Reactive oxygen species at the crossroads of inflammasome and inflammation

Harijith, Anantha; Ebenezer, David L.; Natarajan, Viswanathan

doi:10.3389/fphys.2014.00352

Cited by 377 publications

(283 citation statements)

References 101 publications

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“…It is yet not clear how extreme inactivity is enhancing lung disease but it is tempting to relate these findings to an excess of oxidative stress. A similar phenomenon is observed in skeletal muscles (41,42) in which physical inactivity, through oxidative stress, can lead to activation of inflammatory (43,44) and proteolytic pathways (41,42). Otherwise, enhanced lung inflammation in extremely inactive mice might be related to the fact that hindlimb suspension caused a redistribution of body fluids towards the upper body parts.…”

Section: Discussionmentioning

confidence: 52%

Interaction between Physical Activity and Smoking on Lung, Muscle, and Bone in Mice

Cielen

Maes

Heulens

et al. 2016

Am J Respir Cell Mol Biol

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Physical inactivity is an important contributor to skeletal muscle weakness, osteoporosis and weight loss in chronic obstructive pulmonary disease. However, the effects of physical inactivity, in interaction with smoking, on lung, muscle and bone are poorly understood. To address this issue, male mice were randomly assigned into an active (daily running), moderately inactive (space restriction) or extremely inactive group (space restriction followed by hindlimb suspension to mimic bed rest) during 24 weeks and simultaneously exposed to either cigarette smoke or room air. The effects of different physical activity levels and smoking status and their respective interaction were examined on lung function, body composition, in vitro limb muscle function and bone parameters. Smoking caused emphysema, reduced food intake with subsequent loss of body weight, fat, lean and muscle mass but increased trabecular bone volume. Smoking induced muscle fiber atrophy which did not result in force impairment. Moderate inactivity only affected lung volumes and compliance, whereas extreme inactivity increased lung inflammation, lowered body and fat mass, induced fiber atrophy with soleus muscle dysfunction and reduced exercise capacity and all bone parameters. When combined with smoking, extreme inactivity also aggravated lung inflammation and emphysema, and accelerated body and muscle weight loss. This study shows that extreme inactivity, especially when imposed by absolute rest, accelerates lung damage and inflammation. When combined with smoking, extreme inactivity is deleterious for muscle bulk, bone and lungs. These data highlight that the consequences of physical inactivity during the course of COPD should not be neglected.

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Section: Discussionmentioning

confidence: 52%

Interaction between Physical Activity and Smoking on Lung, Muscle, and Bone in Mice

Cielen

Maes

Heulens

et al. 2016

Am J Respir Cell Mol Biol

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“…In fact, mitochondria is considered a central regulator of NLRP3 inflammasome activation through ROS, Ca 2+ , decrease of NAD + , Mfn or mitochondrial DNA . In patients with diabetes, the inhibition of autophagy results in the accumulation of dysfunctional mitochondria leading to higher ROS production and activating inflammasome (Harijith et al, 2014). On the other hand, Casp-1 activates several pathways that precipitate mitochondrial disassembly, increase ROS production and breaks up mitochondrial network, triggering a vicious cycle in which mitochondrial dysfunction activates inflammasome and Casp-1 induces mitochondrial dysfunction (Yu et al, 2014).…”

Section: Inflammation and Lipid Accumulationmentioning

confidence: 99%

Mitochondrial activity and dynamics changes regarding metabolism in ageing and obesity

López-Lluch

2017

Mechanisms of Ageing and Development

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“…Hyperglycemia activate similar metabolic signaling pathways involving DAG, PKC, NADPH-oxidase and ROS generation. [20][21][22] However, ROS production by TLR4,9 depends on NADPH-oxidase and MAPK signaling pathways. In contrast, the activation of TLR2 leads to ROS production by a mechanism that is dependent on NADPH oxidase but independent of the MAPK.…”

Section: -420mentioning

confidence: 99%

Resveratrol Inhibits the Production of Reactive Oxygen Species in Phorbol Ester- and Toll-Like Receptor-Stimulated Granulocytes from Diabetic Patients

Nogueira-Machado¹

2016

JDMDC

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Although the inflammatory basis of vascular complications in T2DM has been the focus of considerable research, and distinct advances have been made in the development new therapies, the medications currently available are unable to control the serious health AbstractHyperglycemia of diabetes is associated with increase in the generation of reactive oxygen species (ROS) and vascular complications. Resveratrol (RSV) has been proposed as a therapeutic resource for human diseases such as type 2 diabetes mellitus (T2DM). However, the role of hyperglycemia on resveratrol action in cells from innate immunity is poorly studied. The aim of the present study was, to evaluate the effects of RSV on ROS production by granulocytes from T2DM patients "primed" by chronic hyperglycemia "in vivo". The effects of RSV on ROS production in granulocytes were quantified using a luminol assay. The granulocyte activators were phorbol 12,13-dibutyrate (PDB;), and LPS or zymosan (TRL4-and TRL2-activators, respectively). In some experiments, calphostin C were compared with those of RSV. RSV suppressed ROS generation in granulocytes from T2DM patients and non-diabetic (ND) controls in a similar manner (p>0.05). Percentage inhibition values was 85% and 64% in resting cells, 69 and 77% in PDB-stimulated cells, 69 and 67% in TRL4-activated cells, and 76 and 59% in TRL2-activated cells in T2DM patients and ND controls, respectively. The profile of inhibition of ROS production by calphostin C was similar to that obtained with RSV. The effect of RSV is not affected by hyperglycemia. ROS production in granulocytes from T2DM patients and ND controls was inhibited by the polyphenol in a similar manner (p>0.05). The inhibition of ROS generation by RSV was comparable with that observed with calphostin C. PKC and/or NADPHoxidase are targets of RSV action. RSV could be considered a therapeutic option to control innate immune oxidizing response and inflammation in diabetic complications. Keywords Resveratrol inhibits the production of reactive oxygen species in phorbol ester-and toll-like receptorstimulated granulocytes from diabetic patients 148Copyright: ©2016 Gonzaga et al.Citation: Gonzaga RM, Volpe CMO, Villar-Delfino PH, et al. Resveratrol inhibits the production of reactive oxygen species in phorbol ester-and toll-like receptor-stimulated granulocytes from diabetic patients.

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Reactive oxygen species at the crossroads of inflammasome and inflammation

Cited by 377 publications

References 101 publications

Interaction between Physical Activity and Smoking on Lung, Muscle, and Bone in Mice

Interaction between Physical Activity and Smoking on Lung, Muscle, and Bone in Mice

Mitochondrial activity and dynamics changes regarding metabolism in ageing and obesity

Resveratrol Inhibits the Production of Reactive Oxygen Species in Phorbol Ester- and Toll-Like Receptor-Stimulated Granulocytes from Diabetic Patients

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