ABSTRACT
BACKGROUND: Job burnout is associated with job stress but also with mental health symptoms, depression and anxiety. AIMS: This study aims to evaluate the effect of job stress on burnout without the effect of depression and anxiety. METHODS: A cross-sectional study was conducted in 2015 among 673 employees (88% female) from four public service sectors in Pori, Finland. Job burnout was assessed with the Bergen Burnout Indicator (BBI-15). Job stress was assessed by combining psychological risk factors (demand control, effort rewards and mental workload). Respondents who reported symptoms of depression and anxiety were excluded from the analyses. RESULTS: Of the eligible study subjects (nâ =â 617), 10% reported symptoms of at least mild burnout but only 1% severe burnout. The burnout symptoms varied from 6% to 21% by sector of public service. Job burnout was cumulatively associated with job stress factors. One job stress factor increased the risk of burnout 2-fold (relative risk [RR] 2.13; confidence interval [CI] 0.97-4.68), two factors 6-fold (RR 6.56; 2.92-14.8Or), and three factors even more (RR 23.5; CI 8.67-63.8). Similar trends were observed in the analysis of job burnout components (exhaustion, cynicism and professional inadequacy). CONCLUSIONS: Our results indicate that job burnout is also strongly associated with job stress in employees who do not have depressive or anxiety symptoms. As job burnout may precede clinical depression or reduce productivity and well-being at work, it is essential to perform surveys to monitor burnout symptoms among the workforce, and design interventions to prevent remarkable job strain.
Subject(s)
Anxiety , Burnout, Professional , Depression , Occupational Stress , Humans , Finland/epidemiology , Female , Male , Burnout, Professional/psychology , Burnout, Professional/epidemiology , Cross-Sectional Studies , Adult , Depression/epidemiology , Depression/psychology , Middle Aged , Anxiety/epidemiology , Anxiety/psychology , Occupational Stress/psychology , Occupational Stress/epidemiology , Surveys and Questionnaires , Risk Factors , Workload/psychology , Job Satisfaction , Public Sector , Stress, Psychological/psychology , Stress, Psychological/epidemiologyABSTRACT
Infection caused by certain gram-negative bacteria, e.g. Salmonella, can trigger inflammatory joint disease reactive arthritis (ReA). It is suggested that the disease-triggering bacteria or bacterial components persist in patients for an abnormally long time. Development of ReA is strongly associated with tissue antigen HLA-B27. Previously, we reported an enhanced replication of Salmonella enteritidis and altered p38 MAP kinase signalling in HLA-B27-expressing monocytic cells. Here we aimed to investigate the role of HLA-B27 in regulation of double-stranded RNA-activated kinase (PKR)-related signalling in Salmonella-infected or Salmonella lipopolysaccharide (LPS)-stimulated human U937 monocytic cells, as PKR has been reported to modify p38 signalling in Salmonella-infected cells. In cells expressing HLA-B27, PKR is overexpressed and hypophosphorylated, and the expression of transcription factor CCAAT enhancer binding protein beta (C/EBPß) is increased upon Salmonella infection and LPS stimulation. The expression of C/EBPß is PKR-dependent in LPS-stimulated mock cells, whereas in LPS-stimulated B27 cells the majority of C/EBPß is expressed in a PKR-independent manner. Our results show that the expression of HLA-B27 disturbs the PKR-mediated signalling pathway. Moreover, altered signalling is related to misfolding-linked Glu45 in the B pocket of the HLA-B27 heavy chain. We suggest that the expression of HLA-B27 HCs modulates the intracellular environment of monocyte/macrophages and the mechanisms that are important in eliminating intracellular S. enteritidis by altering the intracellular signalling. This phenomenon is at least partly dependent on the misfolding feature of the B27 molecule. These observations offer a novel mechanism by which HLA-B27 may modulate inflammatory response induced by ReA-triggering bacteria.
Subject(s)
CCAAT-Enhancer-Binding Protein-beta/genetics , HLA-B27 Antigen/genetics , Monocytes/immunology , RNA-Binding Proteins/genetics , Salmonella enteritidis/immunology , CCAAT-Enhancer-Binding Protein-beta/immunology , Cell Differentiation/drug effects , Cell Line , Gene Expression Regulation , HLA-B27 Antigen/chemistry , HLA-B27 Antigen/immunology , Humans , Lipopolysaccharides/pharmacology , Monocytes/drug effects , Monocytes/microbiology , Phosphorylation , Plasmids/chemistry , Plasmids/metabolism , Prohibitins , Protein Folding , RNA-Binding Proteins/immunology , Recombinant Proteins/chemistry , Recombinant Proteins/genetics , Recombinant Proteins/immunology , Salmonella Infections/microbiology , Salmonella enteritidis/isolation & purification , Signal Transduction , Tetradecanoylphorbol Acetate/pharmacology , TransfectionABSTRACT
Certain infections play an important role in the pathogenesis of the human leukocyte antigen (HLA)-B27-associated reactive arthritis. Whether infections play a role in other forms of spondyloarthropathies is not as clear. The role of HLA-B27 as an antigen-presenting molecule is important in the pathogenesis of these diseases. Recent evidence has been obtained indicating that this molecule may have other functions unrelated to antigen-presentation in the interaction of reactive arthritis-triggering microbes and host. This paper reviews the recent studies on the role of infection in the spondyloarthropathies.
