Involvement of tumor necrosis factor-α during infection of human monocytic cells by Toxoplasma gondii

Belloni, Aline; Aubert, Dominique; Marín, Jorge Enrique Gómez; Naour, Richard Le; Bonhomme, A.; Guenounou, Moncef; Pinon, J. M.

doi:10.1007/s004360050685

Cited by 15 publications

(11 citation statements)

References 19 publications

(11 reference statements)

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“…34,35 TNF-alpha also contributes to the protection of human monocytic THP-1 cell lines against T. gondii. 36 In in vivo studies with the neutralization of TNF-alpha, fatal encephalitis occurs as a result of reactivation of the latent infection 37 and TNF-alpha was seen to be involved in the prevention of the encephalitis. 38 TNF-alpha along with TNFR1 also presents a protective function in toxoplasmosis.…”

Section: Discussionmentioning

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: Discussionmentioning

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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“…On the other hand, reports have shown that T. gondii-infected macrophages are blocked for production of IL-12 and TNF-αthat are induced by LPS [3,5,13,14]. T. gondii soluble antigen or crude lysates have been shown incapable of inducing IL-12 or TNF-αpro-duction in human monocytes [14,15].…”

Section: Discussionmentioning

confidence: 99%

Suppressed Production of Pro-inflammatory Cytokines by LPS-Activated Macrophages after Treatment with Toxoplasma gondii Lysate

et al. 2008

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During Toxoplasma gondii infection, macrophages, dendritic cells, and neutrophils are important sources of pro-inflammatory cytokines from the host. To counteract the pro-inflammatory activities, T. gondii is known to have several mechanisms inducing down-regulation of the host immunity. In the present study, we analyzed the production of proand anti-inflammatory cytokines from a human myelomonocytic cell line, THP-1 cells, in response to treatment with T. gondii lysate or lipopolysaccharide (LPS). Treatment of THP-1 cells with LPS induced production of IL-12, TNF-α , IL-8, and IL-10. Co-treatment of THP-1 cells with T. gondii lysate inhibited the LPS-induced IL-12, IL-8 and TNF-αexpression, but increased the level of IL-10 synergistically. IL-12 and IL-10 production was down-regulated by anti-human toll-like receptor (TLR)-2 and TLR4 antibodies. T. gondii lysate triggered nuclear factor (NF)-κ B-dependent IL-8 expression in HEK293 cells transfected with TLR2. It is suggested that immunosuppression induced by T. gondii lysate treatment might occur via TLR2-mediated NF-κ B activation.

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“…Treatment of T. gondii-infected monocytes with IFN␥ in combination with LPS reduces the invasion index of T. gondii due to the production of TNF␣. However, a significant decrease in TNF␣ secretion is seen in response to IFN␥/LPS in T. gondii-infected monocytes, in comparison with uninfected cells (18). In addition, active invasion of the parasite is required to mediate the suppression of TNF␣ production in macrophages (19).…”

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confidence: 99%

Roles of Glycosylphosphatidylinositols of Toxoplasma gondii

Debierre‐Grockiego¹,

Azzouz²,

Schmidt³

et al. 2003

Journal of Biological Chemistry

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Toxoplasma gondii is a ubiquitous parasitic protozoan, which causes congenital infectious diseases as well as severe encephalitis, a major cause of death among immune-deficient persons, such as AIDS patients. T. gondii is normally controlled by the immune system of healthy individuals, leading to an asymptomatic infection. T. gondii triggers early cytokine production, which, to a certain extent, protects the host against replication of tachyzoites, the infective form of the parasite. Glycosylphosphatidylinositols (GPIs) constitute a class of glycolipids that have various functions, the most fundamental being to link proteins to eucaryotic cell membranes. GPIs are involved in the pathogenicity of other protozoan parasites and are known to induce tumor necrosis factor-␣ (TNF␣) production. We show that GPIs highly purified from T. gondii tachyzoites, as well as their core glycans, induce TNF␣ production in macrophages. A chemically synthesized GPI of T. gondii lacking its lipid moiety, GPIa, has the same effect as the natural GPIs, whereas a chemically synthesized molecule with dialkylglycerol instead of diacylglycerol as lipid moiety, GPIb, does not induce TNF␣ production. Moreover, GPIb inhibits the TNF␣ production induced by T. gondii GPI or by GPIa. The core glycan prepared from the two chemically synthesized molecules activates macrophages, showing that the lipid moiety may regulate signaling. Stimulation of macrophages with GPIs of T. gondii results in activation of the transcription factor NF-B, which is inhibited by the chemically synthesized GPIb, suggesting the involvement of NF-B in TNF␣ gene expression. Our results support the idea that T. gondii GPIs are bioactive factors that participate in the production of TNF␣ during toxoplasmal pathogenesis.

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Involvement of tumor necrosis factor-α during infection of human monocytic cells by Toxoplasma gondii

Cited by 15 publications

References 19 publications

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

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

Suppressed Production of Pro-inflammatory Cytokines by LPS-Activated Macrophages after Treatment with Toxoplasma gondii Lysate

Roles of Glycosylphosphatidylinositols of Toxoplasma gondii

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