Clinical studies had shown a correlation between mindfulness and changes in the immune response. Other studies had observed an interaction between sensory neurons and neuropeptide-mediated immune response.

This research aims to provide theoretical support to carry out a clinical study based on psychoneuroimmunology.

For this, An epistemological analysis of the concepts of autopoiesis and evocative body was carried out to explain the self-conformation of the organism.

The result of this analysis indicates that the autopoietic process of the organism can be experienced from the three levels proposed by the concept of the evocative body (preontological, ontological and logical). It is posible to generate a nexus between the preontological and the logical in the autopoietic process through the ontological level. Mindfulness is the tool through which it is possible to access the ontological and thus express the preontological in the logical, thereby generating the theoretical possibility of being able to influence our therapeutic process.

This analysis supports the concept of the self-management in health as a measurable therapeutic tool in a clinical study.

No significant relationships.

The study of effects of long-term antipsychotic therapy in patients with schizophrenia is relevant.

To study effects of long-term antipsychotic therapy on parameters of immunity and cytokine levels in patients with schizophrenia.

We examined 20 schizophrenic patients, who received quetiapine (group 1) and 17 - olanzapine (group 2) for more than 6 months before admission in the hospital as the main anti-recurrence therapy. Persons aged 20-63 years with length of the follow-up of the disease ≥1 year were included. The investigations included: phenotyping of immunocompetent cells into CD differentiation clusters by flow cytometry; mitogen-induced, spontaneous production of cytokines (IL2, IFN-γ, IL-4, TNF-α) were identified with use of kits for enzyme-linked immunosorbent assay (ELISA).

It was shown that patients of group 1 in comparison with group 2 were characterized by lower values of СD3- lymphocytes (p=0.049), higher values of the spontaneous production of IFN-γ (p=0.01), mitogen-induced production of IL-2 (p=0.043) and IL-4 (p=0.059). In all examined low level of mitogen-induced of IFN-γ (p=0.0001) and TNFα (p=0.002; p=0.0001), high level of spontaneous production of TNFα (p=0.001) were revealed in relation to control.

It was found that the acute period of schizophrenia after prolonged treatment with atypical antipsychotics is accompanied by immunological imbalance and dysregulation of the cytokine system. More severe immune disorders when hospitalized during the exacerbation period were revealed in patients who had been receiving antipsychotic therapy with the atypical antipsychotic quetiapine for a long time. This can be associated with the features of the mechanism of action of atypical antipsychotics.

No significant relationships.

Encephalitis due to anti-N-methyl-D-aspartate receptor antibodies (ANMDARE) is the most frequent immune-mediated encephalitis. It is distinguished by the subacute onset of neuropsychiatric symptoms.

To evaluate the characteristic neuropsychiatric symptoms and their outcome in patients diagnosed with ANMDARE.

This was a prospective, longitudinal study in patients with a diagnostic suspicion of ANMDARE that presented to the National Institute of Neurology from March 2018 to February 2019. A comparative analysis of two groups (positive N-methyl-D-aspartate receptor [NMDAR] vs. negative NMDAR antibodies in cerebrospinal fluid [CSF]) was done on admission and at discharge. Neuropsychiatric systematic assessments included the Neuropsychiatric Inventory Questionnaire, the Bush Francis Catatonia Rating Scale, the Confusion Assessment Method Severity, the Montreal Cognitive Assessment, and the Overt Agitation Severity Scale.

24 individuals were analysed: 14 had positive NMDAR antibodies, and 10 had negative NMDAR antibodies in CSF. On admission, agitation/aggression, euphoria/exaltation, and disinhibition were more common in patients with positive antibodies. Excited catatonia and delirium were diagnosed more frequently in patients with positive antibodies. At discharge, there was an important decrease in neuropsychiatric symptoms, but substantial cognitive impairment remained. The mean hospitalisation length was 41.71 (SD 39.33) days for patients with definitive ANMDARE (p 0.259).

Neuropsychiatric symptoms profile in ANMDARE was associated with the early onset of euphoria/exaltation and disinhibition, accompanied by marked psychomotor agitation. When ANMDARE was suspected, the presence of excited-type catatonia and delirium showed a tendency to predict definitive ANMDARE. At discharged, most patients recovered from catatonia, delirium, and psychosis, but marked cognitive symptoms, anxiety, and depression persisted at discharge.

Although accumulating evidence supports the hypothesis that immune/inflammatory mechanisms are associated with the pathophysiology of bipolar disorder (BD), data about the profile of chemokines (chemotactic cytokines) and chemokine receptors are still scarce. The current study was designed to evaluate the expression of chemokine receptors on lymphocytes of patients with BD in comparison with controls.

Thirty-three patients with type I BD (N = 21 in euthymia; N = 6 in mania/hypomania; N = 6 in depression) and 22 age- and sex-matched controls were subjected to clinical evaluation and peripheral blood draw. The expression of chemokine receptors CCR3, CCR5, CXCR4, and CXCR3 on CD4+ and CD8+ lymphocytes was assessed by flow cytometry.

Patients with BD had decreased percentage of CD4+CXCR3+ (p = 0.024), CD4+CCR3+ (p = 0.042), and CD4+CCR5+ (0.013) lymphocytes in comparison with controls. The percentage of both CD4+ and CD8+ lymphocytes expressing the chemokine receptor CXCR4 was similar in patients with BD and controls. Likewise, the percentages of CD8+CXCR3+, CD8+CCR3+, and CD8+CCR5+ lymphocytes were similar in patients with BD and controls.

Our findings reinforce the hypothesis that immune pathways, especially involving CD4+ lymphocytes, are involved in the physiopathology of BD.

Immunological theories, particularly the sickness syndrome theory, may explain psychopathology in mood disorders. However, no clinical trials have investigated the association between overall immune system markers with a wide range of specific symptoms including potential gender differences.

We included two similar clinical trials, the lithium treatment moderate-dose use study and clinical and health outcomes initiatives in comparative effectiveness for bipolar disorder study, enrolling 765 participants with bipolar disorder. At study entry, white blood cell (WBC) count was measured and psychopathology assessed with the Montgomery and Aasberg depression rating scale (MADRS). We performed analysis of variance and linear regression analyses to investigate the relationship between the deviation from the median WBC, and multinomial regression analysis between different WBC levels. All analyses were performed gender-specific and adjusted for age, body mass index, smoking, race, and somatic diseases.

The overall MADRS score increased significantly for each 1.0×109/l deviation from the median WBC among 322 men (coefficient=1.10; 95% CI=0.32–1.89; p=0.006), but not among 443 women (coefficient=0.56; 95% CI=−0.19–1.31; p=0.14). Among men, WBC deviations were associated with increased severity of sadness, inner tension, reduced sleep, reduced appetite, concentration difficulties, inability to feel, and suicidal thoughts. Among women, WBC deviations were associated with increased severity of reduced appetite, concentration difficulties, lassitude, inability to feel, and pessimistic thoughts. Both higher and lower WBC levels were associated with increased severity of several specific symptoms.

Immune system alterations were associated with increased severity of specific mood symptoms, particularly among men. Our results support the sickness syndrome theory, but furthermore emphasise the relevance to study immune suppression in bipolar disorder. Due to the explorative nature and cross-sectional design, future studies need to confirm these findings.

The present paper is devoted to evaluation of clinical and immunomodulatory effect of ultra-high dilutions of antibodies to human interferon γ, included in the complex therapy of patients with schizophrenia.

The study was carried out at the Mental Health Research Institute, Tomsk, Russian Federation. This double-blind, placebo-controlled randomised in parallel-group study enrolled 40 patients. As a part of complex therapy, patients from the main group (n=20) received anaferon, a drug containing ultra-high dilutions of affinity-purified antibodies to human interferon γ as the active pharmaceutical ingredient; patients from the comparative group (n=20) received placebo. Duration of the therapy was 30±5 days. Assessment of severity of symptoms and changes in them were made using clinical scales: Positive and Negative Syndrome Scale, Clinical Global Impression, Abnormal Involuntary Movements Scale. Spontaneous and phytohemagglutinin-induced production of interferon γ by immunocompetent cells in supernatants of 48 h whole blood culture of patients was measured by enzyme-linked immunosorbent assay (ELISA) method.

The reduction of interferon-producing potential by immunocompetent cells in comparison with reference normal value was shown in total group of patients (n=40) before combined therapy. During the treatment, increase of spontaneous interferon γ production and favourable changes in psychopathological symptoms as compared with placebo were shown in subjects receiving anaferon. It was found that favourable changes in clinical symptoms assessed using clinical scales with a high degree of confidence correlated with high level of spontaneous interferon γ production.

Anaferon as a part of complex therapy of patients with schizophrenia contributes to enhancement of its efficacy acting via mechanism of psychoimmunomodulation.

Chronic inflammation is implicated in numerous diseases, including major depression and type 2 diabetes mellitus (T2DM). Since depression and T2DM often co-exist, inflammatory pathways are suggested as a possible link. Hence, the establishment of an immune-mediated animal model would shed light on mechanisms possibly linking depression and metabolic alterations.

In this study we investigated a behavioural and metabolic paradigm following chronic infusion with low doses of lipopolysaccharide (LPS) using osmotic minipumps in male rats.

Behavioural testing consisted of evaluating activity level in the open field and depressive-like behaviour in the forced swim test. Metabolic assessment included measurement of body weight, food and water intake, and glucose and insulin levels during an oral glucose tolerance test.

LPS-infused rats showed acute signs of sickness behaviour, but chronic LPS infusion did not induce behavioural or metabolic changes.

These results suggest that although inflammation is immediately induced as indicated by acute sickness, 4 weeks of chronic LPS administration via osmotic minipumps did not result in behavioural changes. Therefore, this paradigm may not be a suitable model for studying the underlying mechanisms that link depression and T2DM.

Although poor sleep accompanies depression, it is unknown which specific sleep abnormalities precede depression. This is similarly the case for depression developing during interferon-α (IFN-α) therapy. Because vulnerability becomes evident in those who slept poorly before IFN-α, we prospectively determined which specific aspect of sleep could predict subsequent depression.

Two nights of polysomnography with quantitative electroencephalogram (EEG) were obtained in 24 adult, euthymic subjects – all subsequently treated with IFN-α for hepatitis C. Every 2 weeks, a Beck Depression Inventory-II (BDI-II) score was obtained, and the maximal increase in BDI-II from pre-treatment baseline – excluding the sleep question – was determined.

The delta sleep ratio (DSR; an index of early-night restorative delta power) was inversely associated with BDI-II increases (p<0.01), as was elevated alpha power (8–12 Hz; p<0.001). Both delta (0.5–4 Hz) and alpha power exhibited high between-night correlations (r=0.83 and 0.92, respectively). In mixed-effect repeated-measure analyses, there was an interaction between alpha power and DSR (p<0.001) – subjects with low alpha power and elevated DSR were resilient to developing depression. Most other sleep parameters – including total sleep time and percentage of time in slow wave sleep – were not associated with subsequent changes in depression.

Both high DSR and low alpha power may be specific indices of resilience. As most other aspects of sleep were not associated with resilience or vulnerability, sleep interventions to prevent depression may need to specifically target these specific sleep parameters.

Previous studies have suggested that somatoform disorders (SFD) might be associated with changes in the function of the central and autonomic nervous systems. The aim of this study was to examine the possible immunological differences between SFD and healthy controls.

Twenty-four patients with SFD and 13 healthy individuals completed the psychological questionnaires to assess symptom reporting [Symptom Checklist-90 Revised (SCL-90-R)] and to diagnose for SFD [Screening for Somatoform Symptoms scale (SOMS-scale)]. Participants also provided a blood sample taken in the morning, which was analysed with an automated cell counter to determine the number of leucocytes per μl and with flow cytometry to determine lymphocyte subsets.

With the exception of a higher T4/T8 ratio in the patient group, which was mainly because of lower CD8 counts, there were no significant differences in the absolute number of lymphocytes (subsets) between patients with SFD and healthy subjects. A positive correlation between B-lymphocyte subsets (CD19+CD22+, CD19+CD5+, CD19+CD3−) to all scales of the SCL-90-R, except somatisation, were found in SFD. Additionally, a positive correlation was found in SFD between CD14+CD16+ monocytes and somatisation (0.573) on the SCL-90-R scale.

These data indicate that patients with SFD have an enhanced humoral immunity as shown by increased B-cell numbers and furthermore an elevated T4/T8 ratio because of lower CD8 suppressor cells. Further studies will be required to determine whether these alterations in lymphocyte subsets are directly involved in the pathophysiology of SFD.

The aim of the current study is to determine whether serum levels of brain-derived neurotrophic factor (BDNF) and interleukin-2 (IL-2) can be biological indicators for the diagnosis of schizophrenia in patients with depressive symptoms.

Forty-seven patients (11 patients diagnosed with schizophrenia, 16 patients diagnosed with schizophrenia and comorbid depression and 20 patients diagnosed with major depressive disorder) and 20 healthy subjects were enrolled. The Positive and Negative Symptoms Scale, the Calgary Depression Scale for Schizophrenia and the Hamilton Depression Rating Scale were used for assessment. The serum BDNF and IL-2 levels of all the subjects were studied.

Decreased levels of serum BDNF and increased levels of serum IL-2 were found in the patients diagnosed with either schizophrenia, schizophrenia with depression, or major depressive disorder (p = 0.049, p = 0.010; p = 0.001 and p = 0.044; p = 0.027, p = 0.003; respectively) compared with control group. There were no significant differences between the patient groups in their serum BDNF and IL-2 levels.

The present study suggests that neurotrophic factors and immune system changes are involved in the pathogenesis of schizophrenia with or without depressive symptomatology. However, the data do not clarify whether depressive symptoms in schizophrenia occur as a dimension of schizophrenia or as symptoms of major depression that is comorbid with schizophrenia.

Recent genetic studies have revealed that the interleukin (IL) 1 gene complex is associated with schizophrenia in the Caucasian population; however, data from the North African population are limited. To further assess the role of interleukin 1 receptor antagonist protein (IL1Ra) in schizophrenia, we examined a functional multiallelic polymorphism localised in intron 2 of this receptor gene associated with an altered level of IL1Ra.

In the present case–control study, we have analysed the (86 bp)n polymorphism of the interleukin 1 receptor antagonist (IL1RN) gene (RS 1794068) by polymerase chain reaction genotyping in 259 patients with schizophrenia and 178 healthy controls from the Tunisian population.

We showed that the frequencies of the IL1RN*2/2 genotype and allele 2 were higher in the patient group compared with the control group, and the difference was statistically significant [13.5% vs. 5.6%, p = 10−3, odds ratio (OR) = 3.2% and 32.8% vs. 21.9%, p = 3 × 10−4, OR = 1.76, respectively). When we evaluated the association between this genetic polymorphism and the clinical variables of schizophrenia, we found that the frequencies of the 2/2 genotype and allele 2 were significantly higher in the male patient group (p = 10−4 and 10−5, respectively) compared with the male control group, indicating a substantially increased risk for sex-onset schizophrenia with inheritance of the IL1RN2 allele. When the association between the genotypes and outcome was evaluated by multiple logistic regression analysis, the adjusted OR for the IL1RN genotypes remained statistically significant [1.39; 95% confidence interval (CI) = 1.11–1.73; p = 0.003].

The intron 2 polymorphism in IL1RN or a genetic polymorphism at proximity seems to be associated specifically with schizophrenia in the Tunisian male population.