Extracellular superoxide anion production contributes to the virulence of Xanthomonas oryzae pv. oryzae

2009 ◽  
Vol 55 (2) ◽  
pp. 110-116 ◽  
Author(s):  
Xin Li ◽  
Xinyue Pang ◽  
Dejuan Zhi ◽  
Jinsheng Wang ◽  
Minquan Li ◽  
...  
Keyword(s):  
Electron Spin Resonance ◽  
Superoxide Anion ◽  
Positive Relationship ◽  
Xanthomonas Oryzae ◽  
Wild Type ◽  
Superoxide Anion Production ◽  
Spin Resonance ◽  
Anion Production ◽  
Type Strains ◽  
Extracellular Fraction

Endogenous superoxide anion production was determined by electron spin resonance in wild-type strains and avrXa7 mutants of Xanthomonas oryzae pv. oryzae . The localization of superoxide anion was carried out in the intra- and extra-cellular fractions. Results showed the presence of superoxide anion in multi-locations of X. oryzae pv. oryzae cells. The extracellular fraction was the major location of superoxide anion production. Furthermore, a positive relationship was shown between the levels of endogenous superoxide anion and the virulence of strains. These indubitable results suggested that the superoxide anion contributes to the virulence of X. oryzae pv. oryzae.

scholarly journals Serum amyloid A3 confers protection against acute lung injury in Pseudomonas aeruginosa-infected mice

2020 ◽  
Vol 318 (2) ◽  
pp. L314-L322 ◽  
Author(s):  
Yu Fan ◽  
Gufang Zhang ◽  
Chi Teng Vong ◽  
Richard D. Ye
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Acute Lung Injury ◽  
Lung Injury ◽  
Knockout Mice ◽  
Superoxide Anion ◽  
Inflammatory Responses ◽  
Serum Amyloid ◽  
Wild Type ◽  
Superoxide Anion Production ◽  
Anion Production

Pseudomonas aeruginosa is a gram-negative bacterium associated with serious illnesses, including ventilator-associated pneumonia and various sepsis syndromes in humans. Understanding the host immune mechanisms against P. aeruginosa is, therefore, of clinical importance. The present study identified serum amyloid A3 (SAA3) as being highly inducible in mouse bronchial epithelium following P. aeruginosa infection. Genetic deletion of Saa3 rendered mice more susceptible to P. aeruginosa infection with decreased neutrophil superoxide anion production, and ex vivo treatment of mouse neutrophils with recombinant SAA3 restored the ability of neutrophils to produce superoxide anions. The SAA3-deficient mice showed exacerbated inflammatory responses, which was characterized by pronounced neutrophil infiltration, elevated expression of TNF-α, KC/CXCL1, and MIP-2/CXCL2 in bronchoalveolar lavage fluid (BALF), and increased lung microvascular permeability compared with their wild-type littermates. BALF neutrophils from Saa3 knockout mice exhibited reduced superoxide anion production compared with neutrophils from wild-type mice. Adoptive transfer of SAA3-treated neutrophils to Saa3 knockout mice ameliorated P. aeruginosa-induced acute lung injury. These findings demonstrate that SAA3 not only serves as a biomarker for infection and inflammation, but also plays a protective role against P. aeruginosa infection-induced lung injury in part through augmentation of neutrophil bactericidal functions.

Abstract 1412: Critical Role Of Extracellular Sod For Protecting The Heart Against Myocardial Hypertrophy And Dysfunction After Myocardial Infarction

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Elza D Deel ◽  
Zhongbing LU ◽  
Xin Xu ◽  
Guangshuo Zhu ◽  
Xinli Hu ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Ejection Fraction ◽  
Superoxide Anion ◽  
Left Ventricular ◽  
Wild Type ◽  
Sod Activity ◽  
Superoxide Anion Production ◽  
Lv Remodeling ◽  
Anion Production ◽  
Lv Ejection Fraction

Extracellular SOD ( SOD3 ) contributes only a small fraction to total SOD activity in the normal heart, but is strategically located to scavenge free radicals in the extracellular compartment. SOD3 expression is decreased in the failing heart, but whether SOD3 can abrogate oxidative stress or modify left ventricular (LV) remodeling following myocardial infarction (MI) is unclear. To examine this question, we studied LV remodeling in SOD3 KO mice and wild type mice following MI. Under unstressed conditions, SOD3 KO had no effect on myocardial total SOD activity, SOD1 or SOD2 protein content, or myocardial nitrotyrosine or superoxide anion production, and caused no change in LV ejection fraction. However, 4 weeks or 8 weeks after MI, SOD3 KO mice developed more LV hypertrophy (8 weeks after MI, ventricular mass increased 1.64-fold in KO mice as compared to 1.35-fold in wild type mice, p<0.01) and had a greater reduction of LV ejection fraction (8 weeks after MI, LV ejection fraction was 35±2.4% in wild type mice as compared to 30±2.0% in KO mice, p<0.01). As compared with wild type mice, SOD3 KO mice had significantly greater increases of myocardial nitrotyrosine and superoxide anion production, a significantly greater decrease of ANP in the peri-infarct zone, and a significant more decrease of SERCA2a in both the peri-infarct and remote zones. In addition, MI caused greater activation of mitogen-activated protein kinase (MAPK) signaling pathways in SOD3 KO mice, as demonstrated by significantly greater increases of p-p38 Thr180/ Tyr182 , p-Erk Thr202/Tyr204 and p-JNK Thr183/Tyr185 in SOD3 KO mice 8 weeks after MI. The finding that SOD3 KO had no effect on myocardial total SOD activity, but significantly exacerbated MI induced LV remodeling implies that the specific extracellular location of SOD3 is more important than its contribution to overall SOD activity in protecting the heart against contractile dysfunction following myocardial infarct.

Abstract W P230: Tetrahydrobiopterin Attenuates Cerebrovascular Oxidative Stress in Tg2576 Mouse Model of Alzheimer’s Disease

Stroke ◽  
2015 ◽  
Vol 46 (suppl_1) ◽  
Author(s):  
Anantha Vijay R Santhanam ◽  
Livius V d'Uscio ◽  
Zvonimir S Katusic
Keyword(s):  
Oxidative Stress ◽  
Enzymatic Activity ◽  
Superoxide Anion ◽  
Wild Type ◽  
Superoxide Anion Production ◽  
Cerebral Microvessels ◽  
Double Mutation ◽  
Enos Uncoupling ◽  
Anion Production ◽  
Tg2576 Mice

Background: The present study was designed to test the hypothesis that supplementation of tetrahydrobiopterin (BH4) to transgenic mice expressing the Swedish double mutation of human amyloid precursor protein (Tg2576 mice) results in restoration of BH4 levels required for activation of endothelial nitric oxide synthase (eNOS), and in turn, prevents oxidative stress in cerebral microvasculature. Methods: Cerebral microvessels were obtained from 4-5 months old female wild-type and Tg2576 mice. Biopterin levels, enzymatic activity of GTP cyclohydrolase I (GTPCH-I) and superoxide production were measured by HPLC. The effects of supplementation of BH4 on oxidative stress were studied by injecting wild-type and Tg2576 mice subcutaneously with 100 mol/kg (b.w.) of BH 4 ([ 6R ]-5,6,7,8-tetrahydro-L-biopterin dihydrochloride; [ 6R ]-BH4). Results: Enzymatic activity of GTPCH-I, rate limiting enzyme in BH4 biosynthesis, was not different between cerebral microvessels of wild-type and Tg2576 mice. However, bioavailability of BH4, was significantly reduced in cerebral microvessels of Tg2576 mice (P<0.05, n=8). Production of superoxide anions was significantly elevated in cerebral microvessels of Tg2576 mice (P<0.01, n=6), indicative of oxidative stress. This increased superoxide anion production was abolished by L-NAME, a NOS inhibitor, suggestive of eNOS uncoupling (P<0.05, n=6). Supplementation of [ 6R ]-BH4 to wild-type and Tg2576 mice resulted in significant increase in BH4 bioavailability (P<0.05, n=6). Notably, supplementation of [ 6R ]-BH4 abrogated the increase in superoxide anion production in cerebral microvessels of Tg2576 mice (P<0.05, n=5), while superoxide anion production remained unchanged in cerebral microvessels of WT mice. Furthermore, the inhibitory effects of L-NAME on superoxide anion production in cerebral microvessels of Tg2576 mice were abolished following [ 6R ]-BH4 supplementation (P<0.05, n=4). Conclusion: Supplementation of [ 6R ]-BH4 restored bioavailability of BH4, thereby abrogating superoxide anion production derived from eNOS. Our results suggest that uncoupling of eNOS contributes to oxidative stress in cerebral microvessels of Tg2576 mice.

Lactate and P o 2 Modulate Superoxide Anion Production in Bovine Cardiac Myocytes

Circulation ◽  
1997 ◽  
Vol 96 (2) ◽  
pp. 614-620 ◽  
Author(s):  
Kamal M. Mohazzab-H. ◽  
Pawel M. Kaminski ◽  
Michael S. Wolin
Keyword(s):  
Cardiac Myocytes ◽  
Superoxide Anion ◽  
Superoxide Anion Production ◽  
Anion Production

scholarly journals Opsonization of Actinobacillus actinomycetemcomitans by Immunoglobulin G Antibody Reactive with Phosphorylcholine

2002 ◽  
Vol 70 (11) ◽  
pp. 6485-6488 ◽  
Author(s):  
Donald Purkall ◽  
John G. Tew ◽  
Harvey A. Schenkein
Keyword(s):  
Streptococcus Pneumoniae ◽  
Immunoglobulin G ◽  
Oxidative Burst ◽  
Superoxide Anion ◽  
Polymorphonuclear Neutrophils ◽  
Actinobacillus Actinomycetemcomitans ◽  
Superoxide Anion Production ◽  
Protective Antibody ◽  
Anion Production ◽  
Human Sera

ABSTRACT We used two strains of Actinobacillus actinomycetemcomitans, one bearing phosphorylcholine (PC) (strain D045D-40) and one devoid of PC antigens (strain DB03A-42), as well as a nonencapsulated strain of Streptococcus pneumoniae (strain 39937), to examine the opsonic properties of physiological concentrations (⩽30 μg/ml) of purified human anti-PC immunoglobulin G (IgG). Anti-PC bound to both A. actinomycetemcomitans DO45D-40 and S. pneumoniae 39937 and induced superoxide anion production by polymorphonuclear neutrophils; induction of the oxidative burst was inhibited by antibodies to either CD16 or CD32. Thus, anti-PC IgG at concentrations present in most human sera promotes the opsonization of PC-expressing strains of A. actinomycetemcomitans in the absence of complement, implying that anti-PC may be a protective antibody against such strains of bacteria.

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