ABSTRACT
The pathophysiology of COVID comprises an exaggerated pro-inflammatory response. Hypothalamic-pituitary-adrenal (HPA) axis has a crucial role in various inflammatory conditions and modulated immunological response. Limited evidence is available regarding the incidence and the effect of HPA dysfunction in COVID-19. Although the cortisol levels have only been estimated in a few studies, the dehydroepiandrosterone sulfate (DHEAS) release from the adrenal gland has not been explored yet. In this mini review, the authors discuss the role of dehydroepiandrosterone (DHEA) and DHEAS in the acute stress response and immunological modulation. Various effects of DHEAS have been demonstrated in different diseases. The specific inhibitory effect of DHEA on interleukin 6 (IL-6) could be of paramount importance in COVID-19. Further, DHEA supplementation has already been proposed in inflammatory conditions, like rheumatoid arthritis. DHEAS levels in COVID-19 may help to understand the HPA axis dysfunction as well as the possibility of repurposing DHEA as a drug for mitigating the pro-inflammatory COVID-19.
Subject(s)
COVID-19 Drug Treatment , COVID-19 , Dehydroepiandrosterone Sulfate/metabolism , Dehydroepiandrosterone/therapeutic use , Hypothalamo-Hypophyseal System , Immunologic Factors/therapeutic use , COVID-19/diagnosis , COVID-19/immunology , COVID-19/metabolism , Humans , Hypothalamo-Hypophyseal System/immunology , Hypothalamo-Hypophyseal System/metabolismABSTRACT
The COVID-19 pandemic has highlighted structural inequalities and racism promoting health disparities among communities of color. Taking cardiovascular disease as an example, we provide a framework for multidisciplinary efforts leveraging translational and epidemiologic approaches to decode the biological impacts of inequalities and racism and develop targeted interventions that promote health equity.
Subject(s)
COVID-19/epidemiology , Health Equity , Health Promotion/methods , Racism , Stress, Physiological/immunology , COVID-19/immunology , COVID-19/metabolism , COVID-19/psychology , Cardiovascular Diseases/epidemiology , Cardiovascular Diseases/immunology , Cardiovascular Diseases/metabolism , Cardiovascular Diseases/psychology , Gene Expression Regulation/genetics , Gene Expression Regulation/immunology , Gene Expression Regulation/physiology , Humans , Hypothalamo-Hypophyseal System/immunology , Hypothalamo-Hypophyseal System/physiology , Racism/psychology , Risk Factors , Sympathetic Nervous System/immunology , Sympathetic Nervous System/physiologyABSTRACT
The emergence of the novel coronavirus (SARS-CoV-2) and the worldwide spread of the coronavirus disease (COVID-19) have led to social regulations that caused substantial changes in manners of daily life. The subsequent loneliness and concerns of the pandemic during social distancing, quarantine, and lockdown are psychosocial stressors that negatively affect the immune system. These effects occur through mechanisms controlled by the sympathetic nervous system (SNS) and the hypothalamic-pituitary-adrenocortical (HPA) axis that alter immune regulation, namely the conserved transcriptional response to adversity (CTRA), which promotes inflammation and diminishes antiviral responses, leading to inadequate protection against viral disease. Unhealthy eating habits, physical inactivity, sleep disturbances, and mental health consequences of COVID-19 add on to the pathological effects of loneliness, making immunity against this ferocious virus an even tougher fight. Therefore, social isolation, with its unintended consequences, has inherently paradoxical effects on immunity in relation to viral disease. Though this paradox can present a challenge, its acknowledgment can serve as an opportunity to address the associated issues and find ways to mitigate the adverse effects. In this review, we aim to explore, in detail, the pathological effects of the new social norms on immunity and present suggested methods to improve our physical, psychological, and healthcare abilities to fight viral infection in the context of the COVID-19 pandemic.
Subject(s)
COVID-19/immunology , COVID-19/psychology , Quarantine/psychology , Stress, Psychological/immunology , Humans , Hypothalamo-Hypophyseal System/immunology , SARS-CoV-2 , Stress, Psychological/psychologyABSTRACT
Cytokine storm in COVID-19 is characterized by an excessive inflammatory response to SARS-CoV-2 that is caused by a dysregulated immune system of the host. We are proposing a new hypothesis that SARS-CoV-2 mediated inflammation of nucleus tractus solitarius (NTS) may be responsible for the cytokine storm in COVID 19. The inflamed NTS may result in a dysregulated cholinergic anti-inflammatory pathway and hypothalamic-pituitary-adrenal axis.