Superoxide anion production by circulating polymorphonuclear leucocytes in rheumatoid arthritis

Cencetti, A.; Martino, Maurizio de; Graziani, Elena; Bongi, Susanna Maddali; Palermo, Carlo; Pavari, E; Zoppi, M.

doi:10.1007/bf02030242

Cited by 9 publications

(3 citation statements)

References 16 publications

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“…25 The production of superoxide is stimulated by cytokines in several cell types, including vascular smooth muscle cells, 26 and has been documented in human RA. 27 However, acutely, cytokines appear to decrease only endothelium-dependent vasodilatation. In normal subjects, generation of an acute systemic inflammatory response by Salmonella typhimurium attenuates vasodilatory responses to bradykinin and ACh but not to the endotheliumindependent agonists verapamil and nitroglycerin.…”

Section: Bergholm Et Al Endothelial Function In Rheumatoid Arthritismentioning

confidence: 99%

Impaired Responsiveness to NO in Newly Diagnosed Patients With Rheumatoid Arthritis

Bergholm

Leirisalo‐Repo

Vehkavaara

et al. 2002

ATVB

194

129

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Objective— Cardiovascular disease is the major cause of excessive mortality in patients with rheumatoid arthritis (RA). We determined whether endothelial dysfunction characterizes patients with newly diagnosed RA (n=10) compared with normal subjects (control group, n=33) and whether it is reversible with 6 months of anti-inflammatory therapy. Methods and Results— Endothelial function was determined by measuring vasodilatory responses to intrabrachial artery infusions of acetylcholine (ACh at 7.5 and 15 μg/min, low and high dose, respectively), an endothelium-dependent vasodilator, and to sodium nitroprusside (SNP, 3 and 10 μg/min), an endothelium-independent vasodilator. Before treatment, blood flow responses (fold increase in flow) to low-dose SNP were 30% lower in the RA versus the control group (4.1±0.4-fold versus 5.9±0.5-fold, respectively), and responses to high-dose SNP were 34% lower in the RA group versus the control group (5.1±0.6-fold versus 7.7±0.7-fold, respectively; P <0.001). The responses to low-dose ACh were 50% lower in the RA group versus the control group (3.0±0.5-fold versus 6.6±0.7-fold, respectively), and responses to high-dose ACh were 37% lower in the RA group versus the control group (5.0±0.4-fold versus 7.9±0.8-fold, respectively; P <0.001). After therapy, clinical and laboratory markers of inflammation had significantly decreased. Blood flow responses to ACh increased significantly ( P =0.02). Conclusions— We conclude that newly diagnosed patients with RA have vascular dysfunction, which is reversible with successful therapy. Therefore, early suppression of inflammatory activity may reduce long-term vascular damage.

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Section: Bergholm Et Al Endothelial Function In Rheumatoid Arthritismentioning

confidence: 99%

Impaired Responsiveness to NO in Newly Diagnosed Patients With Rheumatoid Arthritis

Bergholm

Leirisalo‐Repo

Vehkavaara

et al. 2002

ATVB

194

129

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“…In an Italian study, the O 2 -production from RA "resting" PMNs was greater than control (osteoarthritis [OA] patients on the same nonsteroidal antiinflammatory drugs [NSAIDs]), but the responses to zymosan or PMN stimulation were suppressed; significance was attained only by statistical manipulation in the data analysis. [42] In yet another study, PMNs from patients with Felty's syndrome were said to have impaired superoxide production, [43] but the subjects all had peripheral white blood cell counts below 1, 500/pL with splenomegaly. The circulating peripheral cell mass in such patients clearly represents an abnormal pool of cells with regard to maturity, marrow egress, etc, and it is hard to draw conclusions about disease pathogenesis from such measurements.…”

Section: Oxygen Radical Generation In Rheumatic Diseasesmentioning

confidence: 98%

Role of Nitric Oxide and Reactive Oxygen Species in Arthritis

Cuzzocrea

2006

CPD

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A vast amount of circumstantial evidence implicates oxygen-derived free radicals, especially reactive oxygen species and nitric oxide as mediators of inflammation and/or tissue destruction in inflammatory and arthritic disorders. The aim of the current article is to overview the recent developments in this field, as it relates to the roles of nitric oxide (NO) and reactive oxygen species in the pathogenesis of this condition. The first part of the review focuses on the biochemical impact of NO and reactive oxygen species. The second part of the review deals with the novel findings related to the recently identified regulatory roles of the inducible isoform of nitric oxide synthase (iNOS) in the expression of pro-inflammatory mediators in inflammation. Reactive oxygen species can initiate a wide range of toxic oxidative reactions. These include initiation of lipid peroxidation, direct inhibition of mitochondrial respiratory chain enzymes, inactivation of glyceraldehyde-3phosphate dehydrogenase, inhibition of membrane sodium/potassium ATP-ase activity, inactivation of membrane sodium channels, and other oxidative modifications of proteins. All these toxicities are likely to play a role in the pathophysiology of inflammation. Reactive oxygen species are all potential reactants capable of initiating DNA single strand breakage, with subsequent activation of the nuclear enzyme poly (ADP ribose) synthetase (PARS), leading to eventual severe energy depletion of the cells, and necrotic-type cell death. Recently it has been demonstrated that iNOS inhibitor prevents the activation of poly (ADP ribose) synthetase, and prevents the organ injury associated with inflammation. Although the severity and duration of inflammation may dictate the timing and extent of NOS expression, it is now evident that the up-regulation of NOS can take place during sustained inflammation. Thus, induced nitric oxide, in addition to being a "final common mediator" of inflammation, is essential for the up-regulation of the inflammatory response. Furthermore, a picture of a pathway is evolving that contributes to tissue damage both directly via the formation of reactive oxygen species, with them associated toxicities, and indirectly through the amplification of the inflammatory response.

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“…The acute phase reactant C‐reactive protein (CRP) can activate the endothelium and has been shown in vitro to increase expression of adhesion molecules, such as vascular cell adhesion molecule (VCAM‐1), intercellular adhesion molecule, and E‐selectin, on endothelial cells (15). Neutrophils from RA patients produce high amounts of superoxide free radicals, which may decrease the bioavailability of nitric oxide, thus resulting in blunted vasodilatory responses (16). T lymphocyte responses could also be implicated in endothelial injury in RA.…”

mentioning

confidence: 99%

Anti–tumor necrosis factor α therapy in rheumatoid arthritis: Hitting two birds with one stone?

Warrington¹

2004

Arthritis & Rheumatism

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Superoxide anion production by circulating polymorphonuclear leucocytes in rheumatoid arthritis

Cited by 9 publications

References 16 publications

Impaired Responsiveness to NO in Newly Diagnosed Patients With Rheumatoid Arthritis

Impaired Responsiveness to NO in Newly Diagnosed Patients With Rheumatoid Arthritis

Role of Nitric Oxide and Reactive Oxygen Species in Arthritis

Anti–tumor necrosis factor α therapy in rheumatoid arthritis: Hitting two birds with one stone?

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