Systemic inflammation is characteristic of in vivo T. gondii infection, and increased BBB permeability has been associated with the development of toxoplasmic encephalitis [6]. Ultimately, the parasites enter the brain parenchyma and establish a chronic infection as bradyzoite-containing tissue cysts.…”

Section: Introductionmentioning

confidence: 98%

From the blood to the brain: avenues of eukaryotic pathogen dissemination to the central nervous system

Ueno

Lodoen

2015

Current Opinion in Microbiology

View full text Add to dashboard Cite

Toxoplasma gondii: The severity of toxoplasmic encephalitis in C57BL/6 mice is associated with increased ALCAM and VCAM-1 expression in the central nervous system and higher blood–brain barrier permeability

Cited by 51 publications

References 60 publications

Toxoplasma gondii 70 kDa Heat Shock Protein: Systemic Detection Is Associated with the Death of the Parasites by the Immune Response and Its Increased Expression in the Brain Is Associated with Parasite Replication

Toxoplasma gondii 70 kDa Heat Shock Protein: Systemic Detection Is Associated with the Death of the Parasites by the Immune Response and Its Increased Expression in the Brain Is Associated with Parasite Replication

Multiple Organ Dysfunction During Severe Malaria: The Role of the Inflammatory Response

From the blood to the brain: avenues of eukaryotic pathogen dissemination to the central nervous system

Contact Info

Product

Resources

About