Oncotarget

Research Papers: Immunology:

Toxoplasma gondii excretory/secretory antigens (TgESAs) suppress pro-inflammatory cytokine secretion by inhibiting TLR-induced NF-κB activation in LPS-stimulated murine macrophages

Shuai Wang, Zhenchao Zhang, Yujian Wang, Javaid Ali Gadahi, Qing Xie, Lixin Xu, Ruofeng Yan, Xiaokai Song and Xiangrui Li _

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Oncotarget. 2017; 8:88351-88359. https://doi.org/10.18632/oncotarget.19362

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Abstract

Shuai Wang1,2, Zhenchao Zhang1,2, Yujian Wang1, Javaid Ali Gadahi1, Qing Xie1,2, Lixin Xu1, Ruofeng Yan1, Xiaokai Song1 and Xiangrui Li1

1 College of Veterinary Medicine, Nanjing Agricultural University, Nanjing, Jiangsu, PR China

2 School of Basic Medical Sciences, Xinxiang Medical University, Xinxiang, Henan, PR China

Correspondence to:

Xiangrui Li, email:

Keywords: toxoplasma gondii, excretory/secretory antigens, macrophage, cellular function, immunomodulation, Immunology and Microbiology Section, Immune response, Immunity

Received: December 05, 2016 Accepted: June 20, 2017 Published: July 18, 2017

Abstract

Excretory/secretory antigens (ESAs) produced by Toxoplasma gondii enable this parasite to invade and survive within the host cells through immunomodulation. In this study, the modulating effects of T. gondii excretory/secretory antigens (TgESAs) on the Ana-1 murine macrophage cell line were evaluated. Ana-1 cells were incubated with several concentrations of TgESAs, and the resulting effects on cellular viability, phagocytotic ability, and apoptosis induction were determined. Pro-inflammatory and anti-inflammatory cytokine secretion, nitric oxide production, toll-like receptor expression, and nuclear translocation of NF-κB were all measured after incubation with TgESAs. After TgESAs treatment, the proliferation and phagocytosis ability of Ana-1 cells decreased, and apoptosis was induced in a dose dependent manner. Analysis of Ana-1 cell culture supernatants showed that TgESAs not only upregulated secretion of anti-inflammatory cytokines (interleukin-10 and transforming growth factor-β1), they also inhibited secretion of pro-inflammatory cytokines (tumor necrosis factor-α and interleukin-1β). Additionally, TgESAs inhibited nitric oxide production, toll-like receptor (TLR) 2 and 4 activation, and the nuclear translocation of NF-κB in lipopolysaccharide-stimulated Ana-1 macrophages. These results suggest TgESAs inhibit the functional activity of Ana-1 murine macrophages by inhibiting TLR-induced NF-κB activation, which suppresses pro-inflammatory cytokine secretion.


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