Cytokines in Diseases of the Endocrine System

Igaz, Péter

doi:10.1006/cbir.2000.0536

Cited by 7 publications

(6 citation statements)

References 44 publications

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“…In the early phase of development, the medical intervention also artificially imprints the receptors and not only molecules with DES strength, but by such molecules as perinatal vitamin A and D treatment (McGrath 2001), by surfactants as cortisol, by oxytocin and antihistamines. However, longer is the list of imprinter molecules which were not mentioned, as it is not allowed by the volume of the article, or their imprinter effect was not tested till now, although it would be important, as they are in connection with the endocrine system and/or they act at receptor level (Igaz et al 2000). This flood of imprinting influences the life of people who were the direct victims of imprinting or transgenerationally inherited it (Jirtle and Skinner 2007).…”

Section: Discussionmentioning

confidence: 99%

The biological basis and clinical significance of hormonal imprinting, an epigenetic process

Csaba

2011

Clin Epigenet

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The biological phenomenon, hormonal imprinting, was named and defined by us (Biol Rev, 1980, 55, 47-63) 30 years ago, after many experimental works and observations. Later, similar phenomena were also named to epigenetic imprinting or metabolic imprinting. In the case of hormonal imprinting, the first encounter between a hormone and its developing target cell receptor—usually at the perinatal period—determines the normal receptor-hormone connection for life. However, in this period, molecules similar to the target hormone (members of the same hormone family, synthetic drugs, environmental pollutants, etc), which are also able to bind to the receptor, provoke faulty imprinting also with lifelong—receptorial, behavioral, etc.,—consequences. Faulty hormonal imprinting could also be provoked later in life in continuously dividing cells and in the brain. Faulty hormonal imprinting is a disturbance of gene methylation pattern, which is epigenenetically inherited to the further generations (transgenerational imprinting). The absence of the normal or the presence of false hormonal imprinting predispose to or manifested in different diseases (e.g., malignant tumors, metabolic syndrome) long after the time of imprinting or in the progenies.

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Section: Discussionmentioning

confidence: 99%

The biological basis and clinical significance of hormonal imprinting, an epigenetic process

Csaba

2011

Clin Epigenet

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“…Many physical disorders have been reported to increase the risk for developing a depressive disorder (125) and to activate the production of pro-inflammatory cytokines. Examples are autoimmune and infectious diseases (156–159), endocrine and hormonal diseases (160), cancer (161), diabetes (164), myocardial infarction (165, 196), and physical trauma (166). The treatment of physical disorders, e.g., interferon-based or virostatic treatments for hepatitis C (167, 197), chemotherapy for the treatment of cancer (168), surgery (169) or transplantation (170), can lead to additional cytokine release.…”

Section: Possible Reasons For Cytokine Alterationsmentioning

confidence: 99%

Cytokine Research in Depression: Principles, Challenges, and Open Questions

et al. 2019

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Cytokines have been implicated in the pathology of depression. Currently, the evidence is based on cross-sectional studies and meta-analytic research comparing blood concentrations of T helper type 1 (TH1), T helper type 2 (TH2), pro-inflammatory or anti-inflammatory cytokines of patients with a depressive disorder to those of healthy controls. Additionally, multiple longitudinal studies have investigated cytokine levels during antidepressant treatment. According to the current literature, it seems that peripheral levels of interleukin (IL)-6, IL-10, IL-12, IL-13, and tumor necrosis factor (TNF)-α are elevated and that interferon (IFN)-γ levels are lower in patients with depression compared to healthy controls. However, the overlap of cytokine values between acutely depressed patients, remitted and recovered patients and healthy controls is considerable. Thus, the discriminative power of cytokine concentrations between depressed and non-depressed people is likely weak. Treatment with certain antidepressants appears to decrease peripheral levels of IL-6, IL-10, and TNF-α. However, weight gain-inducing psychopharmacological substances, such as the antidepressant mirtazapine, have been reported to potentially increase the production of pro-inflammatory cytokines. Even though cytokines are often discussed as biomarkers for depression, they have also been shown to be altered in other psychiatric disorders. Moreover, many environmental, social, psychological, biological, and medical factors are also associated with cytokine changes. Thus, cytokine alterations seem extremely unspecific. The interpretation of the results of these studies remains a challenge because it is unknown which type of cells are most responsible for cytokine changes measured in the blood nor have the main target cells or target tissues been identified. The same cytokine can be produced by multiple cell types, and the same cell can produce various cytokines. Additionally, redundancy, synergy, antagonism, and signaling cascades of cytokine signaling must be considered. Cytokines might not be associated with the diagnosis of depression according to the currently used diagnostic manuals, but rather with specific subtypes of depression, or with depressive symptoms across different psychiatric diagnoses. Therefore, the currently available diagnostic systems may not be the ideal starting point for psychiatric cytokine research.

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“…It was found that sheep are a useful model for immunological studies [44], which can be used in leptin-related research because leptin also plays a role in the activation of the immune system, and is a mediator of inflammation. It is generally accepted that leptin is a proinflammatory adipokine [45], and, like other cytokines, may modulate the transduction of signals of different cytokines, affecting both cytokines and the expression of their receptors [46]. Leptin belongs to the long-chain helical cytokines and shows structural similarity to interleukins (IL) 2, 3, 6, 12, 15, granulocyte colony-stimulating factor, oncostatin M, prolactin or the growth hormone [47][48][49].…”

Section: Introductionmentioning

confidence: 99%

“…Furthermore, the mentioned proinflammatory cytokines, including leptin, also influence the pituitary hormonal activity. The action of cytokines in the pituitary influences the production and release of hormones such as gonadotropins [59], the proliferation and survival of hormone-producing cells, tissue modeling, chemotaxis of immune cells infiltrating organs, tissue destruction and development of fibrosis [46]. Research on the rat primary cultures of AP cells showed that TNF inhibits the secretion of pituitary hormones ACTH, GH, LH and PRL in response to hypothalamic stimulation [60], while it was found that IL6 stimulates the secretion of ACTH, GH, PRL, LH and FSH [61][62][63].…”

Section: Introductionmentioning

confidence: 99%

The Impact of Photoperiod on the Leptin Sensitivity and Course of Inflammation in the Anterior Pituitary

Wójcik

Herman

Zieba

et al. 2020

IJMS

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Leptin has a modulatory impact on the course of inflammation, affecting the expression of proinflammatory cytokines and their receptors. Pathophysiological leptin resistance identified in humans occurs typically in sheep during the long-day photoperiod. This study aimed to determine the effect of the photoperiod with relation to the leptin-modulating action on the expression of the proinflammatory cytokines and their receptors in the anterior pituitary under physiological or acute inflammation. Two in vivo experiments were conducted on 24 blackface sheep per experiment in different photoperiods. The real-time PCR analysis for the expression of the genes IL1B, IL1R1, IL1R2, IL6, IL6R, IL6ST, TNF, TNFR1, and TNFR2 was performed. Expression of all examined genes, except IL1β and IL1R2, was higher during short days. The leptin injection increased the expression of all examined genes during short days. In short days the synergistic effect of lipopolysaccharide and leptin increased the expression of IL1B, IL1R1, IL1R2, IL6, TNF, and TNFR2, and decreased expression of IL6ST. This mechanism was inhibited during long days for the expression of IL1R1, IL6, IL6ST, and TNFR1. The obtained results suggest the occurrence of leptin resistance during long days and suggest that leptin modulates the course of inflammation in a photoperiod-dependent manner in the anterior pituitary.

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Cytokines in Diseases of the Endocrine System

Cited by 7 publications

References 44 publications

The biological basis and clinical significance of hormonal imprinting, an epigenetic process

The biological basis and clinical significance of hormonal imprinting, an epigenetic process

Cytokine Research in Depression: Principles, Challenges, and Open Questions

The Impact of Photoperiod on the Leptin Sensitivity and Course of Inflammation in the Anterior Pituitary

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