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Distinct CCL2, CCL5, CCL11, CCL27, IL-17, IL-6, BDNF serum profiles correlate to different job-stress outcomes.

ABSTRACT: Chronic psychosocial stress at workplace is an important factor in the development of physical and mental illness. Objective biological measures of chronic stress are still lacking, but inflammatory response and growth factors are increasingly considered as potential stress biomarkers. Therefore, we investigated the relationship between psychophysical strain and serum levels of 48 chemokines, cytokines and growth factors measured using a multiplex immunoassay, and serum brain-derived neurotrophic factor (BDNF) measured by ELISA. Severity of psychophysical strain was scored in 115 healthy hospital workers using specific scales for anxiety, depression-like emotion, gastrointestinal or cardiac disturbances, and ergonomic dysfunction. Multivariate analysis revealed that higher anxiety scale scores were correlated with lower serum chemokine C-C motif ligand-2 (CCL2/MCP-1), chemokine C-C motif ligand-5 (CCL5/RANTES), chemokine C-C motif ligand-27 (CCL27/CTACK), chemokine C-C motif ligand-11 (CCL11/Eotaxin) and interleukin-6 (IL-6); gastrointestinal disturbances correlated with increased levels of interleukin-17 (IL-17) and reduced CCL11/Eotaxin, CCL27/CTACK and CCL2/MCP-1; while cardiac dysfunctions associate only to reduced CCL27/CTACK, and ergonomic dysfunction correlated with increased BDNF and reduced CCL11/Eotaxin and CCL5/RANTES. Thus, these 7 serum factors may provide a distinct signature for each different stress-related psychophysical outcome giving indications on individual vulnerabilities.

SUBMITTER: Polacchini A

PROVIDER: S-EPMC5834655 | biostudies-literature | 2018 Feb

REPOSITORIES: biostudies-literature

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Distinct CCL2, CCL5, CCL11, CCL27, IL-17, IL-6, BDNF serum profiles correlate to different job-stress outcomes.

Polacchini Alessio A Girardi Damiano D Falco Alessandra A Zanotta Nunzia N Comar Manola M De Carlo Nicola Alberto NA Tongiorgi Enrico E

Neurobiology of stress 20180216

Chronic psychosocial stress at workplace is an important factor in the development of physical and mental illness. Objective biological measures of chronic stress are still lacking, but inflammatory response and growth factors are increasingly considered as potential stress biomarkers. Therefore, we investigated the relationship between psychophysical strain and serum levels of 48 chemokines, cytokines and growth factors measured using a multiplex immunoassay, and serum brain-derived neurotrophi ...[more]

PMID: 29511710

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Project description:BackgroundThe inflammatory chemokines CCL2 (MCP-1) & CCL5 (RANTES) and the inflammatory cytokines TNF? & IL-1? were shown to contribute to breast cancer development and metastasis. In this study, we wished to determine whether there are associations between these factors along stages of breast cancer progression, and to identify the possible implications of these factors to disease course.MethodsThe expression of CCL2, CCL5, TNF? and IL-1? was determined by immunohistochemistry in patients diagnosed with: (1) Benign breast disorders (=healthy individuals); (2) Ductal Carcinoma In Situ (DCIS); (3) Invasive Ducal Carcinoma without relapse (IDC-no-relapse); (4) IDC-with-relapse. Based on the results obtained, breast tumor cells were stimulated by the inflammatory cytokines, and epithelial-to-mesenchymal transition (EMT) was determined by flow cytometry, confocal analyses and adhesion, migration and invasion experiments.ResultsCCL2, CCL5, TNF? and IL-1? were expressed at very low incidence in normal breast epithelial cells, but their incidence was significantly elevated in tumor cells of the three groups of cancer patients. Significant associations were found between CCL2 & CCL5 and TNF? & IL-1? in the tumor cells in DCIS and IDC-no-relapse patients. In the IDC-with-relapse group, the expression of CCL2 & CCL5 was accompanied by further elevated incidence of TNF? & IL-1? expression. These results suggest progression-related roles for TNF? and IL-1? in breast cancer, as indeed indicated by the following: (1) Tumors of the IDC-with-relapse group had significantly higher persistence of TNF? and IL-1? compared to tumors of DCIS or IDC-no-relapse; (2) Continuous stimulation of the tumor cells by TNF? (and to some extent IL-1?) has led to EMT in the tumor cells; (3) Combined analyses with relevant clinical parameters suggested that IL-1? acts jointly with other pro-malignancy factors to promote disease relapse.ConclusionsOur findings suggest that the coordinated expression of CCL2 & CCL5 and TNF? & IL-1? may be important for disease course, and that TNF? & IL-1? may promote disease relapse. Further in vitro and in vivo studies are needed for determination of the joint powers of the four factors in breast cancer, as well as analyses of their combined targeting in breast cancer.

Project description:Pityriasis rubra pilaris (PRP) is a rare inflammatory skin disorder associated with significant patient morbidity. To further characterize the molecular landscape of PRP, we conducted a transcriptomic analysis of epidermis and dermis collected from patients with moderate-to-severe PRP compared to matched healthy controls, on no systemic therapy and then following 24 weeks of treatment with the IL17A inhibitor, ixekizumab. Patients with PRP not only experienced clinical improvements, but also correction of their cutaneous transcriptome dysregulation after therapy. Moreover, those who has >50% improvement in PASI score after treatment demonstrated distinct transcriptomic profiles when compared to those who failed to respond, despite the lack of a discernable phenotypic difference. Pathway enrichment was strongest among DEGs belonging to inflammatory processes for patients with PRP – in particular, enrichment of the Th17 immune response was seen both prior to and following treatment with IL17A inhibition. Positive regulation of natural killer cell chemotaxis was also seen pre- and post-treatment, however, the pathway’s odds of enrichment decreased following treatment in both epidermis and dermis. Additionally, negative regulation of IL-12 production was highly enriched following therapy, suggesting decreased activity of the Th1 axis. Several individual genes of interest similarly displayed marked differential expression by response status. In parallel with their overall normalization in gene expression, responders had a greater normalization toward healthy control skin than non-responders in the Th17 family genes IL17C, IL23A, CCL20, as well as IL36A and IL36F (implicated in pustular psoriasis), Phospholipase A2 group IVD, and the antimicrobial protein S100A7, all of which remained elevated in non-responders. Intriguingly, responders had higher baseline levels of IL17A and IL17F than non-responders. Whereas dermal IL17A/F levels improved in responders, epidermal expression remained high despite the clinical response to IL17A inhibition. In contrast, non-responder IL17A/F epidermal levels normalized and dermal levels were significantly suppressed compared to healthy controls, despite the lack of clinical improvement. This suggests alternative pathways such as specific targeting of IL17C or IL36 may be preferred in some subsets of PRP.

Dataset Information

Distinct CCL2, CCL5, CCL11, CCL27, IL-17, IL-6, BDNF serum profiles correlate to different job-stress outcomes.

Publications

Distinct CCL2, CCL5, CCL11, CCL27, IL-17, IL-6, BDNF serum profiles correlate to different job-stress outcomes.

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