Nitric oxide production increases during Toxoplasma gondii encephalitis in mice

Dinçel, Güngör Çağdaş; Atmaca, Hasan

doi:10.1016/j.exppara.2015.06.009

Cited by 43 publications

(47 citation statements)

References 57 publications

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“…The squash smear technique was used to identify T . gondii tissue cysts in all sacrificed animals as previously described by Dincel and Atmaca . Briefly, five randomly selected small pieces taken from fresh brain tissue were placed onto poly‐L‐lysine‐coated glass slides.…”

Section: Methodsmentioning

confidence: 99%

Increased expressions of ADAMTS‐13 and apoptosis contribute to neuropathology during Toxoplasma gondii encephalitis in mice

Dinçel

Atmaca

2015

Neuropathology

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Toxoplasma gondii (T. gondii) is a protozoan parasite with the potential of causing severe encephalitis among immunocompromised humans and animals. Our previous study showed that T. gondii induces high nitric oxide (NO) production, high glial activation (GFAP) and neurofilament expressions, leading to severe neurodegeneration in toxoplasma encephalitis (TE) in the central nervous system (CNS). The aim of this experimental study was to investigate ADAMTS-13 expression and apoptosis in CNS and to identify whether they have any correlation with toxoplasmosis neuropathology and neurodegeneration. Mice were infected with ME49 strain T. gondii and the levels of ADAMTS-13, caspase 3, caspase 8, caspase 9, TNFR1 and Bcl-xL expressions were examined in brain tissues by immunohistochemistry, during the development and establishment of chronic infections at 10, 30 and 60 days post-infection. Results of the study revealed that the levels of ADAMTS-13 (P < 0.005), caspase 3 (P < 0.05), caspase 8 (P < 0.05), caspase 9 (P < 0.005) and TNFR1 (P < 0.05) expressions in the brain markedly increased while Bcl-xL expression decreased (P < 0.005). The most prominent finding from our study was that 10, 30 and 60 days post-infection ADAMTS-13 increased significantly and this may play an important role in the regulation and protection of the blood-brain barrier integrity and CNS microenvironment in TE. These results also suggest that T. gondii-mediated apoptosis might play a pivotal role and a different type of role in the mechanism of neurodegeneration and neuropathology in the process of TE. Furthermore, expression of ADAMTS-13 might give an idea of the progress and is critical for diagnosis of this disease. To the best of the authors' knowledge, this is the first report on ADAMTS-13 expression in the CNS of T. gondii-infected mice.

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Section: Methodsmentioning

confidence: 99%

Increased expressions of ADAMTS‐13 and apoptosis contribute to neuropathology during Toxoplasma gondii encephalitis in mice

Dinçel

Atmaca

2015

Neuropathology

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“…13 Five representative fields were selected under high-power view and consequtive pictures were captured by the Leica QWin Plus v3 software by a 20× objective (Leica Microsystems Imaging Solutions) at a setting identical to the image system for analysing. For examining the staining of each antibody, we used the same setting for all slides.…”

Section: Histomorphometric Analysis and Statisticsmentioning

confidence: 99%

Role of oxidative stress in the pathophysiology of Toxoplasma gondii infection

Dinçel

Atmaca

2016

Int J Immunopathol Pharmacol

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Oxidative stress (OS) plays an essential role in the pathogenesis of common neurodegenerative diseases. We have previously shown that Toxoplasma gondii (T. gondii) induces high nitric oxide (NO) production, glial activation, and apoptosis that altogether cause severe neuropathology in toxoplasma encephalitis (TE). The objective of this study was to investigate the cytotoxic effect of OS and to identify a correlation between the causes of T. gondii induced neuropathology. Expression levels of glutathione reductase (GR), Cu/Zn superoxide dismutase (SOD1), neuron specific enolase (NSE), and 8-hydroxy-2'-deoxyguanosine (8-OHdG) were investigated. Results of the study revealed that the levels of GR (P <0.005) and NSE (P <0.001) expression in the brain tissue markedly increased while SOD1 activity decreased (P <0.001) in the infected group compared to the non-infected group. In addition, intense staining for 8-OHdG (P <0.05) was observed both in the nucleus and the cytoplasm of neurons and glial cells that underwent OS. These results were reasonable to suggest that T. gondii-mediated OS might play a pivotal role and a different type of role in the mechanism of neurodegeneration/neuropathology in the process of TE. The results also clearly indicated that increased levels of NO and apoptosis might contribute to OS-related pathogenesis of TE. As a result, OS and expression of NSE might give an idea of the disease progress and may have a critical diagnostic significance for patients with T. gondii infection.

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“…The most important mechanism is coming from high affinity of T. gondii to the excitable tissues including nervous system where the parasite forms tissue cysts. Recent evidence indicates that previous opinion regarding the silent status of the parasite in the brain is not true; rather T. gondii has a dynamic status inside the cysts (Watts et al, 2015[32]) thereby can change the function of the neurons by modulation of some neurotransmitters including GABA (Brooks et al, 2015[7]), dopamine (Babaie et al, 2017[3]), serotonin (Gatkowska et al, 2013[17]), noradrenaline (Gatkowska et al, 2013[17]), nitric oxide (Tonin et al, 2014[31]; Dincel and Atmaca 2015[10]), and glutamate (Kannan et al, 2016[21]). Moreover, serum level of pro-inflammatory cytokines also increases during T. gondii infection (Bottari et al, 2015[6]), which contribute to neuropathology of toxoplasmosis.…”

Section: Discussionmentioning

confidence: 99%