High cell surface CD26-associated activities and low plasma adenosine concentration in fibromyalgia

Guieu, Régis; Guedj, Éric; Giorgi, Roch; Dousset, A; Tuzzolino, Véronique; By, Youlet; Lévêque, Jean Marc; Péragut, Jean-Claude; Régis, Jean; Ruf, Jean; Fenouillet, Emmanuel; Roussel, Philippe

doi:10.1136/annrheumdis-2011-201174

Cited by 7 publications

(5 citation statements)

References 10 publications

(11 reference statements)

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“…These results may also help to distinguish ME/CFS from fibromyalgia, because the CD26 activity on PBMC increases in fibromyalgia [19] whereas it decreases in CFS patients. …”

Section: Resultsmentioning

confidence: 99%

“…As previously described [19, 23], PBMCs (1.10 6 cells) were then incubated for 60 min at 37 °C in 75 mM glycine buffer pH 8.7 with three mM Gly-Pro- p -nitroanilide, a colorimetric substrate of the peptidase CD26. The signal background was determined by incubation in acetate buffer pH 5, a condition in which DPPIV is inactive.…”

Section: Methodsmentioning

confidence: 99%

“…These immunological abnormalities also involve a decreased expression of the T cell activation marker CD26 expressed on peripheral blood mononuclear cells (PBMC) [18]. This observation, together with the reports that CD26-expression is increased in patients with fibromyalgia [19] or a metabolic syndrome [20], indicates that CD26-expression changes are present in some muscular disorders.…”

Section: Introductionmentioning

confidence: 99%

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Association of biomarkers with health-related quality of life and history of stressors in myalgic encephalomyelitis/chronic fatigue syndrome patients

et al. 2016

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BackgroundMyalgic encephalomyelitis chronic fatigue syndrome (ME/CFS) is a common debilitating disorder associated with an intense fatigue, a reduced physical activity, and an impaired quality of life. There are no established biological markerof the syndrome. The etiology is unknown and its pathogenesis appears to be multifactorial. Various stressors, including intense physical activity, severe infection, and emotional stress are reported in the medical history of ME/CFS patients which raises the question whether any physiological and biological abnormalities usually found in these patients could be indicative of the etiology and/or the quality-of-life impairment.MethodsThirty-six patients and 11 age-matched healthy controls were recruited. The following variables that appear to address common symptoms of ME/CFS were studied here: (1) muscle fatigue during exercise has been investigated by monitoring the compound muscle action potential (M-wave); (2) the excessive oxidative stress response to exercise was measured via two plasma markers (thiobarbituric acid reactive substances: TBARS; reduced ascorbic-acid: RAA); (3) a potential inflammatory component was addressed via expression of CD26 on peripheral blood mononuclear cells; (4) quality-of-life impairment was assessed using the London Handicap Scale (LHS) and the Medical Outcome Study Short Form-36 (SF-36). The medical history of each patient, including the presence of stressors such as intense sports practice, severe acute infection and/or severe emotional stress was documented.ResultsWe observed that: (1) there were striking differences between cases and controls with regard to three biological variables: post-exercise M-wave, TBARS variations and CD26-expression at rest; (2) each of these three variables correlated with the other two; (3) abnormalities in the biomarkers associated with health-related quality of life: the LHS score was negatively correlated with the exercise-induced TBARS increase and positively correlated with CD26-expression while the pain component of SF-36 was negatively correlated with CD26-expression; (4) the TBARS increase and the M-wave decrease were the highest, and the CD26-expression level the lowest in patients who had been submitted to infectious stressors.ConclusionIn ME/CFS patients, severe alterations of the muscle excitability, the redox status, as well as the CD26-expression level are correlated with a marked impairment of the quality-of-life. They are particularly significant when infectious stressors are reported in the medical history.

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“…These results may also help to distinguish ME/CFS from fibromyalgia, because the CD26 activity on PBMC increases in fibromyalgia [19] whereas it decreases in CFS patients. …”

Section: Resultsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Association of biomarkers with health-related quality of life and history of stressors in myalgic encephalomyelitis/chronic fatigue syndrome patients

et al. 2016

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“…Changes in normal levels of ADA have been reported in a wide variety of pathologies . For example, alterations in the amount of one or both isoenzymes have been observed in a number of diseases such as hereditary hemolytic and Diamond Blackfan anemias, tuberculosis, systemic lupus erythematosus, inflammatory responses, rheumatoid arthritis, heart diseases, acquired immunodeficiency syndrome, autoimmunological thyroid diseases, some types of carcinoma, and neurological disorders, such as multiple sclerosis, meningitis, fibromyalgia, depression, and panic disorder …”

Section: Introductionmentioning

confidence: 99%

Moonlighting Adenosine Deaminase: A Target Protein for Drug Development

Cortés

Gracia

Moreno

et al. 2014

Medicinal Research Reviews

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Interest in adenosine deaminase (ADA) in the context of medicine has mainly focused on its enzymatic activity. This is justified by the importance of the reaction catalyzed by ADA not only for the intracellular purine metabolism, but also for the extracellular purine metabolism as well, because of its capacity as a regulator of the concentration of extracellular adenosine that is able to activate adenosine receptors (ARs). In recent years, other important roles have been described for ADA. One of these, with special relevance in immunology, is the capacity of ADA to act as a costimulator, promoting T-cell proliferation and differentiation mainly by interacting with the differentiation cluster CD26. Another role is the ability of ADA to act as an allosteric modulator of ARs. These receptors have very general physiological implications, particularly in the neurological system where they play an important role. Thus, ADA, being a single chain protein, performs more than one function, consistent with the definition of a moonlighting protein. Although ADA has never been associated with moonlighting proteins, here we consider ADA as an example of this family of multifunctional proteins. In this review, we discuss the different roles of ADA and their pathological implications. We propose a mechanism by which some of their moonlighting functions can be coordinated. We also suggest that drugs modulating ADA properties may act as modulators of the moonlighting functions of ADA, giving them additional potential medical interest.

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“…Interestingly, these functional abnormalities have been also reported at resting-state at individual-level in absence of provoked pain, in hyperalgesic patients with fibromyalgia using SPECT imaging [25]. These abnormalities could be related to metabolism of adenosine [26]. In details, hyperperfusions were found in primary somato-sensory cortices, in regions of the brain known to be involved in the sensory dimension of pain processing, while hypoperfusions were found in frontal, cingulate, medial temporal and cerebellar cortices, in areas assumed to be associated with the affective-attentional dimension of the pain.…”

Section: Functional Neuroimaging Abnormalities In Fibromyalgia and Mamentioning

confidence: 61%

Functional neuroimaging in patients presenting with somatoform disorders: A model for investigating persisting symptoms after tick bites and post-treatment Lyme disease syndrome?

Guedj

Eldin

Raoult

et al. 2019

Médecine et Maladies Infectieuses

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Approximately 10% of patients with Lyme disease will develop fatigue, musculoskeletal pain, difficulties of concentration or deficits in short-term memory within the 6 months after treatment. This entity has been defined as Post Lyme Disease Syndrome or Post Treatment Lyme Disease Syndrome. The pathophysiology of this syndrome is not known, but neither persistence of the bacterium nor efficiency of antibiotics are currently sustained by the existing literature. In France, the Haut Conseil de Santé Publique has recently define a new entity called "persistent polymorphic semiology after tick bite" allowing to design studies to better understand these subjective manifestations, for which objective biomarkers currently lack. This entity encompasses patients suffering from fatigue and global pain in the months following a tick bite, and can be associated to several subjective symptoms with a major impact on quality of life.In interaction with the model of somatoform disorders, this article proposes a review of functional neuroimaging studies in patients with subjective complaints and discusses possible clinical implications for persisting symptoms after tick bites and Post Treatment Lyme Disease Syndrome.

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High cell surface CD26-associated activities and low plasma adenosine concentration in fibromyalgia

Cited by 7 publications

References 10 publications

Association of biomarkers with health-related quality of life and history of stressors in myalgic encephalomyelitis/chronic fatigue syndrome patients

Association of biomarkers with health-related quality of life and history of stressors in myalgic encephalomyelitis/chronic fatigue syndrome patients

Moonlighting Adenosine Deaminase: A Target Protein for Drug Development

Functional neuroimaging in patients presenting with somatoform disorders: A model for investigating persisting symptoms after tick bites and post-treatment Lyme disease syndrome?

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