Interleukin-1β Stimulates Corticotropin-Releasing Hormone (CRH) and Adrenocorticotropin (ACTH) Release by Rat Adrenal Gland in Vitro

Mazzocchi, Giuseppina; Musajo, F; Malendowicz, Ludwik K.; Andreis, P. G.; Nussdorfer, Gastone G.

doi:10.1006/mcne.1993.1034

Cited by 40 publications

(15 citation statements)

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“…Moreover, we have also reported that AHA intrahypothalamic IL-1ß increases at 15 min post-ENDO [27]. Thus, a possible explanation for the present CORT findings is that ENDO could be initiating biologically significant events within locations including the hypothalamus [27], pituitary [25] and the adrenal, acting in the latter in a paracrine mode [18,22,52,53]. For example, there is evidence for very small changes in IL-1ß having relatively large biological effects in, e.g., bioassays [reviewed in 9].…”

Section: Discussionmentioning

confidence: 90%

“…Thus, although systemic IL-1ß at 0.5 h was still statistically similar to 0-hour concentrations, it may have been enough biological action (e.g. individually) to act directly, e.g., produce a paracrine effect of IL-1ß at the adrenal in each rat [18,52,53]. If this type of cytokine-stimulated CORT release was occurring after ENDO administration in the present studies, these results also support the concept that there are three 'layers' of component responses within the HPA axis that enable (or ensure) that there will be an adrenal response, e.g.…”

Section: Discussionmentioning

confidence: 99%

“…During infection and after administration of bacterial ENDO, there are alterations in the release of pituitary hormone secretion patterns and adrenal steroids [1,8,9,29]. However, the mechanisms and locations where ENDO stimulates, e.g., the HPA axis are presently unclear [9,12,18,20,27,38,39]. The present work represents one approach to characterizing a role for the AHA in mediation of neuroendocrine responses to an ENDO immune challenge.…”

Section: Introductionmentioning

confidence: 99%

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Plasma Interleukin-1β, Prolactin, ACTH and Corticosterone Responses to Endotoxin after Damage of the Anterior Hypothalamic Area

Phelps

Chen

Menzies

2001

Neuroimmunomodulation

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This report concerns the use of an animal model described by us [J Submicrosc Cytol Pathol 1995;27:83–89] to investigate neural and endocrine sites for endotoxin (ENDO, E. coli 055:B5, 200 µg/100 g body weight in saline intravenously) effects on immunomodulatory hormone and cytokine release. Plasma interleukin-1β (IL-1β), prolactin (PRL), ACTH and corticosterone responses to ENDO after neurotoxic damage of neurons residing in the anterior hypothalamic area (AHA) were studied in freely behaving male rats. Excitotoxic cell damage in the AHA was produced by bilaterally injecting N-methyl-DL-aspartate (NMA) in artificial cerebrospinal fluid (aCSF) into this brain site. Injections of comparable volumes of aCSF alone served as controls for brain damage associated with the treatment. In both experimental brain manipulations before ENDO challenge the rise in plasma IL-1β concentrations in response to ENDO was reduced by 2-fold at 1 h and 3- to 5-fold at 3 h when compared to controls. Nevertheless, experimental and control brain manipulations did not modulate the expected rise in corticosterone concentrations after ENDO exposure which rose 5-fold above the baseline level in all animals. However, AHA manipulation did reduce plasma ACTH and prolactin concentrations differentially. Introduction of either NMA or the control injection of aCSF alone into AHA reduced plasma ACTH concentrations by 2-fold at 0.5 and 1 h after ENDO. However, there was a greater reduction in the rise of plasma PRL concentrations after ENDO found in NMA-treated groups versus rats receiving control aCSF. These results demonstrate that variable-size hypothalamic damage (a larger lesion produced in AHA by NMA treatment vs. a smaller lesion control after aCSF) can result in a differential blunting of PRL, IL-1β and ACTH release into blood in the face of robust, unmodulated corticosterone increases. In summary, these findings revealed a consistent predominant influence of ENDO on adrenal release of corticosterone as a concomitant to differential IL-1β, ACTH and PRL release after AHA cell loss. In conclusion, these results constitute further evidence for hypothalamic orchestration of a balance between immunotropic and immunosuppressive neuroendocrine-immune events during acute bacterial infection of mammals.

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Section: Discussionmentioning

confidence: 90%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Plasma Interleukin-1β, Prolactin, ACTH and Corticosterone Responses to Endotoxin after Damage of the Anterior Hypothalamic Area

Phelps

Chen

Menzies

2001

Neuroimmunomodulation

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“…It was shown that the effect of interleukin-1 upon the steroidogenesis in the adrenal gland is mediated by the local release of catecholamines (Gwosdow et al, 1992;O'Connell et al, 1994) or by the activation of an intra-adrenal CRH/ACTH system (Andreis et al, 1991a;Mazzocchi et al, 1993c). The role of the local endogenous cytokine production in this process, however, remains unclear.…”

Section: Physiological Relevance Ofmentioning

confidence: 97%

Morphological and functional studies of the paracrine interaction between cortex and medulla in the adrenal gland

Bornstein

Ehrhart‐Bornstein

Scherbaum

1997

Microsc. Res. Tech.

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“…4. CRH and ACTH immunoreactivities are present in rat adrenal glands but not in adrenocortical autotransplants lacking chromaffin cells (Mazzocchi et al, 1993). 5.…”

Section: Factors Regulating Venous Outflowmentioning

confidence: 99%

Vascularization of the adrenal cortex: its possible involvement in the regulation of steroid hormone release

Bassett

West

1997

Microsc. Res. Tech.

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Interleukin-1β Stimulates Corticotropin-Releasing Hormone (CRH) and Adrenocorticotropin (ACTH) Release by Rat Adrenal Gland in Vitro

Cited by 40 publications

References 0 publications

Plasma Interleukin-1β, Prolactin, ACTH and Corticosterone Responses to Endotoxin after Damage of the Anterior Hypothalamic Area

Plasma Interleukin-1β, Prolactin, ACTH and Corticosterone Responses to Endotoxin after Damage of the Anterior Hypothalamic Area

Morphological and functional studies of the paracrine interaction between cortex and medulla in the adrenal gland

Vascularization of the adrenal cortex: its possible involvement in the regulation of steroid hormone release

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