Cyclic Nucleotides in Neurohumoral and Hormonal Regulation of Cells of the Immune System

2020 ◽  
pp. 225-247
Author(s):  
Ronald G. Coffey ◽  
John W. Hadden
Keyword(s):  
Immune System ◽  
Cyclic Nucleotides ◽  
Hormonal Regulation

Hormonal regulation of canine intestinal cholesterol synthesis

1981 ◽  
Vol 240 (4) ◽  
pp. G274-G280
Author(s):  
M. W. Goodman ◽  
W. F. Prigge ◽  
R. L. Gebhard
Keyword(s):  
Cyclic Nucleotides ◽  
Hormonal Regulation ◽  
Cholesterol Synthesis ◽  
Reductase Activity ◽  
In Vivo Studies ◽  
Synthesis Rate ◽  
Ileal Mucosa ◽  
Control Activity

Hormonal regulation of intestinal cholesterol synthesis was studied both in vitro and in vivo. Cholesterol synthesis rate was determined by measurement of 3-hydroxy-3-methylglutaryl-coenzyme A reductase (EC 1.1.1.34) activity and by incorporation [14C]acetate into sterol. In vitro studies utilized organ culture of canine ileal mucosa. During 6-h culture, reductase activity was stimulated sevenfold. Insulin (10-6 M) augmented this rise to 144 +/- 7% of th control activity, while 10(-8) M glucagon, 10(-3) M adenosine 3',5'-cyclic monophosphate, and 3-isobutyl-1-methylxanthine suppressed activity (final reductase activity was 83 +/- 3%, 75 +/- 4%, and 41 +/- 3%, respectively, of cultured control values). In vivo studies utilized dogs with isolated Thiry-Vella ileal fistulas. In vivo, insulin doubled reductase activity while glucagon led to a 42 +/- 9% suppression. It is concluded that insulin and glucagon may be potential physiological regulators of intestinal cholesterol synthesis. The glucagon effect may be mediated by cyclic nucleotides.

Limb regeneration in vertebrates: regulatory factors

1987 ◽  
Vol 65 (8) ◽  
pp. 726-729 ◽  
Author(s):  
Richard A. Liversage
Keyword(s):  
Immune System ◽  
Cyclic Nucleotides ◽  
Limb Regeneration ◽  
Epimorphic Regeneration ◽  
Regulatory Factors ◽  
Adult Newt ◽  
Hormonal Milieu ◽  
Newt Limb ◽  
Bioelectric Fields

Various regulatory factors are required in epimorphic regeneration of an adult newt limb. These factors (namely, amputational injury, the wound and apical epithelium, nerves (mitogenic agents), hormones (the hormonal milieu), bioelectric fields, probably the immune system, and possibly cyclic nucleotides and heretofore unknown regulators) act in concert and contribute to the developing microenvironment of the regenerate in support of normal regrowth and differentiation.

scholarly journals Diet as a Potential Moderator for Genome Stability and Immune Response in Pediatric Leukemia

Cancers ◽  
2021 ◽  
Vol 13 (3) ◽  
pp. 413
Author(s):  
Shanshan Wang ◽  
Christopher A. Maxwell ◽  
Neha M. Akella
Keyword(s):  
Immune System ◽  
Hormonal Regulation ◽  
Genome Stability ◽  
Lymphoblastic Leukemia ◽  
Childhood Development ◽  
Pediatric Leukemia ◽  
Childhood All ◽  
Immune System Development ◽  
Increased Risk ◽  
Essential Components

Pediatric leukemias are the most prevalent cancers affecting children in developed societies, with childhood acute lymphoblastic leukemia (ALL) being the most common subtype. As diet is a likely modulator of many diseases, this review focuses on the potential for diet to influence the incidence and progression of childhood ALL. In particular, the potential effect of diets on genome stability and immunity during the prenatal and postnatal stages of early childhood development are discussed. Maternal diet plays an integral role in shaping the bodily composition of the newborn, and thus may influence fetal genome stability and immune system development. Indeed, higher birth weights of newborns are associated with increased risk of ALL, which suggests in-utero biology may shape the evolution of preleukemic clones. Postnatally, the ingestion of maternal breastmilk both nourishes the infant, and provides essential components that strengthen and educate the developing immune system. Consistently, breast-feeding associates with decreased risk of ALL development. For children already suffering from ALL, certain dietary regimens have been proposed. These regimens, which have been validated in both animals and humans, alter the internal hormonal environment. Thus, hormonal regulation by diet may shape childhood metabolism and immunity in a manner that is detrimental to the evolution or expansion of preleukemic and leukemic ALL clones.

scholarly journals Hormonal Regulation of Oligodendrogenesis I: Effects across the Lifespan

2021 ◽  
Author(s):  
Kimberly Long ◽  
Jocelyn Breton ◽  
Matthew Barraza ◽  
Olga Litvin ◽  
Daniela Kaufer
Keyword(s):  
Immune System ◽  
Hormonal Regulation ◽  
Mechanisms Of Action ◽  
Adult Brain ◽  
Physiological Conditions ◽  
Changing Environments ◽  
Complex Interactions ◽  
Specific Receptors ◽  
The Brain

The brain’s capacity to respond to changing environments via hormonal signaling is critical to fine-tuned function. An emerging body of literature highlights a role for myelin plasticity as a prominent type of experience-dependent plasticity in the adult brain. Myelin plasticity is driven by oligodendrocytes (OLs) and their precursor cells (OPCs). OPC differentiation regulates the trajectory of myelin production throughout development, and importantly, OPCs maintain the ability to proliferate and generate new OLs throughout adulthood. The process of oligodendrogenesis (OLgenesis), the creation of new OLs, can be dramatically influenced during early development and in adulthood by internal and environmental conditions such as hormones. Here, we review the current literature describing hormonal regulation of OLgenesis within physiological conditions, focusing on several classes of hormones: steroid, peptide, and thyroid hormones. We discuss hormonal regulation at each stage of OLgenesis and describe mechanisms of action, where known. Overall, the majority of hormones enhance OLgenesis, increasing OPC differentiation and inducing maturation and myelin production in OLs. The mechanisms underlying these processes vary for each hormone but may ultimately converge upon common signaling pathways, mediated by specific receptors expressed across the OL lineage. However, not all of the mechanisms have been fully elucidated, and here, we note the remaining gaps in the literature, including the complex interactions between hormonal systems and with the immune system. In the companion manuscript in this issue [1], we discuss the implications of hormonal regulation of OLgenesis for neurological and psychiatric disorders characterized by white matter loss. Ultimately, a better understanding of the fundamental mechanisms of hormonal regulation of OLgenesis across the entire lifespan, especially in vivo, will progress both basic and translational research.

scholarly journals Hormonal Regulation of Oligodendrogenesis I: Effects across the Lifespan

Biomolecules ◽  
2021 ◽  
Vol 11 (2) ◽  
pp. 283 ◽  
Author(s):  
Kimberly L. P. Long ◽  
Jocelyn M. Breton ◽  
Matthew K. Barraza ◽  
Olga S. Perloff ◽  
Daniela Kaufer
Keyword(s):  
Immune System ◽  
White Matter ◽  
Hormonal Regulation ◽  
Mechanisms Of Action ◽  
Adult Brain ◽  
Physiological Conditions ◽  
Changing Environments ◽  
Complex Interactions ◽  
Specific Receptors

The brain’s capacity to respond to changing environments via hormonal signaling is critical to fine-tuned function. An emerging body of literature highlights a role for myelin plasticity as a prominent type of experience-dependent plasticity in the adult brain. Myelin plasticity is driven by oligodendrocytes (OLs) and their precursor cells (OPCs). OPC differentiation regulates the trajectory of myelin production throughout development, and importantly, OPCs maintain the ability to proliferate and generate new OLs throughout adulthood. The process of oligodendrogenesis, the creation of new OLs, can be dramatically influenced during early development and in adulthood by internal and environmental conditions such as hormones. Here, we review the current literature describing hormonal regulation of oligodendrogenesis within physiological conditions, focusing on several classes of hormones: steroid, peptide, and thyroid hormones. We discuss hormonal regulation at each stage of oligodendrogenesis and describe mechanisms of action, where known. Overall, the majority of hormones enhance oligodendrogenesis, increasing OPC differentiation and inducing maturation and myelin production in OLs. The mechanisms underlying these processes vary for each hormone but may ultimately converge upon common signaling pathways, mediated by specific receptors expressed across the OL lineage. However, not all of the mechanisms have been fully elucidated, and here, we note the remaining gaps in the literature, including the complex interactions between hormonal systems and with the immune system. In the companion manuscript in this issue, we discuss the implications of hormonal regulation of oligodendrogenesis for neurological and psychiatric disorders characterized by white matter loss. Ultimately, a better understanding of the fundamental mechanisms of hormonal regulation of oligodendrogenesis across the entire lifespan, especially in vivo, will progress both basic and translational research.

Learned Placebo Effects in the Immune System

2014 ◽  
Vol 222 (3) ◽  
pp. 148-153 ◽  
Author(s):  
Sabine Vits ◽  
Manfred Schedlowski
Keyword(s):  
Nervous System ◽  
Immune System ◽  
Associative Learning ◽  
Placebo Response ◽  
Immunosuppressive Drug ◽  
Immune Functions ◽  
Placebo Effects ◽  
New Therapeutic Approaches ◽  
Biological Variables ◽  
Experimental Approaches

Associative learning processes are one of the major neuropsychological mechanisms steering the placebo response in different physiological systems and end organ functions. Learned placebo effects on immune functions are based on the bidirectional communication between the central nervous system (CNS) and the peripheral immune system. Based on this “hardware,” experimental evidence in animals and humans showed that humoral and cellular immune functions can be affected by behavioral conditioning processes. We will first highlight and summarize data documenting the variety of experimental approaches conditioning protocols employed, affecting different immunological functions by associative learning. Taking a well-established paradigm employing a conditioned taste aversion model in rats with the immunosuppressive drug cyclosporine A (CsA) as an unconditioned stimulus (US) as an example, we will then summarize the efferent and afferent communication pathways as well as central processes activated during a learned immunosuppression. In addition, the potential clinical relevance of learned placebo effects on the outcome of immune-related diseases has been demonstrated in a number of different clinical conditions in rodents. More importantly, the learned immunosuppression is not restricted to experimental animals but can be also induced in humans. These data so far show that (i) behavioral conditioned immunosuppression is not limited to a single event but can be reproduced over time, (ii) immunosuppression cannot be induced by mere expectation, (iii) psychological and biological variables can be identified as predictors for this learned immunosuppression. Together with experimental approaches employing a placebo-controlled dose reduction these data provide a basis for new therapeutic approaches to the treatment of diseases where a suppression of immune functions is required via modulation of nervous system-immune system communication by learned placebo effects.

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