scholarly journals Circulating cytokine levels in the treatment of comorbid anxiety disorders

2020 ◽  
pp. 1-7
Author(s):  
Sverre Urnes Johnson ◽  
Asle Hoffart ◽  
Terje Tilden ◽  
Helge Toft ◽  
Sudan P. Neupane ◽  
...  
Keyword(s):  
Treatment Outcome ◽  
Anxiety Disorders ◽  
Interleukin 1 ◽  
Multilevel Modelling ◽  
Self Report ◽  
Necrosis Factor Alpha ◽  
Monocyte Chemoattractant Protein 1 ◽  
Comorbid Anxiety ◽  
Cytokine Levels ◽  
The Relationship

Abstract Psychotherapy research aims to investigate predictors and moderators of treatment outcome, but there are few consistent findings. This study aimed to investigate cytokines in patients undergoing treatment for anxiety disorders and whether the level of cytokines moderated the treatment outcome. Thirty-seven patients with comorbid and treatment-resistant anxiety disorders were investigated using multilevel modelling. Serum cytokine levels were measured three times: pretreatment, in the middle of treatment, and at the end of treatment. Anxiety and metacognitions were measured weekly throughout treatment by self-report. The levels of monocyte chemoattractant protein-1, tumour necrosis factor-alpha, and interleukin-1 receptor antagonist did not change during therapy or were not related to the level of anxiety. Metacognitive beliefs predicted anxiety, but the relationship between metacognitions and anxiety was not moderated by cytokines. Limitations of the study include that the patients were not fasting at blood sampling, and we did not assess body mass index, which may affect cytokine levels. The lack of significance for cytokines as a predictor or moderator may be due to a lack of power for testing moderation hypotheses, a problem associated with many psychotherapy studies. Cytokines did not predict the outcome in the treatment of comorbid anxiety disorders in our sample. Furthermore, cytokines did not moderate the relationship between metacognitions and anxiety.

Triterpenoid CDDO-IM protects against lipopolysaccharide-induced inflammatory response and cytotoxicity in macrophages: The involvement of the NF-κB signaling pathway

2022 ◽  
pp. 153537022110669
Author(s):  
Hassan Ahmed ◽  
Urooj Amin ◽  
Xiaolun Sun ◽  
Demetrius R Pitts ◽  
Yunbo Li ◽  
...  
Keyword(s):  
Septic Shock ◽  
Inflammatory Cytokine ◽  
Interleukin 1 ◽  
Severe Form ◽  
Necrosis Factor Alpha ◽  
Monocyte Chemoattractant Protein 1 ◽  
Tnf Α ◽  
Cytokine Levels ◽  
Factor Alpha ◽  
Gene Expression Levels

Lipopolysaccharide (LPS), also known as endotoxin, can trigger septic shock, a severe form of inflammation-mediated sepsis with a very high mortality rate. However, the precise mechanisms underlying this endotoxin remain to be defined and detoxification of LPS is yet to be established. Macrophages, a type of immune cells, initiate a key response responsible for the cascade of events leading to the surge in inflammatory cytokines and immunopathology of septic shock. This study was undertaken to determine whether the LPS-induced inflammation in macrophage cells could be ameliorated via CDDO-IM (2-cyano-3,12 dioxooleana-1,9 dien-28-oyl imidazoline), a novel triterpenoid compound. Data from this study show that gene expression levels of inflammatory cytokine genes such as interleukin-1 beta (IL-1β), interleukin-8 (IL-8), tumor necrosis factor alpha (TNF-α), and monocyte chemoattractant protein-1 (MCP-1) were considerably increased by treatment with LPS in macrophages differentiated from ML-1 monocytes. Interestingly, LPS-induced increase in expression of pro-inflammatory cytokine levels is reduced by CDDO-IM. In addition, endogenous upregulation of a series of antioxidant molecules by CDDO-IM provided protection against LPS-induced cytotoxicity in macrophages. LPS-mediated nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kB) transcriptional activity was also noted to decrease upon treatment with CDDO-IM in macrophages suggesting the involvement of the NF-κB signaling. This study would contribute to improve our understanding of the detoxification of endotoxin LPS by the triterpenoid CDDO-IM.

scholarly journals The Relationship between Inflammatory Cytokines and Coagulopathy in Patients with COVID-19

2021 ◽  
Vol 10 (9) ◽  
pp. 2020
Author(s):  
Fariba Rad ◽  
Ali Dabbagh ◽  
Akbar Dorgalaleh ◽  
Arijit Biswas
Keyword(s):  
Inflammatory Cytokines ◽  
Interleukin 1 ◽  
Clinical Findings ◽  
Laboratory Findings ◽  
Necrosis Factor Alpha ◽  
Coagulation Parameters ◽  
Increased Risk ◽  
Cytokine Levels ◽  
Α Level ◽  
High Level

Coronavirus disease 2019 (COVID-19), with a broad range of clinical and laboratory findings, is currently the most prevalent medical challenge worldwide. In this disease, hypercoagulability and hyperinflammation, two common features, are accompanied by a higher rate of morbidity and mortality. We assessed the association between baseline inflammatory cytokine levels and coagulopathy and disease outcome in COVID-19. One hundred and thirty-seven consecutive patients hospitalized with COVID-19 were selected for the study. Baseline interleukin-1 (IL-1), IL-6, and tumor necrosis factor alpha (TNF-α) level were measured at time of admission. At the same time, baseline coagulation parameters were also assessed during the patient’s hospitalization. Clinical findings, including development of thrombosis and clinical outcome, were recorded prospectively. Out of 136 patients, 87 (~64%) had increased cytokine levels (one or more cytokines) or abnormal coagulation parameters. Among them, 58 (~67%) had only increased inflammatory cytokines, 12 (~14%) had only coagulation abnormalities, and 17 (19.5%) had concomitant abnormalities in both systems. It seems that a high level of inflammatory cytokines at admission points to an increased risk of developing coagulopathy, thrombotic events, even death, over the course of COVID-19. Early measurement of these cytokines, and timely co-administration of anti-inflammatories with anticoagulants could decrease thrombotic events and related fatal consequences.

Proinflammatory cytokine levels in patients with conversion disorder

2013 ◽  
Vol 25 (3) ◽  
pp. 137-143 ◽  
Author(s):  
Utkan Tiyekli ◽  
Okan Çalıyurt ◽  
Nimet Dilek Tiyekli
Keyword(s):  
Acute Phase ◽  
Proinflammatory Cytokine ◽  
Interleukin 1 ◽  
Conversion Disorder ◽  
Enzyme Linked Immunosorbent Assay ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Significant Difference ◽  
Cytokine Levels ◽  
As Stress

ObjectiveIt was aimed to evaluate the relationship between proinflammatory cytokine levels and conversion disorder both commonly known as stress regulated.MethodBaseline proinflammatory cytokine levels–[Tumour necrosis factor alpha (TNF‐α), Interleukin‐1 beta (IL‐1β), Interleukin‐6 (IL‐6)]–were evaluated with enzyme‐linked immunosorbent assay in 35 conversion disorder patients and 30 healthy controls. Possible changes in proinflammatory cytokine levels were evaluated again, after their acute phase in conversion disorder patients.ResultsStatistically significant decreased serum TNF‐α levels were obtained in acute phase of conversion disorder. Those levels increased after acute conversion phase. There were no statistically significant difference observed between groups in serum IL‐1β and (IL‐6) levels.ConclusionsStress associated with conversion disorder may suppress immune function in acute conversion phase and may have diagnostic and therapeutic value.

scholarly journals Interaction of Neisseria meningitidis with Human Dendritic Cells

2001 ◽  
Vol 69 (11) ◽  
pp. 6912-6922 ◽  
Author(s):  
Annette Kolb-Mäurer ◽  
Alexandra Unkmeir ◽  
Ulrike Kämmerer ◽  
Claudia Hübner ◽  
Thomas Leimbach ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
Neisseria Meningitidis ◽  
Proinflammatory Cytokines ◽  
Interleukin 1 ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Cytokine Levels ◽  
Factor Alpha ◽  
Human Dendritic Cells ◽  
Necrosis Factor

ABSTRACT Infection with Neisseria meningitidis serogroup B is responsible for fatal septicemia and meningococcal meningitis. The severity of disease directly correlates with the production of the proinflammatory cytokines tumor necrosis factor alpha (TNF-α), interleukin-1 (IL-1), IL-6, and IL-8. However, the source of these cytokines has not been clearly defined yet. Since bacterial infection involves the activation of dendritic cells (DCs), we analyzed the interaction of N. meningitidis with monocyte-derived DCs. Using N. meningitidis serogroup B wild-type and unencapsulated bacteria, we found that capsule expression significantly impaired neisserial adherence to DCs. In addition, phagocytic killing of the bacteria in the phagosome is reduced by at least 10- to 100-fold. However, all strains induced strong secretion of proinflammatory cytokines TNF-α, IL-6, and IL-8 by DCs (at least 1,000-fold at 20 h postinfection [p.i.]), with significantly increased cytokine levels being measurable by as early as 6 h p.i. Levels of IL-1β, in contrast, were increased only 200- to 400-fold at 20 h p.i. with barely measurable induction at 6 h p.i. Moreover, comparable amounts of cytokines were induced by bacterium-free supernatants of Neisseria cultures containing neisserial lipooligosaccharide as the main factor. Our data suggest that activated DCs may be a significant source of high levels of proinflammatory cytokines in neisserial infection and thereby may contribute to the pathology of meningococcal disease.

scholarly journals Mitochondrial Transplantation Ameliorates The Development and Progression of Osteoarthritis.

2021 ◽  
Author(s):  
A Ram Lee ◽  
Jin Seok Woo ◽  
Seon-Yeong Lee ◽  
Hyun Sik Na ◽  
Keun-Hyung Cho ◽  
...  
Keyword(s):  
Mitochondrial Dysfunction ◽  
Mitochondrial Function ◽  
Therapeutic Potential ◽  
Interleukin 1 ◽  
Cartilage Destruction ◽  
Degenerative Joint Disease ◽  
Joint Disease ◽  
Necrosis Factor Alpha ◽  
Monocyte Chemoattractant Protein 1 ◽  
Monosodium Iodoacetate

Abstract Objective: Osteoarthritis (OA) is a common degenerative joint disease characterized by breakdown of joint cartilage. Mitochondrial dysfunction of the chondrocyte is a risk factor for OA progression. We examined the therapeutic potential of mitochondrial transplantation for OA.Methods: Mitochondria were injected into the knee joint of monosodium iodoacetate (MIA)-induced OA rats. Chondrocytes from OA rats or patients with OA were cultured to examine mitochondrial function in cellular pathophysiology.Results: Pain, cartilage destruction, and bone loss were improved in mitochondrial transplanted-OA rats. The transcript levels of interleukin 1 beta (IL-1β), tumor necrosis factor alpha (TNF-α), matrix metallopeptidase 13 (MMP13), and monocyte chemoattractant protein-1 (MCP-1) in cartilage were markedly decreased by mitochondrial transplantation. Mitochondrial function, as indicated by membrane potential and oxygen consumption rate, in chondrocytes from OA rats was improved by mitochondrial transplantation. Likewise, the mitochondrial function of chondrocytes from OA patients was improved by coculture with mitochondria. Furthermore, inflammatory cell death was significantly decreased by coculture with mitochondria.Conclusion: Mitochondrial transplantation ameliorated OA progression, which is caused by mitochondrial dysfunction. These results suggest the therapeutic potential of mitochondrial transplantation for OA.

Adolescent Outcome of ADHD: Impact of Childhood Conduct and Anxiety Disorders

CNS Spectrums ◽  
2004 ◽  
Vol 9 (9) ◽  
pp. 668-678 ◽  
Author(s):  
Jeffrey H. Newcorn ◽  
Scott R. Miller ◽  
Iliyan Ivanova ◽  
Kurt P. Schulz ◽  
Jessica Kalmar ◽  
...  
Keyword(s):  
Anxiety Disorder ◽  
Anxiety Disorders ◽  
Child Behavior Checklist ◽  
Social Problems ◽  
Self Report ◽  
Comorbid Condition ◽  
Behavioral Outcome ◽  
Comorbid Anxiety ◽  
The Impact ◽  
Adolescent Outcome

ABSTRACTObjective: This study examines the impact of comorbidity of attention-deficit/hyperactivity disorder (ADHD) with disruptive and anxiety disorders in childhood on clinical course and outcome. We consider the relative contribution of each comorbid symptom constellation, and also their interaction, to assess the following questions: (1) Does early comorbidity with conduct disorder (CD) and anxiety disorders define specific developmental trajectories?; (2) Is comorbid anxiety disorders in childhood continuous with anxiety disorders in adolescence?; (3) Does comorbid anxiety disorders mitigate the negative behavioral outcome of youth with ADHD?; and (4) Is there an interaction between comorbid CD and anxiety disorders, when they occur simultaneously, that predicts a different outcome than either comorbid condition alone?Method: Thirty-two 15- to 18-year-old adolescent males, diagnosed with ADHD between 7 and 11 years of age, were re-evaluated for assessment of adolescent outcome 4.3–9.2 years later. Hierarchical regression analyses were run with each of the eight Child Behavior Checklist and Youth Self-Report problem scales, and the four anxiety symptom subscales of the Multidimensional Anxiety Scale for Children serving as outcome variables.Results: Findings indicate that comorbid CD at baseline predicteds parent reports of behavior problems in adolescence, while comorbid anxiety disorders in childhood predicted youth reports of anxiety and social problems. Anxiety disorders without CD did not predict poor behavioral outcome. Children with both comorbid CD and anxiety disorder had the highest levels of parent-rated symptoms on follow up. In particular, adolescent social problems were best predicted by the combination of comorbid CD and anxiety disorder in childhood.Conclusion: These data provide evidence that children with ADHD plus anxiety disorder do in fact have anxiety disorders, and that the combination of anxiety disorder and CD predicts a more rather than less severe course.

Sexual functioning in male patients suffering from depression and anxiety disorders

2017 ◽  
Vol 41 (S1) ◽  
pp. s848-s849 ◽  
Author(s):  
G. Ciocca ◽  
G. Di Lorenzo ◽  
G. Comite ◽  
E. Limoncin ◽  
D. Mollaioli ◽  
...  
Keyword(s):  
Anxiety Disorders ◽  
Sexual Functioning ◽  
Erectile Function ◽  
Mental Illnesses ◽  
Self Report ◽  
Psychological State ◽  
Sexual Dysfunctions ◽  
Depression And Anxiety ◽  
Male Patients ◽  
The Relationship

IntroductionSexual dysfunctions are frequent in patients with mental illnesses. In particular, anxious and depressive symptomatology often impacts on sexual functioning.ObjectivesThe aim of this study was to evaluate the relationship between sexual function and psychological symptoms in a group of male patients with depression and anxiety disorders.MethodsFrom outpatients program, we consecutively recruited a group of 46 males: 28 patients had major depression and 18 anxiety disorders. Then, we administered two self-report psychometric tools to assess male sexuality, depression and anxiety, i.e., international index of erectile function (IIEF-15), and Depression Anxiety Stress Scales (DASS-21). t-tests and Pearson correlations were performed.ResultsWe found significantly higher score in terms of desire and general sexual wellness in people with anxiety disorder compared to people with depression. However, we found more significant correlations among depressive/anxious symptomatology and sexual impairment in males with anxiety disorders compared to males with depression.ConclusionsOur results revealed that males diagnosed with depression show a decrease of sexual desire, as a vast part of literature previously affirmed. On the contrary, the relationship between psychological symptomatology and sexual dysfunction, as the reduction of erectile function, was higher in males with anxiety disorders. This difference is probably due to a major iatrogenic effect of antidepressive treatments in depressed patients, while in anxious patients could be the psychological state, per se, the main cause of sexual dysfunctions.Disclosure of interestThe authors have not supplied their declaration of competing interest.

scholarly journals Macrophage Inflammatory Protein 1α/CCL3 Is Required for Clearance of an Acute Klebsiella pneumoniae Pulmonary Infection

2001 ◽  
Vol 69 (10) ◽  
pp. 6364-6369 ◽  
Author(s):  
Dennis M. Lindell ◽  
Theodore J. Standiford ◽  
Peter Mancuso ◽  
Zachary J. Leshen ◽  
Gary B. Huffnagle
Keyword(s):  
Klebsiella Pneumoniae ◽  
Alveolar Macrophages ◽  
Interleukin 12 ◽  
Necrosis Factor Alpha ◽  
Monocyte Chemoattractant Protein 1 ◽  
Inflammatory Protein ◽  
Cytokine Levels ◽  
Factor Alpha ◽  
Macrophage Inflammatory Protein

ABSTRACT The objective of these studies was to determine the role of macrophage inflammatory protein 1α/CCL3 in pulmonary host defense during Klebsiella pneumoniae infection. Following intratracheal inoculation, 7-day survival of CCL3−/− mice was less than 10%, compared to 60% for CCL3+/+ mice. Survival of CCR5−/− mice was equivalent to that of controls, indicating that the enhanced susceptibility of CCL3−/− mice to K. pneumoniae is mediated via another CCL3 receptor, presumably CCR1. At day 3, CFU burden in the lungs of CCL3−/− mice was 800-fold higher than in CCL3+/+ mice, demonstrating that CCL3 is critical for control of bacterial growth in the lung. Surprisingly, CCL3−/− mice had no differences in the recruitment of monocytes/macrophages and even showed enhanced neutrophil recruitment at days 1, 2, and 3 postinfection, compared to CCL3+/+ mice. Therefore, the defect in clearance was not due to insufficient recruitment of leukocytes. No significant differences in cytokine levels of monocyte chemoattractant protein 1 (MCP-1), interleukin 12, gamma interferon, or tumor necrosis factor alpha in lung lavages were found between CCL3+/+ and CCL3−/− mice. CCL3−/− alveolar macrophages were found to have significantly lower phagocytic activity toward K. pneumoniae than CCL3+/+alveolar macrophages. These findings demonstrate that CCL3 production is critical for activation of alveolar macrophages to control the pulmonary growth of the gram-negative bacterium K. pneumoniae.

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