Reciprocal modulation of corticotropin-releasing factor and interleukin-1 receptors following ether-laparotomy stress in the mouse

Takao, Toshihiro; Tojo, Chisa; Nishioka, Tatsuya; Kurokawa, Hisayo; Takemura, Taka; Hashimoto, Kozo; Souza, Errol B. De

doi:10.1016/0006-8993(94)90853-2

Cited by 12 publications

(3 citation statements)

References 29 publications

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“…9 Interestingly, the hypothalamus and pituitary are also sites of de novo cytokine synthesis. Pituitary IL-1 and leukemia-inhibitory factor (LIF) are up-regulated by LPS 143,179,180 and macrophage migration inhibitory factor (MIF) is acutely released from pituicytes in vitro and in vivo in response to LPS. 181 Intrapituitary IL-6 is up-regulated by IL-1, 182,183 and, therefore, an intrapituitary network of cytokines is established in the acute phase of endotoxemia, in addition to the circulating, peripherally derived cytokines.…”

Section: 161177178mentioning

confidence: 99%

Review: Endotoxin and the hypothalamo-pituitary-adrenal (HPA) axis

Beishuizen

Thijs

2003

Journal of Endotoxin Research

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Endotoxin is considered to be a systemic (immunological) stressor eliciting a prolonged activation of the hypothalamo-pituitary-adrenal (HPA) axis. The HPA-axis response after an endotoxin challenge is mainly due to released cytokines (IL-1, IL-6 and TNF-a) from stimulated peripheral immune cells, which in turn stimulate different levels of the HPA axis. Controversy exists regarding the main locus of action of endotoxin on glucocorticoid secretion, since the effect of endotoxin on this neuro-endocrine axis has been observed in intact animals and after ablation of the hypothalamus; however, a lack of LPS effect has been described at both pituitary and adrenocortical levels. The resulting increase in adrenal glucocorticoids has well-documented inhibitory effects on the inflammatory process and on inflammatory cytokine release. Therefore, immune activation of the adrenal gland by endotoxin is thought to occur by cytokine stimulation of corticosteroidreleasing hormone (CRH) production in the median eminence of the hypothalamus, which, in turn stimulates the secretion of ACTH from the pituitary. Acute administration of endotoxin stimulates ACTH and cortisol secretion and the release of CRH and vasopressin (AVP) in the hypophysial portal blood. During repeated endotoxemia, tolerance of both immune and HPA function develops, with a crucial role for glucocorticoids in the modulation of the HPA axis. A single exposure to a high dose of LPS can induce a long-lasting state of tolerance to a second exposure of LPS, affecting the response of plasma TNF-a and HPA hormones. Although there are gender differences in the HPA response to endotoxin and IL-1, these responses are enhanced by castration and attenuated by androgen and estrogen replacement. Estrogens attenuate the endotoxin-induced stimulation of IL-6, TNF-a and IL-1ra release and subsequent activation in postmenopausal women. There appears to be a temporal and functional relation between the HPA-axis response to endotoxin and nitric oxide formation in the neuro-endocrine hypothalamus, suggesting a stimulatory role for nitric oxide in modulating the HPA response to immune challenges. demonstrate higher plasma levels of IL-1 and TNF-a. Elevation of plasma glucocorticoids results in suppression of cytokines such as IL-1, IL-6, and TNF-a and in up-regulation of other cytokines, such as IL-4 and IL-10, and cytokine receptors. Thus, by regulation of cytokine production and action, the HPA axis contributes to modulation of the response to inflammation/infection. In addition, the role of HPA activation has been suggested to be a negative feedback system provided by the immunosuppressive activity of glucocorticoids, limiting inflammatory responses and preventing the immune system from over-reacting and causing tissue damage or autoimmunity.As early as 1957, Wexler et al. suggested that LPS could induce ACTH release since they found a depletion of ascorbic acid and cholesterol in the adrenal glands. 10 Moreover, LPS was not able to cause these changes in hypophysectomized rats. ...

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Section: 161177178mentioning

confidence: 99%

Review: Endotoxin and the hypothalamo-pituitary-adrenal (HPA) axis

Beishuizen

Thijs

2003

Journal of Endotoxin Research

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“…These reports suggest that an autoimmune disorder contributes to the pathogenesis of anterior pituitary dysfunction. With respect to ACTH deficiency, pituitary autoimmunity has been suggested as a primary cause in some cases (12)(13)(14)(15)(16). This was corroborated by Richtsmeier et al who described a patient with ACTH deficiency and lymphoid hypophysitis who exhibited a selective loss of corticotropinsecreting cells (4).…”

Section: Discussionmentioning

confidence: 99%

“…The gammaglobulins from the patients and control subjects, resuspended in the DMEM,were added to the cultured cells (final concentration, 2.5 mg/ml) with or without Male Wistar rats (200-240 g) were used. Rat pituitary membranepreparations were prepared as previously described (12). Briefly, 100 |ul of the rat pituitary membrane suspension was added to a 1.5 ml polypropylene microtube containing 100 jul 125I-ovine CRH (final concentration, 100 pM, New England NuclearResearch Products, Boston, MA, USA), 100 jil incubation buffer (PBS with 0.…”

Section: Anterior Pituitary Cell Culturementioning

confidence: 99%

Secretion of Anterior Pituitary Hormones in Patients with Insulin-Dependent Diabetes Mellitus and Polyglandular Autoimmune Syndrome.

et al. 1996

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Anhedonic and Anxiogenic Effects of Cytokine Exposure

Anisman

Merali

1999

Advances in Experimental Medicine and Biology

166

107

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Systemic interleukin IL-1 beta, TNF alpha, and IL-2 profoundly influenced central monoamine activity, as well as behavioral outputs. The effects of the various cytokines were clearly distinguishable from one another, although synergistic effects were detected between several of these cytokines and between the actions of cytokines and stressors. Acutely applied IL-2 appeared to affect reward processes, but did not affect anxiety. When chronically administered, this cytokine markedly influenced working memory in a spatial learning test. In contrast to IL-2, both IL-1 beta and TNF alpha appeared to provoke an anxiogenic action, and provoked clear signs of illness. While these cytokines induced anorexia, they did not appear to affect reward processes. IL-1 beta and TNF alpha were found to act synergistically, and the TNF alpha provoked a sensitization with respect to the action of subsequent TNF alpha treatment. The findings indicated that cytokine treatments profoundly influence extrahypothalamic neurochemical functioning and may thus impact on behavioral outputs. Analyses of the behavioral and neurochemical changes elicited by cytokines, and particularly TNF alpha, need to consider not only the immediate impact of such treatments, but also the proactive effects that may be engendered.

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Reciprocal modulation of corticotropin-releasing factor and interleukin-1 receptors following ether-laparotomy stress in the mouse

Cited by 12 publications

References 29 publications

Review: Endotoxin and the hypothalamo-pituitary-adrenal (HPA) axis

Review: Endotoxin and the hypothalamo-pituitary-adrenal (HPA) axis

Secretion of Anterior Pituitary Hormones in Patients with Insulin-Dependent Diabetes Mellitus and Polyglandular Autoimmune Syndrome.

Anhedonic and Anxiogenic Effects of Cytokine Exposure

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