The pituitary gland is required for protection against lethal effects of Salmonella typhimurium.

Edwards, Carl K.; Yunger, Libby M.; Lorence, Robert M.; Dantzer, Robert; Kelley, Keith W.

doi:10.1073/pnas.88.6.2274

Cited by 116 publications

(53 citation statements)

References 27 publications

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“…Presumably GH provides mechanisms that offer another level of cytokine regulation to protect the host. It has been shown that GH is required for protection against the lethal effects of S. Typhimurium [33]. The consequences of inflammatory pathway activation during disease are often the result of synergic toxicity between cytokines.…”

Section: Discussionmentioning

confidence: 99%

Growth hormone modulates IL- and IFN- release by murine splenocytes activated by LPS or porins of Salmonella Typhimurium

Sommese¹,

Donnarumma²,

L'ero³

et al. 1996

Journal of Medical Microbiology

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The effect of growth hormone (GH) on the release of IL-la and IFN-y from murine splenocytes was investigated. Their release from splenocytes activated by Sulmonella enterica serovar Typhimurium lipopolysaccharide (LPS) 0.5 pg/ml was increased by c. 65% in the presence of GH 100 pg/ml. With splenocytes activated by S. Typhimurium porins 5pg/ml, GH increased the production of both IL-la and IFN-y by c. 56%. Polymyxin treatment abolished the cytokine-releasing activity of LPS but had no effect on the activity of the porin preparation.

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Section: Discussionmentioning

confidence: 99%

Growth hormone modulates IL- and IFN- release by murine splenocytes activated by LPS or porins of Salmonella Typhimurium

Sommese¹,

Donnarumma²,

L'ero³

et al. 1996

Journal of Medical Microbiology

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“…Interruptions of the HPA axis at any level and through multiple mechanisms, whether on a genetic basis, through surgical means such as adrenalectomy or hypophysectomy, or with pharmacological interventions such as treatment with the glucocorticoid receptor antagonist RU 486, can render an inflammatory resistant host susceptible to inflammatory disease (Sternberg 1997a,b). In these circumstances, exposure to the pro-inflammatory stimulus results in high mortality exposure from septic shock within 12 hours (Sternberg et al 1989a, Mason et al 1990, Edwards et al 1991. Conversely, transplantation of fetal hypothalamic tissue from inflammatory resistant F344/N rats into the third ventricle of inflammatory susceptible LEW/N rats reverses both the LEW/N peripheral inflammatory susceptibility and their blunted HPA axis responses to bacterial LPS (Misiewicz et al 1997).…”

Section: Effects Of Blunted Hpa Axis Responses On Immune Function Andmentioning

confidence: 99%

Neuroendocrine regulation of autoimmune/inflammatory disease

Sternberg¹

2001

Journal of Endocrinology

277

162

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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.

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“…Both of these hormones are immunoenhancing (27,33) and are necessary for normal immune system function and resistance to infection. For example, animals deprived of either growth hormone or prolactin, or both, are far more sensitive than control animals to the lethal effects of exper-4 MINIREVIEWS imental Salmonella typhimunium and Listena monocytogenes infections (18).…”

Section: Effects Of Stress On the Immune Responsementioning

confidence: 99%

Central nervous system-immune system interactions: psychoneuroendocrinology of stress and its immune consequences

Black

1994

Antimicrob Agents Chemother

165

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Psychoneuroimmunology is a relatively new discipline which deals with CNS-immune system interactions. The evidence for such interactions was reviewed, as was the neuroendocrinologic response to stress. Recent evidence indicates that the behavioral, nervous system, and neuroendocrine responses to stress are mediated by hypothalamic CRF, which acts on both the sympathetic nervous system and the HPA axis, resulting in increased levels of corticosteroids, catecholamines, and certain opiates, substances which are generally immunosuppressive. Concentrations of growth hormone and prolactin, which are immunoenhancing, are elevated early during the response to stress but are later suppressed. Although several other neuromediators may also be released with stress, the net effect of a variety of acute stressors is down regulation of the immune system function. In the following minireview, I consider whether stress alters the resistance of the host to infection as well as the immunomodulatory effects of released immune system mediators on the brain.

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The pituitary gland is required for protection against lethal effects of Salmonella typhimurium.

Cited by 116 publications

References 27 publications

Growth hormone modulates IL- and IFN- release by murine splenocytes activated by LPS or porins of Salmonella Typhimurium

Growth hormone modulates IL- and IFN- release by murine splenocytes activated by LPS or porins of Salmonella Typhimurium

Neuroendocrine regulation of autoimmune/inflammatory disease

Central nervous system-immune system interactions: psychoneuroendocrinology of stress and its immune consequences

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