Lymphocyte Markers and Natural Killer Cell Activity in Fibromyalgia Syndrome: Effects of Low-Dose, Sublingual Use of Human Interferon-alpha

Russell, I. Jon; Vipraio, Gilbert A.; Michalek, Joel E.; Craig, Fiona E.; Richards, A.

doi:10.1089/107999099313523

Cited by 16 publications

(10 citation statements)

References 37 publications

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“…93,94 In line with these findings, patients with FM have more activated T-cells circulating in blood compared to healthy controls. 95 Epinephrine activates mast cells and stimulates release of IL-1β, IL-6 and other pro-inflammatory cytokines in a β 2 AR-dependent manner. 44 Increased activation of mast cells has been observed in numerous chronic pain disorders, including FM, headache, vestibulodynia, and irritable bowel syndrome.…”

Section: Discussionmentioning

confidence: 99%

Persistent Catechol-O-methyltransferase–dependent Pain Is Initiated by Peripheral β-Adrenergic Receptors

2016

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Background Patients with chronic pain disorders exhibit increased levels of catecholamines alongside diminished activity of catechol-O-methyltransferase (COMT), an enzyme that metabolizes catecholamines. The authors found that acute pharmacologic inhibition of COMT in rodents produces hypersensitivity to mechanical and thermal stimuli via β-adrenergic receptor (βAR) activation. The contribution of distinct βAR populations to the development of persistent pain linked to abnormalities in catecholamine signaling requires further investigation. Methods Here, the authors sought to determine the contribution of peripheral, spinal, and supraspinal βARs to persistent COMT-dependent pain. They implanted osmotic pumps to deliver the COMT inhibitor OR486 (Tocris, USA) for 2 weeks. Behavioral responses to mechanical and thermal stimuli were evaluated before and every other day after pump implantation. The site of action was evaluated in adrenalectomized rats receiving sustained OR486 or in intact rats receiving sustained βAR antagonists peripherally, spinally, or supraspinally alongside OR486. Results The authors found that male (N = 6) and female (N = 6) rats receiving sustained OR486 exhibited decreased paw withdrawal thresholds (control 5.74 ± 0.24 vs. OR486 1.54 ± 0.08, mean ± SEM) and increased paw withdrawal frequency to mechanical stimuli (control 4.80 ± 0.22 vs. OR486 8.10 ± 0.13) and decreased paw withdrawal latency to thermal heat (control 9.69 ± 0.23 vs. OR486 5.91 ± 0.11). In contrast, adrenalectomized rats (N = 12) failed to develop OR486-induced hypersensitivity. Furthermore, peripheral (N = 9), but not spinal (N = 4) or supraspinal (N = 4), administration of the nonselective βAR antagonist propranolol, the β2AR antagonist ICI-118,511, or the β3AR antagonist SR59230A blocked the development of OR486-induced hypersensitivity. Conclusions Peripheral adrenergic input is necessary for the development of persistent COMT-dependent pain, and peripherally-acting βAR antagonists may benefit chronic pain patients.

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Section: Discussionmentioning

confidence: 99%

Persistent Catechol-O-methyltransferase–dependent Pain Is Initiated by Peripheral β-Adrenergic Receptors

2016

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“…The immunological status of individuals suffering from CFS has yielded heterogeneous results [12,17,31,51,52]. Clear examples are data from different CFS cohorts analyzed in a single laboratory [32].…”

Section: Discussionmentioning

confidence: 99%

Screening NK-, B- and T-cell phenotype and function in patients suffering from Chronic Fatigue Syndrome

et al. 2013

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BackgroundChronic Fatigue Syndrome (CFS) is a debilitating neuro-immune disorder of unknown etiology diagnosed by an array of clinical manifestations. Although several immunological abnormalities have been described in CFS, their heterogeneity has limited diagnostic applicability.MethodsImmunological features of CFS were screened in 22 CFS diagnosed individuals fulfilling Fukuda criteria and 30 control healthy individuals. Peripheral blood T, B and NK cell function and phenotype were analyzed by flow cytometry in both groups.ResultsCFS diagnosed individuals showed similar absolute numbers of T, B and NK cells, with minor differences in the percentage of CD4+ and CD8+ T cells. B cells showed similar subset frequencies and proliferative responses between groups. Conversely, significant differences were observed in T cell subsets. CFS individuals showed increased levels of T regulatory cells (CD25+/FOXP3+) CD4 T cells, and lower proliferative responses in vitro and in vivo. Moreover, CD8 T cells from the CFS group showed significantly lower activation and frequency of effector memory cells. No clear signs of T-cell immunosenescence were observed. NK cells from CFS individuals displayed higher expression of NKp46 and CD69 but lower expression of CD25 in all NK subsets defined. Overall, T cell and NK cell features clearly clustered CFS individuals.ConclusionsOur findings suggest that alterations in T-cell phenotype and proliferative response along with the specific signature of NK cell phenotype may be useful to identify CFS individuals. The striking down modulation of T cell mediated immunity may help to understand intercurrent viral infections in CFS.

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“…However, in contrast to the L group they had normal levels of CD4 + CD25 low , but increased numbers of CD4 + expressing HLA-DR, a marker of late cellular activation. It is plausible to consider that discrepant data in the literature of CD4 + CD25 low quantification in FM patients [4,8] might be due to different balances of these two genetic groups in those studies, as those studies considered FM patients as a unique homogeneous population [4,8].…”

Section: Discussionmentioning

confidence: 99%

May genetic factors in fibromyalgia help to identify patients with differentially altered frequencies of immune cells?

Carvalho¹,

Corrêa²,

Silva³

et al. 2008

Clinical and Experimental Immunology

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SummaryThere is common agreement that fibromyalgia (FM) is an extremely heterogeneous entity. Patients differ in their clinical symptoms, endocrine and immune parameters. In this study we evaluated endocrine and immunological features of distinct subsets of FM patients. In contrast to previous attempts to identify subsets of FM patients, based solely on their psychological and cognitive features, herein we propose to separate FM patients by genetic features. Allelic expression of the polymorphic promoter region of the serotonin transporter (5-HTTLPR) was analysed as a relevant genetic factor for FM. Seventy-five patients meeting the American College of Rheumatology criteria and 27 healthy age-matched controls participated in this study. All controls and FM patients were submitted to genotyping of 5-HTTLPR. Twenty-seven FM patients, who were able to discontinue hypnotic, sedative or psychotropic prescription medications for at least 2 weeks, were then subdivided into L (homozygote LL) or S groups (genotypes LS and SS). They were evaluated for salivary cortisol levels, absolute number of leucocyte subpopulations, including natural killer (NK) cells and activated T and B lymphocytes. Both groups presented decreased cortisol levels, more intense in the L group, increased all B lymphocytes subsets and reduced CD4 + CD25 high T lymphocytes. The L group had increased CD4 + CD25 low activated T lymphocytes, while the S group displayed elevated CD4 + human leucocyte antigen D-related (HLA-DR) + activated T lymphocytes and decreased NK cells. We demonstrate that genetic factors may help to identify FM individuals with differentially altered frequencies of immune cells.

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Lymphocyte Markers and Natural Killer Cell Activity in Fibromyalgia Syndrome: Effects of Low-Dose, Sublingual Use of Human Interferon-alpha

Cited by 16 publications

References 37 publications

Persistent Catechol-O-methyltransferase–dependent Pain Is Initiated by Peripheral β-Adrenergic Receptors

Persistent Catechol-O-methyltransferase–dependent Pain Is Initiated by Peripheral β-Adrenergic Receptors

Screening NK-, B- and T-cell phenotype and function in patients suffering from Chronic Fatigue Syndrome

May genetic factors in fibromyalgia help to identify patients with differentially altered frequencies of immune cells?

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