Naloxone‐Reversible Monocyte Dysfunction in Patients with Chronic Fatigue Syndrome

Prieto, Jesús; Subirá, M L; Castilla, Alberto; Serrano, M.

doi:10.1111/j.1365-3083.1989.tb01183.x

Cited by 38 publications

(6 citation statements)

References 56 publications

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“…The existence of a state akin to endotoxin tolerance could also potentially explain a considerable body of data indicating the presence of exhausted or anergic CD4 and CD8 cells in CFS patients (Brenu et al 2011, 2016; Klimas et al 1990; Loebel et al 2014; Prieto et al 1989; Straus et al 1993). This is also true of elevated Foxp3 + Tregs which appear to have been universally reported by researchers using advanced flow cytometry techniques (Brenu et al 2011, 2014b; Curriu et al 2013; Ramos et al 2016).…”

Section: Can Immune and Metabolic Abnormalities Be Explained By Endotmentioning

confidence: 99%

Myalgic encephalomyelitis or chronic fatigue syndrome: how could the illness develop?

et al. 2019

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A model of the development and progression of chronic fatigue syndrome (myalgic encephalomyelitis), the aetiology of which is currently unknown, is put forward, starting with a consideration of the post-infection role of damage-associated molecular patterns and the development of chronic inflammatory, oxidative and nitrosative stress in genetically predisposed individuals. The consequences are detailed, including the role of increased intestinal permeability and the translocation of commensal antigens into the circulation, and the development of dysautonomia, neuroinflammation, and neurocognitive and neuroimaging abnormalities. Increasing levels of such stress and the switch to immune and metabolic downregulation are detailed next in relation to the advent of hypernitrosylation, impaired mitochondrial performance, immune suppression, cellular hibernation, endotoxin tolerance and sirtuin 1 activation. The role of chronic stress and the development of endotoxin tolerance via indoleamine 2,3-dioxygenase upregulation and the characteristics of neutrophils, monocytes, macrophages and T cells, including regulatory T cells, in endotoxin tolerance are detailed next. Finally, it is shown how the immune and metabolic abnormalities of chronic fatigue syndrome can be explained by endotoxin tolerance, thus completing the model.

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Section: Can Immune and Metabolic Abnormalities Be Explained By Endotmentioning

confidence: 99%

Myalgic encephalomyelitis or chronic fatigue syndrome: how could the illness develop?

et al. 2019

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“…While one group reported decreases in delayed hypersensitivity skin reaction to injection of common antigens (38), two others did not (40,61). Of those studies evaluating in vitro peripheral blood mononuclear cell (indicated below by an asterisk) or T-cell function in response to various lymphocyte stimulants, five showed decreases (10,26,38,57,63), one showed increases (24), and seven showed no differences (2, 10,* 16,* 18, 40, 41, 59). The reader should note that one group reported increases in some variables, decreases in others, and no change in yet others (10); moreover, one group reported no significant differences between patients and controls when phytohemagglutinin, concanavalin A, or poke weed antigen were the stimulants but did find significantly lower activity in CFS patients when soluble antigens such as tetanus toxoid were used (16).…”

Section: Inconsistent Immune Markersmentioning

confidence: 99%

Evidence for the Presence of Immune Dysfunction in Chronic Fatigue Syndrome

Natelson¹,

Haghighi

Ponzio

2002

Clin Vaccine Immunol

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Chronic fatigue syndrome is a medically unexplained ailment characterized by new onset of fatigue accompanied by rheumatological, infectious, and neuropsychiatric symptoms. Because the ailment often begins suddenly with a flu-like presentation, early pathophysiological ideas as to cause included viral infection and immune activation. When early reports identified putative immunological abnormalities in this illness, it was given the name of chronic fatigue and immune dysfunction syndrome, or CFIDS.The purpose of this review is to evaluate the immunological literature to determine if strong evidence to support this notion exists. We collected and reviewed 239 published papers, of which only 72 fulfilled a set of criteria for use in this review. For this review, we developed the following criteria: papers had to be published in the peer review literature; patients had to be from a group with substantial fatigue lasting at least 6 months (the vast majority fulfilled either the 1988 [21] or the 1994 [13] case definition of chronic fatigue syndrome [CFS]); papers had to compare CFS patients to healthy controls; and actual data had to be shown with evidence of testing for statistical significance. So, for example, when a paper reported no difference between patients and controls for some immunological variables but actual data were not included, we did not include it. Also, if a report compared patient data to normative values rather than to the study's own control group, we did not include it.The numbers of immunologically active cells and immunologically active substances such as cytokines reported in the literature have mushroomed in the past decade. To keep this review manageable, we are reporting scientific papers only on those variables for which either consistent or inconsistent abnormalities were reported by more than one group. We did not review papers reporting immunological variables to be within normal limits but have listed those studies in which more than one group found such results in a table. We have chosen not to list those variables reported abnormal in only one study because those results have not yet been replicated. When inconsistent results among laboratories were found for any immunological variable, we reviewed the methods described in those papers in an effort to identify reasons for such discrepancies.Note: when a group published more than one paper and it was apparent that the two studies used many if not all of the patients whose data are in the second paper, we chose to include only the more recent paper or the one with the largest number of subjects. To provide several examples, Tirelli published two papers, the first with 205 subjects and the second with 265 patients (66, 67). When data from one variable appeared in both papers, we included data from only the latter. Our own group has published three papers using different statistical methods and making different comparisons when reviewing lymphocyte populations. Thus, we used the one paper that controlled for multiple comparisons (74)...

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“…A number of immunological abnormalities have been described in CFS [5,13. 14,[17][18][19][21][22][23]27,28]. The data have been rather conflicting.…”

mentioning

confidence: 99%

A Comprehensive Immunological Analysis in Chronic Fatigue Syndrome

1991

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A detailed analysis of cell-mediated and antibody-mediated immunity was performed in 20 CDC-defined patients with chronic fatigue syndrome (CFS) and 20 age- and sex-matched healthy controls. CD3+, CD4+, CD8+, and CD20+ lymphocytes were comparable in two groups. Natural killer cells as defined by CD16, CD56 and CD57 antigens were significantly reduced in CFS. A significant increase in the proportions of CD4+ ICAM 1+ T cells was observed in CFS. Monocytes from CFS displayed increased density (as determined by mean fluorescence channel numbers) of intercellular adhesion molecule 1 (ICAM-1) and lymphocyte function associated antigen 1 (LFA-1), but showed decreased enhancing response to recombinant interferon-gamma in vitro. The lymphocyte DNA synthesis in response to phytohaemoglobulin (PHA), Concanavalin A (Con A) and pokeweed mitogen (PWM) was normal but the response to soluble antigens was significantly reduced. Serum IgM, IgG, IgA, and IgG subclasses were normal. In vivo specific antibody response to pneumococcus vaccine was depressed in CFS. Forty percent of patients showed titres of anti-human herpes virus 6 (anti-HHV-6) antibody higher than that in the controls (greater than or equal to 1/80). These data suggest immunological dysfunction in patients with chronic fatigue syndrome. The significance of these observations is discussed.

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Naloxone‐Reversible Monocyte Dysfunction in Patients with Chronic Fatigue Syndrome

Cited by 38 publications

References 56 publications

Myalgic encephalomyelitis or chronic fatigue syndrome: how could the illness develop?

Myalgic encephalomyelitis or chronic fatigue syndrome: how could the illness develop?

Evidence for the Presence of Immune Dysfunction in Chronic Fatigue Syndrome

A Comprehensive Immunological Analysis in Chronic Fatigue Syndrome

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