Is the reactive oxygen species-dependent-NF-κB activation observed in iron-loaded BALB/c mice a key process preventing growth of Leishmania major progeny and tissue-damage?

2006 ◽  
Vol 8 (6) ◽  
pp. 1473-1482 ◽  
Author(s):  
Sylvia Bisti ◽  
Ketty Soteriadou
2006 ◽  
Vol 114 (4) ◽  
pp. 323-328 ◽  
Author(s):  
Gholamreza Kavoosi ◽  
Sussan K. Ardestani ◽  
Amina Kariminia ◽  
Mohssen Abolhassani ◽  
Salvatore J. Turco

2020 ◽  
Vol 21 (9) ◽  
pp. 3161 ◽  
Author(s):  
Luigi Di Luigi ◽  
Paolo Sgrò ◽  
Guglielmo Duranti ◽  
Stefania Sabatini ◽  
Daniela Caporossi ◽  
...  

Oxidative stress linked to vascular damage plays an important role in the pathogenesis of systemic sclerosis (SSc). Indeed, vascular damage at nailfold capillaroscopy in patients with Raynaud’s Phenomenon (RP) is a major risk factor for the development of SSc together with the presence of specific autoantiobodies. Here, we investigated the effects of the phosphodiesterase type 5 inhibitor (PDE5i) sildenafil, currently used in the management of RP, in modulating the proinflammatory response of dermal fibroblasts to oxidative stress in vitro. Human fibroblasts isolated from SSc patients and healthy controls were exposed to exogenous reactive oxygen species (ROS) (100 µM H2O2), in the presence or absence of sildenafil (1 µM). Treatment with sildenafil significantly reduced dermal fibroblast gene expression and cellular release of IL-6, known to play a central role in the pathogenesis of tissue damage in SSc and IL-8, directly induced by ROS. This reduction was associated with suppression of STAT3-, ERK-, NF-κB-, and PKB/AKT-dependent pathways. Our findings support the notion that the employment of PDE5i in the management of RP may be explored for its efficacy in modulating the oxidative stress-induced proinflammatory activation of dermal fibroblasts in vivo and may ultimately aid in the prevention of tissue damage caused by SSc.


2011 ◽  
Vol 360 (1-2) ◽  
pp. 189-195 ◽  
Author(s):  
Sudhakar Baluchamy ◽  
Prabakaran Ravichandran ◽  
Vani Ramesh ◽  
Zhenhua He ◽  
Ye Zhang ◽  
...  

2008 ◽  
Vol 120 (1) ◽  
pp. 62-66 ◽  
Author(s):  
Gholamreza Kavoosi ◽  
Sussan K. Ardestani ◽  
Amina Kariminia ◽  
Majid Zeinali ◽  
Mohammad Hossein Alimohammadian

2020 ◽  
Author(s):  
Sandrine Huot ◽  
Cynthia Laflamme ◽  
Paul R. Fortin ◽  
Eric Boilard ◽  
Marc Pouliot

AbstractAutoimmune complexes are an important feature of several autoimmune diseases such as lupus, as they contribute to tissue damage through the activation of immune cells. Neutrophils, key players in lupus, interact with immune complexes through Fc gamma receptors (FcgR). Incubation of neutrophils with aggregated-IgGs caused degranulation and increased the surface expression of FcgRI within minutes in a concentration-dependent fashion. After 30 min, IgG aggregates (1 mg/ml) up-regulated FcgRI by 4.95 ± 0.45-fold. FcgRI-positive neutrophils reached 67.24% ± 6.88% on HA-IgGs stimulated neutrophils, from 3.12% ± 1.62% in non-stimulated cells, ranking IgG-aggregates among the most potent known agonists. FcgRIIa, and possibly FcgRIIIa, appeared to mediate this up-regulation. Also, FcgRI-dependent signaling proved necessary for reactive oxygen species (ROS) production in response to IgG-aggregates. Finally, combinations of bacterial materials with aggregates dramatically boosted ROS production. This work suggests FcgRI as an essential component in the response of human neutrophils to immune complexes leading to the production of ROS, which may help explain how neutrophils contribute to tissue damage associated with immune complex-associated diseases, such as lupus.


2008 ◽  
Vol 48 (12) ◽  
pp. 539-545 ◽  
Author(s):  
Takeshi AOYAMA ◽  
Kazutoshi HIDA ◽  
Satoshi KURODA ◽  
Toshitaka SEKI ◽  
Shunsuke YANO ◽  
...  

2004 ◽  
Vol 10 (14) ◽  
pp. 1611-1626 ◽  
Author(s):  
Carlo Bergamini ◽  
Stefania Gambetti ◽  
Alessia Dondi ◽  
Carlo Cervellati

2017 ◽  
Vol 63 (3) ◽  
pp. 229-235 ◽  
Author(s):  
Roberta Cattaneo Horn ◽  
Gabriela Tassotti Gelatti ◽  
Natacha Cossettin Mori ◽  
Ana Caroline Tissiani ◽  
Mariana Spanamberg Mayer ◽  
...  

Summary Introduction: Obesity refers to the accumulation of fatty tissues and it favors the occurrence of oxidative stress. Alternatives that can contribute to body weight reduction have been investigated in order to reduce the production of reactive oxygen species responsible for tissue damage. The aim of the current study was to assess whether the oxidant and antioxidant markers of obese women before and after bariatric surgery were able to reduce oxidative damage. Method: We have assessed 16 morbidly obese women five days before and 180 days after the surgery. The control group comprised 16 non-obese women. Levels of thiobarbituric acid-reactive substances, carbonylated proteins, reduced glutathione and ascorbic acid were assessed in the patients' plasma. Results: Levels of lipid peroxidation and protein carbonylation in the pre-surgical obese women were higher than those of the controls and post-surgical obese women. Levels of reduced glutathione in the pre-surgical obese women were high compared to the controls, and declined after surgery. Levels of ascorbic acid fell in the pre--surgical obese women compared to the control and post-surgical obese women. Conclusion: Body weight influences the production of reactive oxygen species. Bariatric surgery, combined with weight loss and vitamin supplementation, reduces cellular oxidation, thus reducing tissue damage.


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