Major depression is characterized by multifarious symptoms and symptoms clusters, such as the melancholic and anxiety symptom clusters. There is a strong comorbidity and a biological similarity between major depression and myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS).The aim of the present study was to examine "psychosomatic" symptoms reminiscent of ME/CFS in major depression.Toward this end, we examined the 12-item Fibromyalgia and Chronic Fatigue Syndrome Rating (FF) Scale and the Hamilton Depression Rating Scale (HDRS) in 103 major depressed patients by means of multivariate pattern recognition methods. results: Our findings support the existence of two factors, i.e. a fatigue and somatic (F&S) factor, i.e aches and pain, muscular tension, fatigue, concentration difficulties, failing memory, irritability, irritable bowel, headache, and a subjective experience of infection; and a depression factor, i.e. sadness, irritability, sleep disorders, autonomic symptoms, and a subjective experience of infection. Cluster analysis performed on the 12 FF items found two different clusters, which were separated by highly significant differences in the F&S items, the most significant being a subjective experience of infection, aches and pain, muscular tension, fatigue, concentration difficulties and failing memory. Multivariate analyses showed that the differences between both clusters were quantitatively, and not qualitatively, and reflected the severity of the F&S dimension. There was a strong association between the F&S symptoms and melancholia and chronic depression. Treatment resistant depression was characterized by higher scores on the depression factor score. There was a strong correlation between the HDRS score and the FF items, fatigue, a subjective experience of infection, and sadness. Our findings show that F&S symptoms are a major feature of depression and largely predict severity of illness, and chronic and melancholic depression.It is concluded that the diagnostic criteria of depression and melancholia and rating scales to measure severity of illness should be modified to include the F&S symptom profile.
Severe socioeconomic deprivation (SED) and adverse childhood experiences (ACE) are significantly associated with the development in adulthood of (i) enhanced inflammatory status and/or hypothalamic-pituitary-adrenal (HPA) axis dysfunction and (ii) neurological, neuroprogressive, inflammatory and autoimmune diseases. The mechanisms by which these associations take place are detailed. The two sets of consequences are themselves strongly associated, with the first set likely contributing to the second. Mechanisms enabling bidirectional communication between the immune system and the brain are described, including complex signalling pathways facilitated by factors at the level of immune cells. Also detailed are mechanisms underpinning the association between SED, ACE and the genesis of peripheral inflammation, including epigenetic changes to immune system-related gene expression. The duration and magnitude of inflammatory responses can be influenced by genetic factors, including single nucleotide polymorphisms, and by epigenetic factors, whereby pro-inflammatory cytokines, reactive oxygen species, reactive nitrogen species and nuclear factor-κB affect gene DNA methylation and histone acetylation and also induce several microRNAs including miR-155, miR-181b-1 and miR-146a. Adult HPA axis activity is regulated by (i) genetic factors, such as glucocorticoid receptor polymorphisms; (ii) epigenetic factors affecting glucocorticoid receptor function or expression, including the methylation status of alternative promoter regions of NR3C1 and the methylation of FKBP5 and HSD11β2; (iii) chronic inflammation and chronic nitrosative and oxidative stress. Finally, it is shown how severe psychological stress adversely affects mitochondrial structure and functioning and is associated with changes in brain mitochondrial DNA copy number and transcription; mitochondria can act as couriers of childhood stress into adulthood.
Commentary| July 24 2001 Psychological stress and the inflammatory response system MICHAEL MAES MICHAEL MAES 1Department of Psychiatry and Neuropsychology, University Hospital of Maastricht, Postbus 5800, 6202 AZ Maastricht, The Netherlands(ON BEHALF OF THE EDITORIAL BOARD) Search for other works by this author on: This Site PubMed Google Scholar Clin Sci (Lond) (2001) 101 (2): 193–194. https://doi.org/10.1042/cs1010193 Views Icon Views Article contents Figures & tables Video Audio Supplementary Data Peer Review Share Icon Share Facebook Twitter LinkedIn Email Cite Icon Cite Get Permissions Citation MICHAEL MAES; Psychological stress and the inflammatory response system. Clin Sci (Lond) 1 August 2001; 101 (2): 193–194. doi: https://doi.org/10.1042/cs1010193 Download citation file: Ris (Zotero) Reference Manager EasyBib Bookends Mendeley Papers EndNote RefWorks BibTex toolbar search Search Dropdown Menu toolbar search search input Search input auto suggest filter your search All ContentAll JournalsClinical Science Search Advanced Search This content is only available as a PDF. The Biochemical Society and the Medical Research Society © 20012001 Article PDF first page preview Close Modal You do not currently have access to this content.
AbstractMaes M, Bosmans E, Scharpé S, Hendriks D, Cooremans W, Neels H, De Meyer F, D'Hondt P, Peeters D. Components of biological variation in serum soluble transferrin receptor: relationships to serum iron, transferrin and ferritin concentrations, and immune and haematological variables. Scand J Clin Lab Invest 1997:57:31–41.We investigated the components of biological variation in serum soluble transferrin receptor (TfR) in relation to serum iron, transferrin (Tf), ferritin, soluble interleukin-2 receptor (sIL-2R), sIL-6R, and number of erythrocytes, haemoglobin (Hb), haematocrit (Ht), mean corpuscular volume (MCV), mean cell haemoglobin (MCH), and erythrocyte distribution width (RDW). We took monthly blood samples during 1 calendar year from 26 healthy subjects for assay of the above variables. The estimated CVs for TfR were interindividual CVg=20.8%, and intra-individual CVi=13.6%; for Tf, CVg=14.4% and CVi=6.7%; for iron, CVg=16.8% and CVi=29.2%; and for ferritin, CVg=71.1% and CVi=26.5%. There was a statistically significant seasonal pattern in the four variables with significant annual, biannual and/or trimonthly rhythms, which were expressed as a group phenomenon. The peak-trough differences in the yearly variations, expressed as a percentage of the mean, were: for TfR, 11.7%; for iron, 39.2%; for Tf, 11.7%; and for ferritin, 29.3%. Up to 34.2% of the within-subject variability in TfR (which reflects changes over time) could be explained by the regression on iron, ferritin, Tf, sIL-2R, sIL-6R and MCH values. Up to 67.2% of the between-subject variability in TfR (which reflects differences in the homeostatic setpoint during the study year) could be explained by the regression on gender, iron, Tf, and ferritin values.Key Words: chronobiologyferritininterleukin-2interleukin-6receptorseasonalitysource of variationtransferrin
Background: Immune dysregulation is a component of Major Depressive Disorder (MDD). Cannabidiol (CBD) has immunomodulatory and putative antidepressant effects. The relationship between apoptotic and exhaustion immune markers and the clinical features of MDD and the effects of CBD on these markers are still unknown. Objectives: To assess pro-apoptotic (CD95) and T cell exhaustion (TIM3) markers on immune cells in patients with MDD, as well as the impact of in vitro CBD administration on these markers. Methods: We recruited healthy controls and MDD patients and evaluated the immunophenotypes of T/B lymphocytes using flow cytometry in unstimulated and anti-CD3/CD28 stimulated conditions. We evaluated the immune profiles of M1 macrophages, T helper (Th)17 cells, immune-inflammatory response system (IRS), T cell proliferation, and immune-related neurotoxicity (IRN). We investigated the in vitro effects of CBD on immune cell subsets at concentrations of 0.1 ug/mL, 1 ug/mL, and 10.0 ug/mL. Results: The stimulated CD3+CD95+ cell percentages were substantially correlated with the number of depressive episodes, recurrence of illness, and suicidal behaviors. The stimulated CD8+TIM-3+ cell percentages were substantially and inversely associated with the M1, IRS, CIRS, T cell growth, and IRN immune profiles. TIM-3+ bearing CD3+, CD4+, CD8+, and CD20+ cells were significantly suppressed by lower CBD concentrations (0.1 to 1 ug/mL). TIM3+ and all CD95+ bearing cells, with the exception of CD3+CD95+, were suppressed by the higher CBD concentrations. Discussion: Aberrations in immune checkpoint molecular processes impact the features of MDD. CBD significantly impacts apoptotic and exhaustion processes thereby possibly interfering with immune homeostasis.
Abstract Background Neuro-immune pathways are engaged in antenatal and postpartum depression. Aims: To determine if immune profiles influence the severity of prenatal depression above and beyond the effects of adverse childhood experiences (ACE), premenstrual syndrome (PMS) and current psychological stressors. Methods Using the Bio-Plex Pro human cytokine 27-plex test kit, we assayed M1 macrophage, T helper (Th)-1, Th-2, Th-17, growth factor, chemokine, T cell growth immune profiles as well as indicators of the immune inflammatory response system (IRS) and compensatory immunoregulatory system (CIRS) in 120 pregnant females in the early (<16 weeks) and late (> 24 weeks) pregnancy. The Edinburgh Postnatal Depression Scale (EPDS) was used to assess severity of antenatal depression. Results Cluster analyses showed that the combined effects of ACE, relationship dissatisfaction, unwanted pregnancy, PMS, and upregulated M1, Th-1, Th-2 and IRS immune profiles and the ensuing early depressive symptoms shape a stress-immune-depression phenotypic class. Elevated IL-4, IL-6, IL-8, IL-12p70, IL-15, IL-17 and GM-CSF are the primary cytokines associated with this new phenotypic class. All immune profiles (except CIRS) were significantly associated with the early EPDS score, independent of the effects of psychological variables and PMS. There was a shift in immune profiles from early to late pregnancy, with an increase in the IRS/CIRS ratio. The late EPDS score was predicted by the early EPDS score, adverse experiences, and immune profiles, mainly the Th-2 and Th-17 phenotypes. Conclusions Activated immune phenotypes contribute to early and late perinatal depressive symptoms above and beyond the effects of psychological stressors and PMS.
