Hormesis and immunity: A review

Csaba, G.

doi:10.1556/030.65.2018.036

Cited by 16 publications

(11 citation statements)

References 107 publications

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“…The immune system is continuously influenced by hormetic effects of environmental compounds (e.g., chemicals), physical influences (background irradiations, major change of temperature), or medical (drugs) and food interactions [44]. Low-level ROS activates the main cellular antioxidant pathways (e.g., thioredoxin (TRX) and GSH) as well as their transcriptional regulator Nrf2 [45].…”

Section: Other Hormetic Effects In the Immune Systemmentioning

confidence: 99%

Less Can Be More: The Hormesis Theory of Stress Adaptation in the Global Biosphere and Its Implications

Schirrmacher¹

2021

Biomedicines

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A dose-response relationship to stressors, according to the hormesis theory, is characterized by low-dose stimulation and high-dose inhibition. It is non-linear with a low-dose optimum. Stress responses by cells lead to adapted vitality and fitness. Physical stress can be exerted through heat, radiation, or physical exercise. Chemical stressors include reactive species from oxygen (ROS), nitrogen (RNS), and carbon (RCS), carcinogens, elements, such as lithium (Li) and silicon (Si), and metals, such as silver (Ag), cadmium (Cd), and lead (Pb). Anthropogenic chemicals are agrochemicals (phytotoxins, herbicides), industrial chemicals, and pharmaceuticals. Biochemical stress can be exerted through toxins, medical drugs (e.g., cytostatics, psychopharmaceuticals, non-steroidal inhibitors of inflammation), and through fasting (dietary restriction). Key-lock interactions between enzymes and substrates, antigens and antibodies, antigen-presenting cells, and cognate T cells are the basics of biology, biochemistry, and immunology. Their rules do not obey linear dose-response relationships. The review provides examples of biologic stressors: oncolytic viruses (e.g., immuno-virotherapy of cancer) and hormones (e.g., melatonin, stress hormones). Molecular mechanisms of cellular stress adaptation involve the protein quality control system (PQS) and homeostasis of proteasome, endoplasmic reticulum, and mitochondria. Important components are transcription factors (e.g., Nrf2), micro-RNAs, heat shock proteins, ionic calcium, and enzymes (e.g., glutathion redox enzymes, DNA methyltransferases, and DNA repair enzymes). Cellular growth control, intercellular communication, and resistance to stress from microbial infections involve growth factors, cytokines, chemokines, interferons, and their respective receptors. The effects of hormesis during evolution are multifarious: cell protection and survival, evolutionary flexibility, and epigenetic memory. According to the hormesis theory, this is true for the entire biosphere, e.g., archaia, bacteria, fungi, plants, and the animal kingdoms.

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Section: Other Hormetic Effects In the Immune Systemmentioning

confidence: 99%

Less Can Be More: The Hormesis Theory of Stress Adaptation in the Global Biosphere and Its Implications

Schirrmacher¹

2021

Biomedicines

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“…38 Perinatal psychosocial stress has been reported to increase vulnerability to disease, while mild predictable stressors allowed for better coping for future stressors (considering hormesis?). 39,40 There is an interplay between programming and stress for the HPA axis and immune and inflammatory diseases during development. 41 Perinatal stress has been reported to impact later immune functions of offspring 42 and to open a window for fetal programming of immune function.…”

Section: Early Life Stress Results In Immune Alterations In Later Lifementioning

confidence: 99%

“…The uncontrolled proliferation of endocrine disruptors could lead to more harmful effects of faulty imprinters. 10,39,84 A special problem is the transgenerational inheritance 85 of the perinatal actions studied. Faulty hormonal imprinting is inherited to the progenies up to the third generation in mammals and up to the 1000th generation in unicellular ciliate, cells such as Tetrahymena pyriformis.…”

Section: Discussionmentioning

confidence: 99%

Reprogramming of the Immune System by Stress and Faulty Hormonal Imprinting

Csaba

2020

Clinical Therapeutics

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Purpose: Hormonal imprinting is taking place perinatally at the first encounter between the developing hormone receptors and their target hormones. However, in this crucial period when the developmental window for physiological imprinting is open, other molecules, such as synthetic hormones and endocrine disruptors can bind to the receptors, leading to faulty imprinting with lifelong consequences, especially to the immune system. This review presents the factors of stress and faulty hormonal imprinting that lead to reprogramming of the immune system. Methods: Relevant publications from Pubmed since 1990 were reviewed and synthesized. Findings: The developing immune system is rather sensitive to hormonal effects. Faulty hormonal imprinting is able to reprogram the original developmental program present in a given cell, with lifelong consequences, manifested in alteration of hormone binding by receptors, susceptibility to certain (non-infectious) diseases, and triggering of other diseases. As stress mobilizes the hypothalamicpituitary-adrenal axis if it occurred during gestation or perinatally, it could lead to faulty hormonal imprinting in the immune system, manifested later as allergic and autoimmune diseases or weakness of normal immune defenses. Hormonal imprinting is an epigenetic process and is carried to the offspring without alteration of DNA base sequences. This means that any form of early-life stress alone or in association with hormonal imprinting could be associated with the developmental origin of health and disease (DOHaD). As puberty is also a period of reprogramming, stress or faulty imprinting can change the original (developmental) program, also with lifelong consequences. Implications: Considering the continuous differentiation of immune cells (from blast-cells) during the whole life, there is a possibility of lateimprinting or stress-activated reprogramming in the immune system at any periods of life, with later pathogenetic consequences.

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“…High-dose radiation exposure is known to suppress the immune system, while LDIR may stimulate it. This is evident from multiple experimental studies (Hosoi and Sakamoto, 1993;Cui et al 2017;Csaba 2019). The therapeutic potential of LDIR has been actively investigated for decades in various animal models of immune-associated pathological conditions, including autoimmune disorders and malignant tumors (for review, see Cui 2017).…”

Section: Immune Responsementioning

confidence: 88%