Reactive Oxygen Species and Endotoxic Shock: Effect of Dimethylthiourea

Pattanaik, Uttara; Prasad, Kailash

doi:10.1177/107424840100600308

Cited by 10 publications

(6 citation statements)

References 43 publications

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“…Upon contact with microbes, excessive production of ROS might also become detrimental to the host itself. For example, ROS contribute to endotoxemic shock [13, 14], whereas Jurkat T cells undergo necroptosis upon contact with pathogenic amoebae as a result of a strong ROS response [15]. Likewise, the nematode Caenorhabditis elegans is killed during infection with S. Typhimurium through a massive ROS response filling the whole nematode, almost resembling a primordial septic shock [16].…”

Section: Reactive Oxygen Speciesmentioning

confidence: 99%

Salmonella and Reactive Oxygen Species: A Love-Hate Relationship

Rhen¹

2019

J Innate Immun

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Salmonella enterica represents an enterobacterial species including numerous serovars that cause infections at, or initiated at, the intestinal epithelium. Many serovars also act as facultative intracellular pathogens with a tropism for phagocytic cells. These bacteria not only survive in phagocytes but also undergo de facto replication therein. Phagocytes, through the activities of phagocyte NADPH-dependent oxidase and inducible nitric oxide synthase, are very proficient in converting molecular oxygen to reactive oxygen (ROS) and nitrogen species (RNS). These compounds represent highly efficient effectors of the innate immune defense. Salmonella is by no means resistant to these effectors, which may stand in contrast to the host niches chosen. To cope with this paradox, these bacteria rely on an array of detoxification and repair systems. Combination these systems allows for a high enough tolerance to ROS and RNS to enable establishment of infection. In addition, salmonella possesses protein factors that have the potential to dampen the infection-associated inflammation, which evidently results in a reduced exposure to ROS and RNS. This review attempts to summarize the activities and strategies by which salmonella tries to cope with ROS and RNS and how the bacterium can make use of these innate defense factors.

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Section: Reactive Oxygen Speciesmentioning

confidence: 99%

Salmonella and Reactive Oxygen Species: A Love-Hate Relationship

Rhen¹

2019

J Innate Immun

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“…The concentrations of superoxide dismutase, catalase, and DMTU were 0.02 mg/mL, 80 µg/mL, and 10 mg/mL of blood, respectively. Amounts of superoxide dismutase, catalase, and DMTU that are approximately similar to the amounts used here have been used by previous investigators (23)(24)(25).…”

Section: Methodsmentioning

confidence: 99%

C-Reactive Protein Increases Oxygen Radical Generation by Neutrophils

Prasad

2004

J Cardiovasc Pharmacol Ther

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C-reactive protein (CRP) has been suggested to play a role in the pathogenesis of atherosclerosis. Neutrophil respiratory burst and levels of CRP are increased during infection. The increase in the neutrophil respiratory burst may be due to factors that are elevated in infection, such as cytokines, tumor necrosis factor, platelet-activating factor, and CRP. The direct effect of CRP on the release of oxygen radicals by neutrophils is not known. This investigation was made to determine if CRP affects the generation of oxygen radicals by neutrophils and if this effect is blocked by antioxidants. The effect of various concentrations (1 to 200 microg/mL blood) of CRP on the generation of oxygen radicals by neutrophils was measured as luminol-dependent chemiluminescence (chemiluminescent activity) on a luminometer (Auto Lumat LB953, EG & G Berthold, Gaithersburg, MD). The unit of chemiluminescent activity is the relative light unit and was expressed as relative light unit/white blood cell (RLU/WBC). Chemiluminescent activity of blood without CRP was slightly higher than that of buffer with or without CRP. CRP markedly increased the chemiluminescent activity of blood. There was no significant change in the chemiluminescent activity of WBCs with 1 microg/mL of CRP. The chemiluminescent activity increased significantly with higher concentrations of CRP. The percent increases in the chemiluminescent activity with 2, 5, 10, 25, 50, 100 and 200 microg/mL of CRP were 45%, 72%, 50%, 70%, 52%, 67%, and 68% respectively. Antioxidants (superoxide dismutase, catalase, and dimethylthiourea) blocked CRP-induced oxygen radicals by WBCs. These results suggest that CRP increases the generation of oxygen radicals from the WBCs. CRP-induced atherosclerosis may be mediated through generation of oxygen radicals by neutrophils.

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“…the impaired myocardial function during sepsis including accumulation of (i) bacterial wall fragments like LPS, 42 (ii) various cytokines such as IL-1b and TNF-a 9 , and (iii) reactive oxygen/nitrogen species. 43,44 Altered NO production within the heart is believed to participate in the pathogenesis of heart failure originated from sepsis. 11 There is good evidence that the endocrine, immune, and nervous system are in concert to depress cardiac contractility under inflammatory conditions.…”

Section: Myocardial Inos Mrna Expressionmentioning

confidence: 99%

Infection – Inflammation

2012

Revue des Maladies Respiratoires Actualités

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Aims Myocardial function is severely compromised during sepsis. Several underlying mechanisms have been proposed. The innate immune system, i.e. Toll-like receptor (TLR) 2 and 4, significantly contributes to cardiac dysfunction. Little is known regarding TLR9 and its pathogenic ligand bacterial DNA in the myocardium. We therefore studied the role of TLR9 in myocardial inflammation and cardiac contractility.Methods and results Wild-type (WT, C57BL/6) and TLR9-deficient (TLR9-D) mice and isolated cardiomyocytes were challenged with synthetic bacterial DNA (CpG-ODN). Myocardial contractility as well as markers of inflammation/signalling were determined. Isolated cardiomyocytes incorporated fluorescence-marked CpG-ODN. In WT mice, CpG-ODN caused a robust response in hearts demonstrated by increased levels of tumour necrosis factor (TNF-a), interleukin (IL)-1b, IL-6, inducible nitric oxide synthase (iNOS), and nuclear factor kB activity. This inflammatory response was absent in TLR9-D mice. Under similar conditions, contractility measurements of isolated ventricular cardiomyocytes demonstrated a TLR9-dependent loss of sarcomeric shortening after CpG-ODN exposure. This observation was iNOS dependent as the application of a specific iNOS inhibitor reversed sarcomeric shortening to normal levels. Conclusion Our data suggest that bacterial DNA contributes to myocardial cytokine production and loss of cardiomyocyte contractility via TLR9.

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Reactive Oxygen Species and Endotoxic Shock: Effect of Dimethylthiourea

Cited by 10 publications

References 43 publications

<b><i>Salmonella</i></b> and Reactive Oxygen Species: A Love-Hate Relationship

<b><i>Salmonella</i></b> and Reactive Oxygen Species: A Love-Hate Relationship

C-Reactive Protein Increases Oxygen Radical Generation by Neutrophils

Infection – Inflammation

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