Aflatoxin B1-activated heterophil extracellular traps result in the immunotoxicity to liver and kidney in chickens

Gao, Xinxin; Jiang, Liqiang; Xu, Jingnan; Liu, Wei; Li, Shurou; Huang, Wenlong; Zhao, Hongbin; Yang, Zhengtao; Yu, Xianjun; Wei, Zhengkai

doi:10.1016/j.dci.2021.104325

Cited by 19 publications

(11 citation statements)

References 48 publications

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“…Similar to NETs in mammals, chickens could also generate avian-specific HETs. 12,32,33 However, immune defences against T. gondii in chickens is poorly understood. In this study, we investigated the effect of T. gondii on the release of HETs in chickens.…”

Section: Discussionmentioning

confidence: 99%

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Toxoplasma gondii triggers heterophil extracellular traps via NADPH oxidase, ERK_1/2 and P38 signalling pathways, glycolysis and autophagy in chickens

Chen

Jin

et al. 2023

Parasite Immunology

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Toxoplasma gondii is a zoonotic parasite with a global distribution. Heterophil extracellular traps (HETs) are a novel innate immune mechanism of chickens against pathogens, but whether T. gondii can induce HETs release in chickens has not been reported. The effects of T. gondii on heterophils viability were assessed by using Cell Counting Kit‐8. T. gondii‐induced HETs were observed and analysed by the immunofluorescence method. T. gondii‐induced reactive oxygen species (ROS) was determined by the DCFH‐DA method. The mechanisms underlying T. gondii‐triggered HETs were investigated by inhibitors and fluorescence microplate reader. T. gondii did not significantly affect heterophils viability at a 1:1 ratio within 1 h. It was demonstrated for the first time that T. gondii could induce HETs release in chicken, and the structure of HETs was comprised of DNA, elastase and citrullinated histone 3 (citH3). T. gondii increased ROS production in a dose‐dependent manner. Inhibitors of NADPH oxidase, extracellular signal‐regulated kinase 1/2 (ERK1/2) and P38 signalling pathways, glycolysis and autophagy significantly decreased the release of T. gondii‐induced HETs. Taken together, T. gondii can induce HETs release in chickens, and ROS, NADPH oxidase, ERK1/2 and P38 signalling pathways, glycolysis and autophagy participate in the process of HETs release, which provides new insights into the innate immune mechanism of chickens against T. gondii infection.

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Section: Discussionmentioning

confidence: 99%

“…Heterophil extracellular traps (HETs) play an important role in the innate immune system of chickens against pathogens. 12 Until now, the effects and mechanism of T. gondii-induced HETs release in chickens remains unclear.…”

Section: Introductionmentioning

confidence: 99%

Toxoplasma gondii triggers heterophil extracellular traps via NADPH oxidase, ERK_1/2 and P38 signalling pathways, glycolysis and autophagy in chickens

Chen

Jin

et al. 2023

Parasite Immunology

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“…AFB 1 also impaired the physiological functions of freshly isolated swine alveolar macrophages (SAM), and consumption of AFB 1 -contaminated feed increased the risk of secondary infections in pigs ( Pang, Chiang & Chang, 2020 ). In addition, AFB 1 activated the release of heterophil extracellular traps (HETs) in chicks, and induced the expression of TNFα, IL6 and IL1β, iNOS, COX2, NLRP3, caspase1, caspase3 and caspase11, which resulted in liver and kidney damage ( Gao et al, 2022 ).…”

Section: Afb 1 -Induced Toxicitymentioning

confidence: 99%

Research progress in toxicological effects and mechanism of aflatoxin B₁ toxin

Liu

et al. 2022

PeerJ

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Fungal contamination of animal feed can severely affect the health of farm animals, and result in considerable economic losses. Certain filamentous fungi or molds produce toxic secondary metabolites known as mycotoxins, of which aflatoxins (AFTs) are considered the most critical dietary risk factor for both humans and animals. AFTs are ubiquitous in the environment, soil, and food crops, and aflatoxin B1(AFB1) has been identified by the World Health Organization (WHO) as one of the most potent natural group 1A carcinogen. We reviewed the literature on the toxic effects of AFB1 in humans and animals along with its toxicokinetic properties. The damage induced by AFB1 in cells and tissues is mainly achieved through cell cycle arrest and inhibition of cell proliferation, and the induction of apoptosis, oxidative stress, endoplasmic reticulum (ER) stress and autophagy. In addition, numerous coding genes and non-coding RNAs have been identified that regulate AFB1 toxicity. This review is a summary of the current research on the complexity of AFB1 toxicity, and provides insights into the molecular mechanisms as well as the phenotypic characteristics.

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“…23 Neutrophil extracellular traps are the newly discovered antiviral, antibacterial, antifungal, and antiparasitic mechanisms by neutrophils. 24 There are many mechanisms of Neutrophil extracellular traps (NETs) formation, including suicidal cellular NETs and living cell or vital NETs. 25 Activated neutrophils release NETs composed mainly of DNA, histone H3 (H3), myeloperoxidase (MPO), and neutrophil elastase (NE).…”

Section: ■ Introductionmentioning

confidence: 99%

“…Neutrophil extracellular traps are the newly discovered antiviral, antibacterial, antifungal, and antiparasitic mechanisms by neutrophils . There are many mechanisms of Neutrophil extracellular traps (NETs) formation, including suicidal cellular NETs and living cell or vital NETs .…”

Section: Introductionmentioning

confidence: 99%

Antagonistic Effect of Selenium on Fumonisin B1 Promotes Neutrophil Extracellular Traps Formation in Chicken Neutrophils

Zhu

Qiao

Ouyang

et al. 2022

J. Agric. Food Chem.

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Neutrophils are an important component of the innate immune system, and one of their defense mechanisms, neutrophil extracellular traps (NETs), is a hot topic of the current research. This study explored the effects of fumonisin B1 (FB1) on chicken neutrophil production of NETs and its possible molecular mechanism of action. Scanning electron microscopy and fluorescence microscopy were used to observe morphological changes in neutrophils, and a fluorescence microplate reader was used to detect reactive oxygen species (ROS) and extracellular DNA release from neutrophils. Quantitative PCR (qPCR) and western blot were used to determine the expression levels of selenoproteins. The results indicate that FB1 inhibited the zymosan-induced formation of NETs in chicken neutrophils by preventing ROS burst and histone H3 (H3) and neutrophil elastase (NE) release. Moreover, the mRNA expression levels of glutathione peroxidase (GPX), thioredoxin reductase (TXNRD), and deiodinase (DIO) were downregulated in the FB1 group. The protein expression levels of GPX1, GPX2, GPX3, DIO3, and TXNRD1 were consistent with the changes in their gene expressions, suggesting an abnormal selenoprotein expression in response to the toxic effects of FB1. Conversely, selenium (Se) supplementation reduced the toxic effects of FB1 and restored the NETs formation, indicating that Se can be used as a potential drug to prevent and control FB1 toxicity in livestock farming.

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Aflatoxin B1-activated heterophil extracellular traps result in the immunotoxicity to liver and kidney in chickens

Cited by 19 publications

References 48 publications

Toxoplasma gondii triggers heterophil extracellular traps via NADPH oxidase, ERK_1/2 and P38 signalling pathways, glycolysis and autophagy in chickens

Toxoplasma gondii triggers heterophil extracellular traps via NADPH oxidase, ERK_1/2 and P38 signalling pathways, glycolysis and autophagy in chickens

Research progress in toxicological effects and mechanism of aflatoxin B₁ toxin

Antagonistic Effect of Selenium on Fumonisin B1 Promotes Neutrophil Extracellular Traps Formation in Chicken Neutrophils

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Aflatoxin B1-activated heterophil extracellular traps result in the immunotoxicity to liver and kidney in chickens

Cited by 19 publications

References 48 publications

Toxoplasma gondii triggers heterophil extracellular traps via NADPH oxidase, ERK1/2 and P38 signalling pathways, glycolysis and autophagy in chickens

Toxoplasma gondii triggers heterophil extracellular traps via NADPH oxidase, ERK1/2 and P38 signalling pathways, glycolysis and autophagy in chickens

Research progress in toxicological effects and mechanism of aflatoxin B1 toxin

Antagonistic Effect of Selenium on Fumonisin B1 Promotes Neutrophil Extracellular Traps Formation in Chicken Neutrophils

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Product

Resources

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Toxoplasma gondii triggers heterophil extracellular traps via NADPH oxidase, ERK_1/2 and P38 signalling pathways, glycolysis and autophagy in chickens

Toxoplasma gondii triggers heterophil extracellular traps via NADPH oxidase, ERK_1/2 and P38 signalling pathways, glycolysis and autophagy in chickens

Research progress in toxicological effects and mechanism of aflatoxin B₁ toxin