scholarly journals Nicotinamide Adenine Dinucleotide-Dependent Flavin Oxidoreductase of Mycoplasma hyopneumoniae Functions as a Potential Novel Virulence Factor and Not Only as a Metabolic Enzyme

2021 ◽  
Vol 12 ◽  
Author(s):  
Xing Xie ◽  
Fei Hao ◽  
Rong Chen ◽  
Jingjing Wang ◽  
Yanna Wei ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Virulence Factor ◽  
Polyclonal Antibody ◽  
Nicotinamide Adenine Dinucleotide ◽  
Mycoplasma Hyopneumoniae ◽  
Nicotinamide Adenine ◽  
Metabolic Enzyme ◽  
Multiple Sequence ◽  
Enzootic Pneumonia ◽  
Flavin Oxidoreductase

Mycoplasma hyopneumoniae (Mhp) is the main pathogen that causes enzootic pneumonia, a disease that has a significant impact on the pig industry worldwide. The pathogenesis of enzootic pneumonia, especially possible virulence factors of Mhp, has still not been fully elucidated. The transcriptomic and proteomic analyses of different Mhp strains reported in the literature have revealed differences in virulence, and differences in RNA transcription levels between high- and low-virulence strains initially indicated that nicotinamide adenine dinucleotide (NADH)-dependent flavin oxidoreductase (NFOR) was related to Mhp pathogenicity. Prokaryotic expression and purification of the NFOR protein from Mhp were performed, a rabbit-derived polyclonal antibody against NFOR was prepared, and multiple sequence alignment and evolutionary analyses of Mhp NFOR were performed. For the first time, it was found that the NFOR protein was conserved among all Mhp strains, and NFOR was localized to the cell surface and could adhere to immortalized porcine bronchial epithelial cells (hTERT-PBECs). Adhesion to hTERT-PBECs could be specifically inhibited by an anti-NFOR polyclonal antibody, and the rates of adhesion to both high- and low-virulence strains, 168 and 168L, significantly decreased by more than 40%. Moreover, Mhp NFOR not only recognized and interacted with host fibronectin and plasminogen but also induced cellular oxidative stress and apoptosis in hTERT-PBECs. The release of lactate dehydrogenase by hTERT-PBECs incubated with Mhp NFOR was significantly positively correlated with the virulence of Mhp. Overall, in addition to being a metabolic enzyme related to oxidative stress, NFOR may also function as a potential novel virulence factor of Mhp, thus contributing to the pathogenesis of Mhp; these findings provide new ideas and theoretical support for studying the pathogenic mechanisms of other mycoplasmas.

scholarly journals NADH-Dependent Flavin Oxidoreductase of Mycoplasma Hyopneumoniae Functions as a Potential Novel Virulence Factor and not Only as a Metabolic Enzyme

2021 ◽  
Author(s):  
Xing Xie ◽  
Fei Hao ◽  
Rong Chen ◽  
Jingjing Wang ◽  
Yanna Wei ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Virulence Factor ◽  
Polyclonal Antibody ◽  
Mycoplasma Hyopneumoniae ◽  
Metabolic Enzyme ◽  
Evolutionary Analysis ◽  
Feed Conversion ◽  
Multiple Sequence ◽  
Poor Growth ◽  
Flavin Oxidoreductase

Abstract Background: Mycoplasma hyopneumoniae (Mhp) is the main pathogen of enzootic pneumonia, pigs infected with Mhp demonstrate mainly poor growth and a reduced feed conversion rate, a disease that has a significant impact on the pig industry and pock production worldwide. The pathogenesis, especially possible virulence factors of Mhp, has still not been fully clarified.Results: The transcriptome and proteomic analysis of Mhp strains differed in virulence based on reported literature, and RNA transcription expression levels between high- and low-virulence strains initially indicated that nicotinamide adenine dinucleotide (NADH)-dependent flavin oxidoreductase (NFOR) was related to Mhp pathogenicity. Prokaryotic expression and purification of the NFOR protein of Mhp were performed, a rabbit-origin polyclonal antibody of NFOR was prepared, and multiple sequence alignment and evolutionary analysis of Mhp NFOR were performed. For the first time, it was found that the NFOR protein was conserved among all Mhp strains, and NFOR was localized on the cell surface and could adhere to immortalized porcine bronchial epithelial cells (hTERT-PBECs). Adhesion to hTERT-PBECs could be specifically inhibited by an NFOR polyclonal antibody, and the adhesion rates of both high- and low-virulence strains, 168 and 168L, significantly decreased by more than 40%. Moreover, Mhp NFOR could not only recognize and interact with host fibronectin and plasminogen but could also induce cellular oxidative stress and apoptosis in hTERT-PBECs. Lactate dehydrogenase release of Mhp NFOR in hTERT-PBECs was significantly positively correlated with the virulence of Mhp.Conclusions: Overall, in addition to being a metabolic enzyme related to oxidative stress, NFOR may also function as a potential novel virulence factor of Mhp, thus contributing to the pathogenesis process of Mhp, providing new ideas and theoretical support for studying the pathogenic mechanisms of other mycoplasmas.

Polymorphism C242T of the gene of the p22phox subunit for nicotinamide adenine dinucleotide phosphate oxidase, and erythrocytic antioxidant enzymes, in patients with tetralogy of Fallot

2007 ◽  
Vol 17 (3) ◽  
pp. 295-300 ◽  
Author(s):  
António Guerra ◽  
Carla Rego ◽  
Constança Coelho ◽  
Nuno Guimarães ◽  
Catarina Thiran ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Tetralogy Of Fallot ◽  
Nicotinamide Adenine Dinucleotide ◽  
Reductase Activity ◽  
Tyrosine Phosphatase ◽  
Nicotinamide Adenine Dinucleotide Phosphate ◽  
Nicotinamide Adenine ◽  
Long Term Follow Up ◽  
Markers Of Oxidative Stress ◽  
Blood Pressures

Background:Nicotinamide adenine dinucleotide phosphate oxidase of the vascular cell membrane is an important source of reactive oxygen species. The aim of our study was to evaluate the possible influence of the p22phox C242T gene polymorphism on blood pressure and some markers of oxidative stress in children with tetralogy of Fallot.Methods:After surgical repair in early life, we recruited 38 children, aged 11.7 plus or minus 3.2 years, including 185 healthy individuals as controls for the purposes of establishing frequencies of alleles and genotypes. From this latter group, we matched a sub-sample of 53 healthy caucasian children, aged 11.0 plus or minus 1.0 years, in order to compare enzymic activities.Results:The children with tetralogy of Fallot showed significantly lower values of low-molecular-weight protein tyrosine phosphatase, particularly in carriers of CC genotype for the p22phox gene, with values of 145.2 plus or minus 77.4 μmol/g Hb/h, compared to controls, at 344.4 plus or minus 100.4 μmol/g Hb/h (p less than 0.001). Methemoglobin reductase activity in the patients with tetralogy was also lower in those with the CC genotype, at 9.8 plus or minus 3.2 μmol/g Hb−1min−1compared to 24.2 plus or minus 11.8 μmol/g Hb−1min−1as measured in the controls (p less than 0.01). Lower systolic (p less than 0.05) and diastolic (p less than 0.01) blood pressures were also observed in the patients with tetralogy of Fallot.Conclusions:Patients with tetralogy of Fallot having the CC genotype may be at a higher state of oxidative stress than T allele carriers, a finding which could have prognostic implications. Long term follow-up of these patients, however, may be necessary in order to draw definite conclusions.

Effect on oxidative stress, hepatic chemical metabolizing parameters, and genotoxic damage of mad honey intake in rats

2017 ◽  
Vol 37 (9) ◽  
pp. 991-1004 ◽  
Author(s):  
G Eraslan ◽  
M Kanbur ◽  
M Karabacak ◽  
K Arslan ◽  
Y Siliğ ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Nicotinamide Adenine Dinucleotide ◽  
Nicotinamide Adenine Dinucleotide Phosphate ◽  
Exposure Period ◽  
Acute Stage ◽  
Nicotinamide Adenine ◽  
Control Group ◽  
Antioxidant Enzyme Activities ◽  
Subacute Stage ◽  
Mad Honey

A total of 66 male Wistar rats were used and six groups (control: 10 animals and experimental: 12 animals) were formed. While a separate control group was established for each study period, mad honey application to the animals in the experimental group was carried out with a single dose (12.5 g kg−1 body weight (b.w.); acute stage), at a dose of 7.5 g kg−1 b.w. for 21 days (subacute stage), and at a dose of 5 g kg−1 b.w. for 60 days (chronic stage). Tissue and blood oxidative stress markers (malondialdehyde (MDA), nitric oxide (NO), 4-hydroxynonenal (HNE), superoxide dismutase, catalase, glutathione (GSH) peroxidase, and glucose-6-phosphate dehydrogenase), hepatic chemical metabolizing parameters in the liver (cytochrome P450 2E1, nicotinamide adenine dinucleotide (NADH)-cytochrome b5 reductase, nicotinamide adenine dinucleotide phosphate (NADPH)-cytochrome c reductase (CYTC), GSH S-transferase (GST), and GSH), and micronucleus and comet test in some samples were examined. Findings from the study showed that single and repeated doses given over the period increased MDA, NO, and HNE levels while decreasing/increasing tissue and blood antioxidant enzyme activities. From hepatic chemical metabolizing parameters, GST activity increased in the subacute and chronic stages and CYTC activity increased in the acute period, whereas GSH level decreased in the subacute stage. Changes in tail and head intensities were found in most of the comet results. Mad honey caused oxidative stresses for each exposure period and made some significant changes on the comet test in certain periods for some samples obtained. In other words, according to the available research results obtained, careless consumption of mad honey for different medical purposes is not appropriate.

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