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

Wei Ye; Jinhui Sun; Chunchao Li; Xuanyan Fan; Fan Gong; Xinqia Huang; Mingzhu Deng; Jia-Qi Chu

추천

검색

질문

자료유형: 학술저널

저자정보: Wei Ye (Affiliated Hospital of Guangdong Medical University) Jinhui Sun (Affiliated Hospital of Guangdong Medical University) Chunchao Li (Affiliated Hospital of Guangdong Medical University) Xuanyan Fan (Affiliated Hospital of Guangdong Medical University) Fan Gong (Affiliated Hospital of Guangdong Medical University) Xinqia Huang (Affiliated Hospital of Guangdong Medical University) Mingzhu Deng (Affiliated Hospital of Guangdong Medical University) Jia-Qi Chu (Affiliated Hospital of Guangdong Medical University)

저널정보: 대한기생충학열대의학회 Parasites, Hosts and Diseases The Korean Journal of Parasitology Vol.58 No.4

발행연도: 2020.8

수록면: 393 - 402 (10page)

이용수

📌

연구주제

📖

연구배경

🔬

연구방법

🏆

연구결과

초록· 키워드

오류제보하기

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.

#Toxoplasma gondii #adenosine A₃ receptor #TNF-α #HTR8/SVneo trophoblast cell #MAPK

참고문헌 (25)

참고문헌 신청

Flegr J / 2014 / Toxoplasmosis--a global threat. Correlation of latent toxoplasmosis with specific disease burden in a set of 88 countries / PLoS One 9:e90203

Milian ICB / 2019 / Increased Toxoplasma gondii intracellular proliferation in human extravillous trophoblast cells(HTR8/SVneo Line)is sequentially triggered by MIF, ERK1/2, and COX-2 / Front Microbiol 10:852

Barbosa BF / 2008 / BeWo trophoblast cell susceptibility to Toxoplasma gondii is increased by interferon-gamma, interleukin-10 and transforming growth factor-beta1 / Clin Exp Immunol 151:536~545

Nishikawa Y / 2007 / Toxoplasma gondii infection induces apoptosis in noninfected macrophages : role of nitric oxide and other soluble factors / Parasite Immunol 29:375~385

Abbasi M / 2003 / Infection of placental trophoblasts by Toxoplasma gondii / J Infect Dis 188:608~616

함께 읽어보면 좋을 논문

논문 유사도에 따라 DBpia 가 추천하는 논문입니다. 함께 보면 좋을 연관 논문을 확인해보세요!