Biomolecular basis of the role of chronic psychological stress hormone ‘‘glucocorticoid’’ in alteration of cellular immunity during cancer

Ahsan, Md. Rubayet; Mahmud-Al-Rafat, Abdullah; Sobhani, Mahbub-E-; Molla, Md. A. W.

doi:10.1007/s12254-013-0075-y

Cited by 3 publications

(8 citation statements)

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“…During stress conditions, the HPA axis is activated, followed by signaling, generation, and release of adrenocorticotropic hormone which stimulates the adrenal gland to release CATs (adrenaline, noradrenaline). Also, other stress mediators like glucocorticoids (e.g., cortisol) participate in tumor growth and metastasis [6, 54, 56]. Cortisol arises from cholesterol and is released in response to stress and glucose from the adrenal gland acting as enhancers and suppressors of the immune system [56].…”

Section: Discussionmentioning

confidence: 99%

“…Also, other stress mediators like glucocorticoids (e.g., cortisol) participate in tumor growth and metastasis [6, 54, 56]. Cortisol arises from cholesterol and is released in response to stress and glucose from the adrenal gland acting as enhancers and suppressors of the immune system [56]. In turn, the SNS stimulates secretion of noradrenaline in the blood stream [54].…”

Section: Discussionmentioning

confidence: 99%

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Psychological Stress and Cellular Aging in Cancer: A Meta-Analysis

Kruk

Aboul‐Enein

Bernstein

et al. 2019

Oxidative Medicine and Cellular Longevity

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Background Epidemiological evidence continues to accumulate on the effect of psychosocial and behavioral factors in relation to cancer risk, progression, and mortality. Material and Methods This article presents the current evidence on the relationship between psychological stress and the risk of cancer and cellular aging process. Ten databases were searched to identify publications up to September 2019. References from retrieved articles were also reviewed. We included nine review papers and 26 cohort or case-control studies based on inclusion/exclusion criteria. Results Results of previously published review articles did not show consistent evidence for the association between cancer risk and psychological stress, while previous evidence is stronger regarding the role of chronic psychological stress on cancer growth and metastasis and aging. In seven observational studies, severe life events, anxiety, depression, insufficient social support perception, or avoiding coping strategy were significantly associated with breast cancer risk. For other specific types of cancer, 11 studies reported increased risk factors for stressful life events, and two others found increased mortality or a decline in treatment adherence. Conclusions Recent epidemiological evidence generally suggests psychosocial factors may be considered risk factors for specific types of cancer and play a key role in the cellular aging process. Understanding molecular mechanisms of the stress interaction is important in cancer management and prevention. The psychological stressors should be considered when developing or evaluating change in psychosocial practice.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Psychological Stress and Cellular Aging in Cancer: A Meta-Analysis

Kruk

Aboul‐Enein

Bernstein

et al. 2019

Oxidative Medicine and Cellular Longevity

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“…+ lymphocyte-mediated antiviral responses ( Figure 1) [108,109,110,111]. GCs cause a polarization of CD4 + lymphocyte subsets from Th1 to Th2 and increase production of Th2 cytokines which further stimulate alternatively activated M2 macrophages [109,111,112,113].…”

mentioning

confidence: 99%

mentioning

confidence: 99%

“…GCs cause a polarization of CD4 + lymphocyte subsets from Th1 to Th2 and increase production of Th2 cytokines which further stimulate alternatively activated M2 macrophages [109,111,112,113]. M2 macrophages are characterized by excessive synthesis of IL-10 and TGF-β, which is triggered mainly by elevated levels of GCs which suppress activity of classically activated M1 macrophages [80,111,114,115]. High mortality rates attributable to an exaggerated proinflammatory response and efficient virus clearance are both observed in the absence of GCs, as demonstrated experimentally for other viral infections [116,117].This clearly indicates the critical function of GCs to viral persistence and in establishing an equitable balance in the host-pathogen interaction.…”

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confidence: 99%

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Effects of Anthropogenic Events and Viral Persistence on Rodent Reservoirs of Hantavirus Infection: Understanding Host-Pathogen Interactions Facilitates Novel Approaches to Intervention Strategies

Mahmud-Al-Rafat¹,

E-Sobhani²,

Taylor‐Robinson³

2015

AJIDM

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Hantaviruses are primarily rodent-borne pathogens which have received considerable attention recently due to their high mortality rates in humans. In order to find the causes of rapid transmission and emergence of hantavirus-associated diseases anthropogenic changes are a priority. These include deforestation, urbanization, noise pollution, light pollution and electromagnetic fields, all of which have been shown to profoundly affect rodent physiology and immunology. Moreover, anthropogenic events promote human-rodent co-habitation and thereby provide a driver to increase rates of transmission and, by extrapolation, levels of infection in humans. Such environmental disruption acts as a chronic stressor to rodents and causes elevated concentrations of glucocorticoids, which are a major class of immunosuppressive hormone. Glucocorticoids are responsible for altering the immune tolerance of rodents, thereby rendering them susceptible to infection. Glucocorticoids induce regulatory T lymphocytes to reduce inflammatory and antiviral responses and to activate regulatory responses, principally through production of the cytokines interleukin-10 and transforming growth factor-β to support viral persistence. In order to develop a low-cost intervention strategy for hantavirus infection consideration should be given to a systemic approach to therapy. This would both aim to achieve a reduction of anthropogenic stressors and to gain a greater understanding of host-pathogen interactions.

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Physical exercise and catecholamines response: benefits and health risk: possible mechanisms

Kruk

Kotarska

Aboul‐Enein

2020

Free Radical Research

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Beneficial effect of regular moderate physical exercise (PE) and negative effect of severe exercise and/or overtraining as an activator of the sympathetic nervous system (SNS) have been shown in numerous aspects of human health, including reduced risk of cardiovascular disease, neurological disease, depression, and some types of cancer. Moderate-to-vigorous PE stimulates the SNS activation, releasing catecholamines (CATs) adrenaline, noradrenaline, dopamine that play an important regulatory and modulatory actions by affecting metabolic processes and the immune system. Summary of the dispersed literature in this area and explanation of the biological mechanisms operating between PE-CATs and the immune system would lead to a better understanding of the beneficial and negative effects of PE on health. This overview aimed to: demonstrate representative literature findings on the exercise released CATs levels, major functions performed by these hormones, their interactions with immune system and their effects on carbohydrate and lipid metabolism. Also, mechanisms of cytotoxic free radicals and reactive oxygen species generation during CATs oxidation, and molecular mechanisms of CATs response to exercise are discussed to demonstrate positive and negative on human health effects. Owing to the large body of the subject literature, we present a representative cross-section of the published studies in this area.The results show a significant role of CATs in carbohydrate and lipid metabolism, immunity and as generators of reactive oxygen species, depending on PE intensity and duration. Further investigation of the PE-CATs relationship should validate CATs levels to optimize safe intensity and duration of exercise and individualize their prescription, considering CATs to be applied as markers for a dose of exercise. Also, a better understanding of the biological mechanisms is also needed.

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Biomolecular basis of the role of chronic psychological stress hormone ‘‘glucocorticoid’’ in alteration of cellular immunity during cancer

Cited by 3 publications

References 122 publications

Psychological Stress and Cellular Aging in Cancer: A Meta-Analysis

Psychological Stress and Cellular Aging in Cancer: A Meta-Analysis

Effects of Anthropogenic Events and Viral Persistence on Rodent Reservoirs of Hantavirus Infection: Understanding Host-Pathogen Interactions Facilitates Novel Approaches to Intervention Strategies

Physical exercise and catecholamines response: benefits and health risk: possible mechanisms

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