scholarly journals NEUROIMMUNE MECHANISMS OF COGNITIVE IMPAIRMENT AT AFFECTIVE DISORDERS

2019 ◽  
Vol 19 (1S) ◽  
pp. 76-78
Author(s):  
B G Goldin
Keyword(s):  
Cognitive Impairment ◽  
Functional Activity ◽  
Affective Disorders ◽  
Proliferative Activity ◽  
Mononuclear Cells ◽  
Control Function ◽  
Radioactive Label ◽  
Immune System Dysfunction ◽  
Tnf Α ◽  
Blood Mononuclear Cells

The aim of this study was the identification of the neuroimmune mechanisms of cognitive impairment on the basis of investigation of an of cognitive disorders association with functional activity of blood mononuclear cells and the synthesis of tumor necrosis factor - α (TNF-α) in patients with affective disorders in the form of depressive reactions and depression.TNF-α expression level in blood mononuclear cells of patients conducted with using the reverse transcriptase polymerase chain reaction method. The proliferative activity of blood mononuclear cells was investigated by a standard method based on the inclusion of a radioactive label. Cognitive function was assessed on the basis of perception, memory, praxis, speech, and control function. The severity of affective symptoms was measured by the Hamilton scale. It was found that patients with depressive reactions were characterized by the mild non-elemental cognitive impairment; while, in patients with depression, more severe non-elemental cognitive impairments in the form of decreased attention, memory, and daily activity were observed. In patients with affective disorders in the form of depression, an increase in the synthesis of TNF-α in blood mononuclear cells was detected, both an increase of the expression frequency of its gene and an increase in mRNA level, as well as an increase of the proliferative activity of blood mononuclear cells, which indicates the presence of immune system dysfunction in this category of patients.Thus, in patients with depression, activation of the TNF-α synthesis in blood mononuclear cells occurs: an increase in the frequency of its expression and an increase of the level of mRNA; these changes are accompanied by the increasing of immune cells functional activity and moderate non-delicate cognitive disorder in the form of cognitive impairment.

scholarly journals Phenotypic and Functional Alterations of Immune Effectors in Periodontitis; A Multifactorial and Complex Oral Disease

2021 ◽  
Vol 10 (4) ◽  
pp. 875
Author(s):  
Kawaljit Kaur ◽  
Shahram Vaziri ◽  
Marcela Romero-Reyes ◽  
Avina Paranjpe ◽  
Anahid Jewett
Keyword(s):  
Periodontal Disease ◽  
Peripheral Blood ◽  
Mononuclear Cells ◽  
Oral Disease ◽  
Healthy Controls ◽  
Healthy Individuals ◽  
Tnf Α ◽  
Blood Mononuclear Cells ◽  
Ifn Γ ◽  
And Function

Survival and function of immune subsets in the oral blood, peripheral blood and gingival tissues of patients with periodontal disease and healthy controls were assessed. NK and CD8 + T cells within the oral blood mononuclear cells (OBMCs) expressed significantly higher levels of CD69 in patients with periodontal disease compared to those from healthy controls. Similarly, TNF-α release was higher from oral blood of patients with periodontal disease when compared to healthy controls. Increased activation induced cell death of peripheral blood mononuclear cells (PBMCs) but not OBMCs from patients with periodontal disease was observed when compared to those from healthy individuals. Unlike those from healthy individuals, OBMC-derived supernatants from periodontitis patients exhibited decreased ability to induce secretion of IFN-γ by allogeneic healthy PBMCs treated with IL-2, while they triggered significant levels of TNF-α, IL-1β and IL-6 by untreated PBMCs. Interaction of PBMCs, or NK cells with intact or NFκB knock down oral epithelial cells in the presence of a periodontal pathogen, F. nucleatum, significantly induced a number of pro-inflammatory cytokines including IFN-γ. These studies indicated that the relative numbers of immune subsets obtained from peripheral blood may not represent the composition of the immune cells in the oral environment, and that orally-derived immune effectors may differ in survival and function from those of peripheral blood.

TNF-α decreases hsp 27 in human blood mononuclear cells: Involvement of protein kinase c

Life Sciences ◽  
2006 ◽  
Vol 80 (3) ◽  
pp. 181-186 ◽  
Author(s):  
Masayuki Niwa ◽  
Koichi Hotta ◽  
Akira Hara ◽  
Kouseki Hirade ◽  
Hidenori Ito ◽  
...  
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Human Blood ◽  
Mononuclear Cells ◽  
Hsp 27 ◽  
Kinase C ◽  
Tnf Α ◽  
Blood Mononuclear Cells

scholarly journals Viability and Functional Activity of Cryopreserved Mononuclear Cells

2000 ◽  
Vol 7 (4) ◽  
pp. 714-716 ◽  
Author(s):  
Adriana Weinberg ◽  
Li Zhang ◽  
Darby Brown ◽  
Alejo Erice ◽  
Bruce Polsky ◽  
...  
Keyword(s):  
Clinical Trial ◽  
Functional Activity ◽  
Lymphocyte Proliferation ◽  
Mononuclear Cells ◽  
Cell Number ◽  
Peripheral Blood Mononuclear ◽  
Blood Mononuclear Cells ◽  
And Function ◽  
Functional Analyses ◽  
Cd4 Cell

ABSTRACT Factors that influence viability and function of cryopreserved peripheral blood mononuclear cells (PBMC) were identified on 54 samples from 27 AIDS Clinical Trial Units. PBMC viability ranged from 1 to 96% with a median of 70%, was higher in laboratories with experienced staff, and was not significantly associated with CD4 cell number. Function of cryopreserved PBMC, measured by lymphocyte proliferation, was associated with viability. Preparations with viability greater than or equal to 70% had consistent proliferative responses and were suitable for functional analyses.

Exercise elevates plasma levels but not gene expression of IL-1β, IL-6, and TNF-α in blood mononuclear cells

2000 ◽  
Vol 89 (4) ◽  
pp. 1499-1504 ◽  
Author(s):  
Andrei I. Moldoveanu ◽  
Roy J. Shephard ◽  
Pang N. Shek
Keyword(s):  
Gene Expression ◽  
Oxygen Uptake ◽  
Mononuclear Cells ◽  
Plasma Concentrations ◽  
Peak Oxygen Uptake ◽  
Cytokine Gene Expression ◽  
Mrna Accumulation ◽  
Peripheral Blood Mononuclear ◽  
Tnf Α ◽  
Blood Mononuclear Cells

Physical activity induces a subclinical inflammatory response, mediated in part by leukocytes, and manifested by elevated concentrations of circulating proinflammatory cytokines, including interleukin (IL)-1β, IL-6, and tumor necrosis factor-α (TNF-α). However, the source of the cytokines that appear during exercise remains unknown. In this study, we examined exercise-induced changes in plasma cytokine concentrations and their corresponding mRNA expression in peripheral blood mononuclear cells. Ten healthy [peak oxygen uptake = 48.8 ± 6.5 (SD) ml · kg−1 · min−1] but untrained men [age = 25 ± 5 (SD) yr] undertook 3 h of exercise (cycling and inclined walking) at 60–65% peak oxygen uptake. Circulating leukocyte subset counts were elevated during and 2 h postexercise but returned to normal within 24 h. Plasma concentrations of IL-1β, IL-6, and TNF-α peaked at the end of exercise and remained elevated at 2 h (IL-6) and up to 24 h (IL-1β and TNF-α) postexercise. Cytokine gene expression in circulating mononuclear cells was measured by using the reverse transcriptase-polymerase chain reaction; mRNA accumulation did not change with exercise. In conclusion, mRNA accumulation of IL-1β, IL-6, and TNF-α in circulating mononuclear cells is not affected by 3 h of moderate endurance exercise and does not seem to account for the observed increases in plasma cytokines.

Extracellular ubiquitin inhibits the TNF-α response to endotoxin in peripheral blood mononuclear cells and regulates endotoxin hyporesponsiveness in critical illness

Blood ◽  
2003 ◽  
Vol 101 (5) ◽  
pp. 1882-1890 ◽  
Author(s):  
Matthias Majetschak ◽  
Ulrich Krehmeier ◽  
Mark Bardenheuer ◽  
Christof Denz ◽  
Michael Quintel ◽  
...  
Keyword(s):  
Critical Illness ◽  
Peripheral Blood Mononuclear Cells ◽  
Inhibitory Activity ◽  
Mononuclear Cells ◽  
Inhibitory Effect ◽  
Trauma Patients ◽  
Peripheral Blood Mononuclear ◽  
Healthy Donors ◽  
Tnf Α ◽  
Blood Mononuclear Cells

Ubiquitin is suggested to play a key role in essential intracellular functions, such as heat shock response, protein breakdown, and regulation of immune responses. Ubiquitin has also been detected in the extracellular space, but the function and biologic significance is unclear. We describe a new function of extracellular ubiquitin and show that extracellular ubiquitin specifically inhibits ex vivo secretion of tumor necrosis factor-α (TNF-α) and TNF-α mRNA expression from peripheral blood mononuclear cells (PBMNCs) in response to endotoxin in a dose-dependent manner. In contrast, the TNF-α response to zymosan or Staphylococcus aureus as well as the interleukin-6 (IL-6) and IL-8 responses to endotoxin were unaffected by ubiquitin. Measurement of serum ubiquitin levels showed a significant 5- to 7-fold increase in sepsis and trauma patients, to the level required for inhibition of the PBMNC TNF-α response to endotoxin by ubiquitin. Elevated ubiquitin levels in serum were significantly correlated with a reduced TNF-α production. Antibodies to ubiquitin were able to (1) significantly increase (2- to 5-fold) the TNF-α response to endotoxin in whole blood from trauma and sepsis patients, (2) completely neutralize the inhibitory effect of trauma patients' serum on healthy donors' TNF-α production, and (3) partially neutralize the inhibitory effect of sepsis patients' serum on healthy donors' TNF-α production. Ubiquitin-depleted serum from trauma patients lost the inhibitory activity for TNF-α production, whereas extracted endogenous ubiquitin exerts the inhibitory activity. The results demonstrate that extracellular ubiquitin acts as a cytokinelike protein with anti-inflammatory properties and indicate that extracellular ubiquitin is involved in the regulation of immunodepression in critical illness.

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