Mycoplasma ovipneumoniae induces sheep airway epithelial cell apoptosis through an ERK signalling-mediated mitochondria pathway

Li, Yanan; Jiang, Zhongjia; Xue, Ding; Deng, Guangcun; Li, Min; Liu, Xiaoming; Wang, Yujiong

doi:10.1186/s12866-016-0842-0

Cited by 30 publications

(21 citation statements)

References 61 publications

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“…This observation is of particular mentioning to importance due to the fact that an inhibitor of ERK1/2 signaling is incapable of reducing the activation of caspase-3, indicating that CPS-induced apoptosis can be independent of ERK1/2 signaling and can progress alternatively through the JNK and p38 pathways. Of note, this observation was different from the M. ovipneumoniae bacteria-induced cell apoptosis determined in our recent study, in which M. ovipneumoniae was demonstrated to induce the cell apoptosis through an ERK-mediated MAPK pathway [ 15 ]. The discrepancy suggested distinct pathogenic roles of CPS of M. ovipneumoniae , as compared with its parent pathogen bacteria cells.…”

Section: Discussioncontrasting

confidence: 90%

“…In the present study, we interrogated the biological activity and mechanism of capsular polysaccharides (CPS) of M. ovipneumoniae- induced respiratory epithelial cell apoptosis using air-liquid interface- (ALI-) cultured epithelial cells generated with primary bronchial epithelial cells of Tan sheep [ 14 , 15 ]. The results showed that CPS of M. ovipneumoniae could induce sheep bronchial epithelial cell apoptosis through ROS-dependent JNK/P38 MAPK- but not ERK MAPK-mediated apoptotic pathways.…”

Section: Introductionmentioning

confidence: 99%

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Capsular Polysaccharide of Mycoplasma ovipneumoniae Induces Sheep Airway Epithelial Cell Apoptosis via ROS‐Dependent JNK/P38 MAPK Pathways

Jiang

Song

et al. 2017

Oxidative Medicine and Cellular Longevity

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In an attempt to better understand the pathogen-host interaction between invading Mycoplasma ovipneumoniae (M. ovipneumoniae) and sheep airway epithelial cells, biological effects and possible molecular mechanism of capsular polysaccharide of M. ovipneumoniae (CPS) in the induction of cell apoptosis were explored using sheep bronchial epithelial cells cultured in air-liquid interface (ALI). The CPS of M. ovipneumoniae was first isolated and purified. Results showed that CPS had a cytotoxic effect by disrupting the integrity of mitochondrial membrane, accompanied with an increase of reactive oxygen species and decrease of mitochondrial membrane potential (ΔΨm). Of importance, the CPS exhibited an ability to induce caspase-dependent cell apoptosis via both intrinsic and extrinsic apoptotic pathways. Mechanistically, the CPS induced extrinsic cell apoptosis by upregulating FAS/FASL signaling proteins and cleaved-caspase-8 and promoted a ROS-dependent intrinsic cell apoptosis by activating a JNK and p38 signaling but not ERK1/2 signaling of mitogen-activated protein kinases (MAPK) pathways. These findings provide the first evidence that CPS of M. ovipneumoniae induces a caspase-dependent apoptosis via both intrinsic and extrinsic apoptotic pathways in sheep bronchial epithelial cells, which may be mainly attributed by a ROS-dependent JNK and p38 MAPK signaling pathways.

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Section: Discussioncontrasting

confidence: 90%

Section: Introductionmentioning

confidence: 99%

Capsular Polysaccharide of Mycoplasma ovipneumoniae Induces Sheep Airway Epithelial Cell Apoptosis via ROS‐Dependent JNK/P38 MAPK Pathways

Jiang

Song

et al. 2017

Oxidative Medicine and Cellular Longevity

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“…The ERK pathway has been shown to directly affect mitochondrial function by inhibiting mitochondrial respiration [ 25 ] and reducing mitochondrial membrane potential [ 26 ]. The phosphorylation of ERK1/2 leads to the disruption of mitochondrial membranes and release of cytochrome c [ 27 , 28 ]. The activation of ERK1/2 can upregulate a proapoptotic protein, such as Bax [ 29 , 30 ], and downregulate an antiapoptosis protein such as Bcl-2 [ 31 , 32 ], which facilitate the release of cytochrome c and apoptosis.…”

Section: Discussionmentioning

confidence: 99%

Poly-L-Arginine Induces Apoptosis of NCI-H292 Cells via ERK1/2 Signaling Pathway

Wang

Zhang

Fan

et al. 2018

Journal of Immunology Research

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Cationic protein is a cytotoxic protein secreted by eosinophils and takes part in the damage of airway epithelium in asthma. Poly-L-arginine (PLA), a synthetic cationic protein, is widely used to mimic the biological function of the natural cationic protein in vitro. Previous studies demonstrated the damage of the airway epithelial cells by cationic protein, but the molecular mechanism is unclear. The purpose of this study aimed at exploring whether PLA could induce apoptosis of human airway epithelial cells (NCI-H292) and the underlying mechanism. Methods. The morphology of apoptotic cells was observed by transmission electron microscopy. The rate of apoptosis was analyzed by flow cytometry (FCM). The expressions of the phosphorylation of extracellular signal-regulated kinase 1/2 (ERK1/2), Bcl-2/Bax, and cleaved caspase-3 were assessed by western blot. Results. PLA can induce apoptosis in NCI-H292 cells in a concentration-dependent manner. Moreover, the phosphorylation of the ERK1/2 and the unbalance of Bcl2/Bax, as well as the activation of caspase-3, were involved in the PLA-induced apoptosis. Conclusions. PLA can induce the apoptosis in NCI-H292 cells, and this process at least involved the ERK1/2 and mitochondrial pathway. The results could have some indications in revealing the apoptotic damage of the airway epithelial cells. Besides, inhibition of cationic protein-induced apoptotic death in airway epithelial cells could be considered as a potential target of anti-injury or antiremodeling in asthmatics.

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“…At present, the main methods for detecting M. ovipneumoniae are pathogen diagnosis, enzyme linked immunosorbent assay (ELISA), and PCR (Jiang et al 2016 ) (Jiang et al 2016 ; Ziegler et al 2014 ; Li et al 2016 ; Yang et al 2014 ; Kılıc et al 2013 ). Furthermore, the research of M. ovipneumoniae has mainly concentrated on the isolation, identification, and detection technology of pathogenic bacteria (Butler et al 2017 ).…”

Section: Introductionmentioning

confidence: 99%

Loop-mediated isothermal amplification-lateral-flow dipstick (LAMP-LFD) to detect Mycoplasma ovipneumoniae

Zhang

Cao

Zhu

et al. 2019

World J Microbiol Biotechnol

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In order to establish a rapid detection method for Mycoplasma ovipneumoniae , this study used the loop-mediated isothermal amplification (LAMP) technique to carry out nucleic acid amplification and chromatographic visualization via a lateral flow dipstick (LFD) assay. The M. ovipneumoniae elongation factor TU gene ( EF-TU ) was detected using a set of specific primers designed for the EF-TU gene, and the EF-TU FIP was detected by biotin labeling, which was used in the LAMP amplification reaction. The digoxin-labeled probe specifically hybridized with LAMP products, which were visually detected by LFD. Here, we established the M. ovipneumoniae LAMP-LFD rapid detection method and tested the specificity, sensitivity, and clinical application of this method. Results showed that the optimized LAMP performed at 60 °C for 60 min, and LFD can specifically and visually detect M. ovipneumoniae with a minimum detectable concentration at 1.0 × 10 2 CFU/mL. The sensitivity of LAMP-LFD was 1000 times that of the conventional PCR detection methods, and the clinical lung tissue detection rate was 86% of 50 suspected sheep infected with M. ovipneumoniae . In conclusion, LAMP-LFD was established in this study to detect M. ovipneumoniae , a method that was highly specific, sensitive, and easy to operate, and provides a new method for the prevention and diagnosis of M. ovipneumoniae infection. Electronic supplementary material The online version of this article (10.1007/s11274-019-2601-5) contains supplementary material, which is available to authorized users.

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Mycoplasma ovipneumoniae induces sheep airway epithelial cell apoptosis through an ERK signalling-mediated mitochondria pathway

Cited by 30 publications

References 61 publications

Capsular Polysaccharide of Mycoplasma ovipneumoniae Induces Sheep Airway Epithelial Cell Apoptosis via ROS‐Dependent JNK/P38 MAPK Pathways

Capsular Polysaccharide of Mycoplasma ovipneumoniae Induces Sheep Airway Epithelial Cell Apoptosis via ROS‐Dependent JNK/P38 MAPK Pathways

Poly-L-Arginine Induces Apoptosis of NCI-H292 Cells via ERK1/2 Signaling Pathway

Loop-mediated isothermal amplification-lateral-flow dipstick (LAMP-LFD) to detect Mycoplasma ovipneumoniae

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