PENINGKATAN TNF-α DAN INDEKS APOPTOSIS PADA TULANG MENCIT YANG DIINFEKSI Toxoplasma gondii

Suwanti‬, ‪Lucia Tri; Mufasirin, M.

doi:10.21157/j.ked.hewan.v9i2.2808

Cited by 4 publications

(6 citation statements)

References 9 publications

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“…In this study, it showed that congenitally T. gondii infection induced increased expression of TNF-α and IFN-γ in the skull of pups. This discovery completed our previous studies that also showed that T. gondii infection increased expression of TNF-α and IFN-γ (Suwanti, 2006;Suwanti, 2008;Suwanti and Mufasirin, 2015).…”

Section: A B a B Discussionsupporting

confidence: 61%

“…However reduced or increased apoptosis from normal may result in a particular pathology (Favaloro et al, 2012). Previous studies showed that acute toxoplasmosis induced apoptosis in liver and spleen (Mordue et al, 2001), trophoblast (Suwanti et al, 2006) or femur (Suwanti and Mufasirin 2015). On the other hand, accoding to Mordue et al (2001) and Nishikawa et al (2007), apoptosis in toxoplasmosis occurs in noninfected cells.…”

Section: A B a B Discussionmentioning

confidence: 99%

“…Our previous study showed that pregnant mice infected by T.gondii displayed increased apoptosis of trophoblast and the trophoblasts apoptosis was associated with increased expression of FAS in the trophoblast and IFN-γ and TNF-α in decidual cells (Suwanti, 2005). Apoptosis that caused by T. gondii infection also occured in femur bone cells of mice and it was associated with increased TNF-α expression (Suwanti and Mufasirin, 2015).…”

Section: Introductionmentioning

confidence: 99%

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). Increased Apoptosis Skull of Pups Born to Toxoplasma Gondii-Infected Mice Associated With Increased Expression of Interferon Gamma, but Not Tumor Necrosis Factor Alfa

Suwanti¹,

Mufasirin²

2018

AJID

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Bacground: Toxoplasma gondii is an intracellular obligate protozoan parasite that infects most warm-blooded animals including humans. It can cause congenital infection with clinical symptoms ranging from mild to severe including microcephaly. At the cellular level, infection T. gondii causes apoptosis in some tissues and it is induced by proinflammatory cytokines, such as IFN-γ and TNF-α. The purpose of this study is to determine the role of proinflammatory cytokines (TNF-α and IFN-γ) to apoptosis skull of newborn from T. gondii-infected mice. Materials and Methods: Twenty pregnant mice were divided into two groups. The first group was the control group which was not infected with T. gondii tachizoites. The second group was the infected mice, which was infected with T. gondii tachizoites on the day 11.5 of gestation. All mice were cared until delivery. Subsequenly, pups of the mice were sacrificed and their skullcap tissues were taken for histological preparation. The tissues were stained by TUNEL Assay and IHC. Observed variables were apoptotic index and the percentage of skull cell expressing TNF-α and IFN-γ. Data were analyzed with t-test and regression. Results: Compared to the control group, the skull of the pups born to T. gondii-infected mice showed that the number of apoptotic index and percentage of expressing TNF-α and IFN-γ cells were higher than the control group. There is no correlation between increasing expression of TNF-α and apoptosis skull of pups. However, an increasing expression of IFN-γ affected the increased apoptosis of skull pups born to T.gondii-infected mice. Conclusion: Congenital toxoplasmosis in mice increased apoptotic index of skull and the apoptosis of skull associated with increasing expression of IFN-γ, but not associated with increasing expression of TNF-α.

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Section: A B a B Discussionsupporting

confidence: 61%

Section: A B a B Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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). Increased Apoptosis Skull of Pups Born to Toxoplasma Gondii-Infected Mice Associated With Increased Expression of Interferon Gamma, but Not Tumor Necrosis Factor Alfa

Suwanti¹,

Mufasirin²

2018

AJID

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“…It means that T. gondii infection inhibits the apoptosis process in the retina [Tabel 1 and Figure 2]. The decreasing of apoptosis index in this research may be the explanation about the failed development of the newborn mice retina [ Figure 1c] and it is different with the result of the previous research that T. gondii infection caused increasing apoptosis in the skull and brain of newborn mice [8,9].…”

Section: Vmic 2017mentioning

confidence: 54%

Inhibition of Apoptosis in Retinal of Newborn Mice Due to Congenital Toxoplasmosis

Suwanti

Mufasirin

Plumeriastuti

2017

KLS

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Toxoplasma gondii infection in pregnant women cause defects in the newborn, such as hydrocephalus and eye damaged, even blindness. Histologically damage due to congenital infection of T. gondii need to be examined. Twenty pregnant mice were divided into two groups which are the treatment group and the control group. Each mouse in treatment group was infected with 10 takizoit by intraperitoneal. Each of the newborn were sacrified, their head were taken and their eye tissue were fixed in 10% of buffered formalin and the histological sample were made in HE and TUNEL staining. The result showed that the retina of the eye of the newborn from infected mice damage. The damages include: hemorrhage, infected retinal cells, eye growth inhibition and decreased of apoptosis index of the retina cells. Keywords: Apoptosis in retinal, Newborn, Congenital Toxoplasmosis, Ocular Toxoplasmosis

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“…In pregnant mice infected by T. gondii, increased trophoblast apoptosis was observed and was associated with increased FAS expression in trophoblast cells and IFN-γ and TNF-α in decidual cells [5]. T. gondii infection-induced apoptosis was also observed in femur bone marrow cells of mice and was associated with increased TNF-α expression [6]. TNF-α, a multifunctional cytokine, has been detected in many tissues including ovary, oviduct, uterus, and placenta and is expressed in embryonic tissues.…”

Section: Introductionmentioning

confidence: 99%

Adenosine A3 Receptor Mediates ERK1/2- and JNK-Dependent TNF-α Production in Toxoplasma gondii-Infected HTR8/SVneo Human Extravillous Trophoblast Cells

Sun

et al. 2020

Korean J Parasitol

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Toxoplasma gondii is an intracellular parasite that causes severe disease when the infection occurs during pregnancy. Adenosine is a purine nucleoside involved in numerous physiological processes; however, the role of adenosine receptors in T. gondii-induced trophoblast cell function has not been investigated until now. The goal of the present study was to evaluate the intracellular signaling pathways regulated by adenosine receptors using a HTR-8/SVneo trophoblast cell model of T. gondii infection. HTR8/SVneo human extravillous trophoblast cells were infected with or without T. gondii and then evaluated for cell morphology, intracellular proliferation of the parasite, adenosine receptor expression, TNF-α production and mitogen-activated protein (MAP) kinase signaling pathways triggered by adenosine A3 receptor (A3AR). HTR8/SVneo cells infected with T. gondii exhibited an altered cytoskeletal changes, an increased infection rate and reduced viability in an infection time-dependent manner. T. gondii significantly promoted increased TNF-α production, A3AR protein levels and p38, ERK1/2 and JNK phosphorylation compared to those observed in uninfected control cells. Moreover, the inhibition of A3AR by A3AR siRNA transfection apparently suppressed the T. gondii infection-mediated upregulation of TNF-α, A3AR production and MAPK activation. In addition, T. gondii-promoted TNF-α secretion was dramatically attenuated by pretreatment with PD098059 or SP600125. These results indicate that A3AR-mediated activation of ERK1/2 and JNK positively regulates TNF-α secretion in T. gondii-infected HTR8/SVneo cells.

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PENINGKATAN TNF-α DAN INDEKS APOPTOSIS PADA TULANG MENCIT YANG DIINFEKSI Toxoplasma gondii

Cited by 4 publications

References 9 publications

). Increased Apoptosis Skull of Pups Born to Toxoplasma Gondii-Infected Mice Associated With Increased Expression of Interferon Gamma, but Not Tumor Necrosis Factor Alfa

). Increased Apoptosis Skull of Pups Born to Toxoplasma Gondii-Infected Mice Associated With Increased Expression of Interferon Gamma, but Not Tumor Necrosis Factor Alfa

Inhibition of Apoptosis in Retinal of Newborn Mice Due to Congenital Toxoplasmosis

Adenosine A3 Receptor Mediates ERK1/2- and JNK-Dependent TNF-α Production in Toxoplasma gondii-Infected HTR8/SVneo Human Extravillous Trophoblast Cells

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