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Esther M. Sternberg - One of the best experts on this subject based on the ideXlab platform.

  • Neuroendocrine Regulation of Immunity
    Annual Review of Immunology, 2001
    Co-Authors: Jeanette I. Webster, Leonardo H. Tonelli, Esther M. Sternberg
    Abstract:

    A reciprocal Regulation exists between the central nervous and immune systems through which the CNS signals the immune system via hormonal and neuronal pathways and the immune system signals the CNS through cytokines. The primary hormonal pathway by which the CNS regulates the immune system is the hypothalamic-pituitary-adrenal axis, through the hormones of the Neuroendocrine stress response. The sympathetic nervous system regulates the function of the immune system primarily via adrenergic neurotransmitters released through neuronal routes. Neuroendocrine Regulation of immune function is essential for survival during stress or infection and to modulate immune responses in inflammatory disease. Glucocorticoids are the main effector end point of this Neuroendocrine system and, through the glucocorticoid receptor, have multiple effects on immune cells and molecules. This review focuses on the Regulation of the immune response via the Neuroendocrine system. Particular details are presented on the effects of ...

  • Neuroendocrine Regulation of autoimmune/inflammatory disease.
    The Journal of endocrinology, 2001
    Co-Authors: Esther M. Sternberg
    Abstract:

    Interactions between the immune and nervous systems play an important role in modulating host susceptibility and resistance to inflammatory disease. Neuroendocrine Regulation of inflammatory and immune responses and disease occurs at multiple levels: systemically, through the anti-inflammatory action of glucocorticoids released via hypothalamic-pituitary-adrenal axis stimulation; regionally, through production of glucocorticoids within and sympathetic innervation of immune organs such as the thymus; locally, at sites of inflammation. Estrogens also play an important role in immune modulation, and contribute to the approximately 2- to 10-fold higher incidence of autoimmune/inflammatory diseases seen in females of all mammalian species. During inflammation, cytokines from the periphery activate the central nervous system through multiple routes. This results in stimulation of the hypothalamic-pituitary-adrenal axis which, in turn through the immunosuppressive effects of the glucocorticoids, generally inhibits inflammation. Recent studies indicate that physiological levels of glucocorticoids are immunomodulatory rather than solely immunosuppressive, causing a shift in patterns of cytokine production from a TH1- to a TH2-type pattern. Interruptions of this loop at any level and through multiple mechanisms, whether genetic, or through surgical or pharmacological interventions, can render an inflammatory resistant host susceptible to inflammatory disease. Over-activation of this axis, as occurs during stress, can also affect severity of infectious disease through the immunosuppressive effects of the glucocorticoids. These interactions have been clearly demonstrated in many animal models, across species, strains and diseases, and are also relevant to human inflammatory, autoimmune and allergic illnesses, including rheumatoid arthritis, systemic lupus crythematosus, Sjogren's syndrome, allergic asthma and atopic skin disease. While many genes and environmental factors contribute to susceptibility and resistance to autoimmune/ inflammatory diseases, a full understanding of the molecular effects on immune responses of combinations of neuropeptides, neurohormones and neurotransmitters at all levels has opened up new therapcutic approaches and are essential for the design of future therapies based on such principles.

  • Neuroendocrine Regulation of autoimmune inflammatory disease
    Journal of Endocrinology, 2001
    Co-Authors: Esther M. Sternberg
    Abstract:

    Interactions between the immune and nervous systems play an important role in modulating host susceptibility and resistance to inflammatory disease. Neuroendocrine Regulation of inflammatory and immune responses and disease occurs at multiple levels: systemically, through the anti-inflammatory action of glucocorticoids released via hypothalamic-pituitary-adrenal axis stimulation; regionally, through production of glucocorticoids within and sympathetic innervation of immune organs such as the thymus; locally, at sites of inflammation. Estrogens also play an important role in immune modulation, and contribute to the approximately 2- to 10-fold higher incidence of autoimmune/inflammatory diseases seen in females of all mammalian species. During inflammation, cytokines from the periphery activate the central nervous system through multiple routes. This results in stimulation of the hypothalamic-pituitary-adrenal axis which, in turn through the immunosuppressive effects of the glucocorticoids, generally inhibits inflammation. Recent studies indicate that physiological levels of glucocorticoids are immunomodulatory rather than solely immunosuppressive, causing a shift in patterns of cytokine production from a TH1- to a TH2-type pattern. Interruptions of this loop at any level and through multiple mechanisms, whether genetic, or through surgical or pharmacological interventions, can render an inflammatory resistant host susceptible to inflammatory disease. Over-activation of this axis, as occurs during stress, can also affect severity of infectious disease through the immunosuppressive effects of the glucocorticoids. These interactions have been clearly demonstrated in many animal models, across species, strains and diseases, and are also relevant to human inflammatory, autoimmune and allergic illnesses, including rheumatoid arthritis, systemic lupus crythematosus, Sjogren's syndrome, allergic asthma and atopic skin disease. While many genes and environmental factors contribute to susceptibility and resistance to autoimmune/ inflammatory diseases, a full understanding of the molecular effects on immune responses of combinations of neuropeptides, neurohormones and neurotransmitters at all levels has opened up new therapcutic approaches and are essential for the design of future therapies based on such principles.

  • EUROSTERONE MEETING Neuroendocrine Regulation of autoimmune/inflammatory disease
    2001
    Co-Authors: Esther M. Sternberg
    Abstract:

    Interactions between the immune and nervous systems play an important role in modulating host susceptibility and resistance to inflammatory disease. Neuroendocrine Regulation of inflammatory and immune responses and disease occurs at multiple levels: systemically, through the anti-inflammatory action of glucocorticoids released via hypothalamic‐pituitary‐adrenal axis stimulation; regionally, through production of glucocorticoids within and sympathetic innervation of immune organs such as the thymus; locally, at sites of inflammation. Estrogens also play an important role in immune modulation, and contribute to the approximately 2- to 10-fold higher incidence of autoimmune/inflammatory diseases seen in females of all mammalian species. During inflammation, cytokines from the periphery activate the central nervous system through multiple routes. This results in stimulation of the hypothalamic‐pituitary‐adrenal axis which, in turn through the immunosuppressive effects of the glucocorticoids, generally inhibits inflammation. Recent studies indicate that physiological levels of glucocorticoids are immunomodulatory rather than solely immunosuppressive, causing a shift in patterns of cytokine production from a TH1- to a TH2-type pattern. Interruptions of this loop at any level and through multiple mechanisms, whether genetic, or through surgical or pharmacological interventions, can render an inflammatory resistant host susceptible to inflammatory disease. Over-activation of this axis, as occurs during stress, can also affect severity of infectious disease through the immunosuppressive effects of the glucocorticoids. These interactions have been clearly demonstrated in many animal models, across species, strains and diseases, and are also relevant to human inflammatory, autoimmune and allergic illnesses, including rheumatoid arthritis, systemic lupus erythematosus, Sjogren’s syndrome, allergic asthma and atopic skin disease. While many genes and environmental factors contribute to susceptibility and resistance to autoimmune/ inflammatory diseases, a full understanding of the molecular effects on immune responses of combinations of neuropeptides, neurohormones and neurotransmitters at all levels has opened up new therapeutic approaches and are essential for the design of future therapies based on such principles.

Tetsu Ando - One of the best experts on this subject based on the ideXlab platform.

  • Selectivity and Neuroendocrine Regulation of the precursor uptake by pheromone glands from hemolymph in geometrid female moths, which secrete epoxyalkenyl sex pheromones.
    Insect biochemistry and molecular biology, 2004
    Co-Authors: Wei Wei, Masanobu Yamamoto, Tetsuhiro Asato, Takeshi Fujii, Tetsu Ando
    Abstract:

    Macrolepidopteran female moths in families such as Geometridae produce epoxyalkenyl sex pheromones, which are biosynthesized via epoxidation of polyunsaturated hydrocarbons in their pheromone glands. The precursors, however, are expected to be produced outside of the pheromone glands, probably in oenocytes or in the fat body, and transported to the glands via hemolymph. Based on these facts, the selectivity of the epoxidation substrates and of the precursor uptake by pheromone glands was examined with two geometrid species, Hemerophila artilineata and Ascotis selenaria cretacea, using binary mixtures of deuterated precursors and their analogs, which were topically applied to the pheromone glands or injected into the abdomen. GC-MS measurements of pheromone extracts showed equal epoxidation of two polyenes, indicating a low selectivity for both processes, while the epoxidation proceeded at only one double bond specific to each species. This result makes it possible to conclude that the formation of species-specific epoxyalkenyl pheromones results from the rigid formation of polyunsaturated precursors and their epoxidation at a fixed position. Next, the Neuroendocrine Regulation of these processes was studied with in vivo and in vitro experiments using decapitated females. The epoxy pheromones disappeared completely within 36 h of decapitation, and epoxidation of the injected precursors was not detected in the decapitated females, which restarted the reaction by treatment with a pheromone biosynthesis-activating neuropeptide (PBAN). The precursors topically applied to glands of the decapitated females, however, were converted into epoxy pheromones without PBAN, indicating that this neuropeptide hormone accelerated the precursor uptake by pheromone glands but not the epoxidation already underway in the glands.

Ei Terasawa - One of the best experts on this subject based on the ideXlab platform.

  • 5.14 – Neuroendocrine Regulation of Puberty
    Hormones Brain and Behavior, 2017
    Co-Authors: Ei Terasawa, Jon E. Levine
    Abstract:

    Steroid hormone secretions during the transition between the juvenile and pubertal period direct the acquisition of secondary sex characteristics and modify brain circuitries to mediate the transition to adult behavioral phenotypes. The neural mechanisms that prompt the pubertal activation of pulsatile GnRH release, and hence the hypothalamic–pituitary–gonadal axis, remain the subject of intense study. Species differences exist in the physiological juvenile restraint mechanism, with gonadal feedback-dependent mechanisms predominating in rodents and a steroid hormone-independent central brake operating in primates. Recent work has clarified the roles of kisspeptin and neurokinin B neurons in the Regulation of the pubertal increase in GnRH release, and the somatic and environmental factors that may in turn alter their activity and hence, the timing of puberty. Future work remains to elucidate the mechanism governing central inhibition prior to puberty onset, and to understand the similarities and differences between mechanisms that operate in different species.

  • Neuroendocrine Regulation of Puberty
    Hormones Brain and Behavior, 2009
    Co-Authors: Ei Terasawa, Sergio R. Ojeda
    Abstract:

    Puberty is a developmental phase during which profound hormonal, physical, behavioral, and psychological changes occur. The individual becomes capable of reproduction, that is, viable gametes are produced and transferred through a mature reproductive system.

Wei Wei - One of the best experts on this subject based on the ideXlab platform.

  • Selectivity and Neuroendocrine Regulation of the precursor uptake by pheromone glands from hemolymph in geometrid female moths, which secrete epoxyalkenyl sex pheromones.
    Insect biochemistry and molecular biology, 2004
    Co-Authors: Wei Wei, Masanobu Yamamoto, Tetsuhiro Asato, Takeshi Fujii, Tetsu Ando
    Abstract:

    Macrolepidopteran female moths in families such as Geometridae produce epoxyalkenyl sex pheromones, which are biosynthesized via epoxidation of polyunsaturated hydrocarbons in their pheromone glands. The precursors, however, are expected to be produced outside of the pheromone glands, probably in oenocytes or in the fat body, and transported to the glands via hemolymph. Based on these facts, the selectivity of the epoxidation substrates and of the precursor uptake by pheromone glands was examined with two geometrid species, Hemerophila artilineata and Ascotis selenaria cretacea, using binary mixtures of deuterated precursors and their analogs, which were topically applied to the pheromone glands or injected into the abdomen. GC-MS measurements of pheromone extracts showed equal epoxidation of two polyenes, indicating a low selectivity for both processes, while the epoxidation proceeded at only one double bond specific to each species. This result makes it possible to conclude that the formation of species-specific epoxyalkenyl pheromones results from the rigid formation of polyunsaturated precursors and their epoxidation at a fixed position. Next, the Neuroendocrine Regulation of these processes was studied with in vivo and in vitro experiments using decapitated females. The epoxy pheromones disappeared completely within 36 h of decapitation, and epoxidation of the injected precursors was not detected in the decapitated females, which restarted the reaction by treatment with a pheromone biosynthesis-activating neuropeptide (PBAN). The precursors topically applied to glands of the decapitated females, however, were converted into epoxy pheromones without PBAN, indicating that this neuropeptide hormone accelerated the precursor uptake by pheromone glands but not the epoxidation already underway in the glands.

Sergio R. Ojeda - One of the best experts on this subject based on the ideXlab platform.