Cytokines and cardiovascular disease

Mehra, Vishal C.; Ramgolam, Vinod S.; Bender, Jeffrey R.

doi:10.1189/jlb.0405182

Cited by 133 publications

(106 citation statements)

References 200 publications

(211 reference statements)

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“…While gender-specific differences in the psychobiological stress response have not been clearly identified, they may provide valuable insight towards understanding the differential cardiovascular risk in men and women. Processes associated to CVDǡ such as TCR signaling, defense response, response to wounding, cytokine production and interferon signaling (Mehra et al, 2005) ʹͳ were differently regulated by acute stress in males and females in our study (Fig. 3).…”

Section: Gender-specificity Of the Acute Stress Response At The Transmentioning

confidence: 72%

Acute psychological stress induces short-term variable immune response

Breen

Beliakova-Bethell

Mujica‐Parodi

et al. 2016

Brain, Behavior, and Immunity

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Please cite this article as: Breen, M.S., Beliakova-Bethell, N., Mujica-Parodi, L.R., Carlson, J.M., Ensign, W.Y., Woelk, C.H., Rana, B.K., Acute psychological stress induces short-term variable immune response, Brain, Behavior, and Immunity (2015), doi: http://dx.doi.org/10.1016/j.bbi. 2015.10.008 This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. AbstractIn spite of advances in understanding the cross-talk between the peripheral immune system and the brain, the molecular mechanisms underlying the rapid adaptation of the immune system to an acute psychological stressor remain largely unknown.Conventional approaches to classify molecular factors mediating these responses have targeted relatively few biological measurements or explored cross-sectional study designs, and therefore have restricted characterization of stress-immune interactions.This exploratory study analyzed transcriptional profiles and flow cytometric data of peripheral blood leukocytes with physiological (endocrine, autonomic) measurements collected throughout the sequence of events leading up to, during, and after short-term exposure to physical danger in humans. Immediate immunomodulation to acute psychological stress was defined as a short-term selective up-regulation of Natural Killer (NK) cell-associated cytotoxic and IL-12 mediated signaling genes that correlated with increased cortisol, catecholamines and NK cells into the periphery. In parallel, we observed down-regulation of innate immune toll-like receptor genes and genes of the MyD88-dependent signaling pathway. Focusing analyses on discrete groups of coordinately expressed genes (modules) throughout the time-series revealed immune stress responses in modules associated to immune/defense response, response to wounding, cytokine production, TCR signaling and NK cell cytotoxicity which differed between males and females. These results offer a spring-board for future research towards improved treatment of stress-related disease including the impact of stress on cardiovascular and autoimmune disorders, and identifies an immune mechanism by which vulnerabilities to these diseases may be gender-specific.͵

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Section: Gender-specificity Of the Acute Stress Response At The Transmentioning

confidence: 72%

Acute psychological stress induces short-term variable immune response

Breen

Beliakova-Bethell

Mujica‐Parodi

et al. 2016

Brain, Behavior, and Immunity

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“…For instance, cardiovascular disease (Mehra et al ., 2005) and AD (Swardfager et al ., 2010) are consistently associated with elevated levels of pro‐inflammatory cytokines.…”

Section: Omics and Agingmentioning

confidence: 99%

Integration of ‘omics’ data in aging research: from biomarkers to systems biology

et al. 2015

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SummaryAge is the strongest risk factor for many diseases including neurodegenerative disorders, coronary heart disease, type 2 diabetes and cancer. Due to increasing life expectancy and low birth rates, the incidence of age‐related diseases is increasing in industrialized countries. Therefore, understanding the relationship between diseases and aging and facilitating healthy aging are major goals in medical research. In the last decades, the dimension of biological data has drastically increased with high‐throughput technologies now measuring thousands of (epi) genetic, expression and metabolic variables. The most common and so far successful approach to the analysis of these data is the so‐called reductionist approach. It consists of separately testing each variable for association with the phenotype of interest such as age or age‐related disease. However, a large portion of the observed phenotypic variance remains unexplained and a comprehensive understanding of most complex phenotypes is lacking. Systems biology aims to integrate data from different experiments to gain an understanding of the system as a whole rather than focusing on individual factors. It thus allows deeper insights into the mechanisms of complex traits, which are caused by the joint influence of several, interacting changes in the biological system. In this review, we look at the current progress of applying omics technologies to identify biomarkers of aging. We then survey existing systems biology approaches that allow for an integration of different types of data and highlight the need for further developments in this area to improve epidemiologic investigations.

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“…І хоча ме-ханізми дестабілізації бляшки в основному відносяться до процесів, що відбуваються всередині неї, моноцити та лімфоцити, котрі циркулюють у периферичній крові, також здатні генерувати і секретувати медіатори, що залучаються до процесів дестабілізації, включаючи запалення, матриксну деградацію і тромбогенез. Взаємодія мононуклеарів з іншими клітинами крові ендотеліальними і гладеньком'язовими клітинами стінки судини реалізуються при безпосередньому контакті за допомогою цитокінів [12]. Перед залу-ченням моноцитів до патогенезу гострого інфаркту міокарда (ГІМ) вони проходять фенотипічну трансформацію, що призводить до їх активації.…”

Section: вступunclassified

“…Прозапальним ци-токінам мононуклеарів властива синергічна дія, вони контролюють усі етапи формування локального запалення. До них відносяться: а) продукція чинників активації гемокоагуляції [16,18], б) індукція молекул адгезії клітин [3,5], в) посилення активності нейтрофілів і моноцитів/макрофагів [3,12], г ) ініціація системної запальної відповіді і синтез білків гострої фази запалення в гепатоцитах [2], д) індукція морфологічних і функціональних змін в ендотеліальних клітинах [5,8,10].…”

Section: результати та їх обговоренняunclassified