scholarly journals 1082-181 Production of reactive oxygen species by mononuclear cells correlates with the severity of coronary heart disease and NADPH oxidase expression

2004 ◽  
Vol 43 (5) ◽  
pp. A476
Author(s):  
Joerg Kreuzer ◽  
Olaf Jandt ◽  
Sanja Jovic ◽  
Daniel Teupser ◽  
Klaus Dugi ◽  
...  
2010 ◽  
Vol 79 (2) ◽  
pp. 767-773 ◽  
Author(s):  
Stefanie S. V. Henriet ◽  
Peter W. M. Hermans ◽  
Paul E. Verweij ◽  
Elles Simonetti ◽  
Steven M. Holland ◽  
...  

ABSTRACTInvasive aspergillosis is a major threat for patients suffering from chronic granulomatous disease (CGD). AlthoughAspergillus fumigatusis the most commonly encounteredAspergillusspecies, the presence ofA. nidulansappears to be disproportionately high in CGD patients. The purpose of this study was to investigate the involvement of the NADPH oxidase and the resulting reactive oxygen species (ROS) in host defense against fungi and to clarify their relationship towardA. nidulans. Murine CGD alveolar macrophages (AM) and polymorphonuclear leukocytes (PMN) and peripheral blood mononuclear cells (PBMC) from healthy controls and CGD patients were challenged with eitherA. fumigatusorA. nidulans. Analysis of the antifungal effects of ROS revealed thatA. nidulans, in contrast toA. fumigatus, is not susceptible to ROS. In addition, infection with liveA. nidulansdid not result in any measurable ROS release. Remarkably, human CGD PMN and PBMC and murine CGD AM were at least equipotent at arresting conidial germination compared to healthy controls. Blocking of the NADPH oxidase resulted in significantly reduced damage ofA. fumigatusbut did not affectA. nidulanshyphae. Furthermore, the microbicidal activity of CGD PMN was maintained towardA. nidulansbut notA. fumigatus. In summary, antifungal resistance toA. nidulansis not directly ROS related. The etiology ofA. nidulansinfections in CGD cannot be explained by the simple absence of the direct microbicidal effect of ROS.In vivo, the NADPH oxidase is a critical regulator of innate immunity whose unraveling will improve our understanding of fungal pathogenesis in CGD.


2020 ◽  
Vol 169 (4) ◽  
pp. 535-538 ◽  
Author(s):  
A. A. Savchenko ◽  
M. D. Goncharov ◽  
Yu. I. Grinsthein ◽  
I. I. Gvozdev ◽  
T. S. Mongush ◽  
...  

2012 ◽  
Vol 130 (2) ◽  
pp. 210-215 ◽  
Author(s):  
Jonathan Watt ◽  
Marie-Ann Ewart ◽  
Fiona H. Greig ◽  
Keith G. Oldroyd ◽  
Roger M. Wadsworth ◽  
...  

2000 ◽  
Vol 151 (1) ◽  
pp. 229
Author(s):  
Błaszczyk ◽  
J. Kȩdziora ◽  
B. Westfal ◽  
J. Zasłonka ◽  
J. Kowalski ◽  
...  

Cells ◽  
2021 ◽  
Vol 10 (4) ◽  
pp. 936
Author(s):  
Olga Witkowska-Piłaszewicz ◽  
Rafał Pingwara ◽  
Jarosław Szczepaniak ◽  
Anna Winnicka

Clenbuterol, the β2-adrenoceptor agonist, is gaining growing popularity because of its effects on weight loss (i.e., chemical liposuction). It is also popular in bodybuilding and professional sports, due to its effects that are similar to anabolic steroids. However, it is prohibited by anti-doping control. On the other hand, it is suggested that clenbuterol can inhibit the inflammatory process. The cells from 14 untrained and 14 well-trained race horses were collected after acute exercise and cultured with clenbuterol. The expressions of CD4, CD8, FoxP3, CD14, MHCII, and CD5 in PBMC, and reactive oxygen species (ROS) production, as well as cell proliferation, were evaluated by flow cytometry. In addition, IL-1β, IL-4, IL-6, IL-10, IL-17, INF-γ and TNF-α concentrations were evaluated by ELISA. β2-adrenoceptor stimulation leads to enhanced anti-inflammatory properties in well-trained horses, as do low doses in untrained animals. In contrast, higher clenbuterol doses create a pro-inflammatory environment in inexperienced horses. In conclusion, β2-adrenoceptor stimulation leads to a biphasic response. In addition, the immune cells are more sensitive to drug abuse in inexperienced individuals under physical training.


2013 ◽  
Vol 2013 ◽  
pp. 1-7 ◽  
Author(s):  
Shan Chen ◽  
Xian-Fang Meng ◽  
Chun Zhang

Proteinuria is an independent risk factor for end-stage renal disease (ESRD) (Shankland, 2006). Recent studies highlighted the mechanisms of podocyte injury and implications for potential treatment strategies in proteinuric kidney diseases (Zhang et al., 2012). Reactive oxygen species (ROS) are cellular signals which are closely associated with the development and progression of glomerular sclerosis. NADPH oxidase is a district enzymatic source of cellular ROS production and prominently expressed in podocytes (Zhang et al., 2010). In the last decade, it has become evident that NADPH oxidase-derived ROS overproduction is a key trigger of podocyte injury, such as renin-angiotensin-aldosterone system activation (Whaley-Connell et al., 2006), epithelial-to-mesenchymal transition (Zhang et al., 2011), and inflammatory priming (Abais et al., 2013). This review focuses on the mechanism of NADPH oxidase-mediated ROS in podocyte injury under different pathophysiological conditions. In addition, we also reviewed the therapeutic perspectives of NADPH oxidase in kidney diseases related to podocyte injury.


Sign in / Sign up

Export Citation Format

Share Document