Activation of the hypothalamus-pituitary-adrenal axis by bacterial endotoxins: Routes and intermediate signals

Tilders, F. J. H.; DeRuk, Roel H.; Dam, Anne Marie Van; Vincent, V.A.M.; Schotanus, K.; Persoons, Jek H. A.

doi:10.1016/0306-4530(94)90010-8

Cited by 263 publications

(138 citation statements)

References 126 publications

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“…Our results also demonstrate that LPS produced a marked depletion of CRH-41 ME content, which reflects its release into the portal vessels (Chappell et al 1986), with a concomitant elevation in plasma corticosterone levels. This result is also consistent with many previous studies, which reported that LPS produces marked alterations in all components of the HPA axis, including the secretion of CRH, ACTH, and glucocorticoids (Tilders et al 1994), as well as an impairment in the glucocorticoid negative feedback regulation of adrenocortical responses (Weidenfeld and Yirmiya 1996). Taken together, these behavioral and neuroendocrine symptoms resemble the characteristics of depression; therefore, we Figure 5.…”

Section: Discussionsupporting

confidence: 92%

“…Although the role of CRH in mediating the anorexic effects of LPS has not been studied directly, there are indications that CRH mediates the anorexic effects of IL-1 (Bluthe et al 1992;Uehara et al 1989). Moreover, ample evidence indicates that CRH mediates LPS-induced adrenocortical activation (Tilders et al 1994). Thus, it may be suggested that fluoxetine-induced attenuation of CRH neuronal activation is involved in the reduction of LPS-induced anorexia and adrenocortical activation.…”

Section: Discussionmentioning

confidence: 99%

Section: Antidepressants Produce Various Immunomodulatory Effects Asmentioning

confidence: 99%

“…One aim of the present study was to extend these findings by examining the effects of the SSRI fluoxetine (Prozac) on LPS-induced sickness behavior. Because LPS also produces marked changes in body temperature and activation of the hypothalamus-pituitary-adrenal (HPA) axis (Kluger 1991;Tilders et al 1994), another aim of the present study was to examine the effects of antidepressant treatment on these thermoregulatory and neuroendocrine components of the acute phase response.Some of the effects of antidepressants are probably mediated by a direct action on immune cells. For example, TCAs were found to inhibit spontaneous secretion of IL-2 and IFN ␥ from T-cells, as well as spontaneous and LPS-induced secretion of IL-1 ␤ , IL-6 and TNF ␣ from monocytes (Xia et al 1996).…”

mentioning

confidence: 99%

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Effects of Antidepressant Drugs on the Behavioral and Physiological Responses to Lipopolysaccharide (LPS) in Rodents

Yirmiya

Pollak

Barak

et al. 2001

Neuropsychopharmacology

203

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Antidepressants produce various immunomodulatory effects, as well as an attenuation of the behavioral responses to immune challenges, such as lipopolysaccharide (LPS). To explore further the effects of antidepressants on neuroimmune interactions, rats were treated daily with either fluoxetine (Prozac) or saline for 5 weeks, and various behavioral, neuroendocrine, and immune functions were measured following administration of either LPS or saline. Chronic fluoxetine treatment significantly attenuated the anorexia and body weight loss, as well as the depletion of CRH-41 from the median eminence and the elevation in serum corticosterone levels induced by LPS. Chronic treatment with imipramine also attenuated LPS-induced adrenocortical activation. In rats and in mice, which normally display a biphasic body temperature response to LPS (initial hypothermia followed by hyperthermia), chronic treatment with fluoxetine completely abolished the hypothermic response and facilitated and strengthened the hyperthermic response. The effects of antidepressants on the responsiveness to LPS are probably not mediated by their effects on peripheral proinflammatory cytokine production, because LPS-induced expression of TNFSeveral lines of evidence indicate that antidepressants produce various immunomodulatory effects. In depressed patients, the effects of antidepressants are variable and seem to be related to the immune status of the patients at the initiation of the treatment. When depression was associated with immune activation, antidepressants reduced immune function and cytokine secretion. For example, the increased plasma levels of IL-6 during acute depression were normalized by 8-week treatment with fluoxetine (Sluzewska et al. 1995), the increased monocyte counts in depressed patients were reduced following 6-weeks treatment with tricyclic antidepressants (TCAs) (Seidel et al. 1996), and the increased numbers of leukocytes and neutrophils were also reduced by antidepressant treatment (Maes et al. 24 , NO . 5 1997). On the other hand, when immune functions were found to be normal, antidepressants had no immunological effects; for example, chronic moclobemide treatment had no effect on monocytes functions, TNF ␣ production or IFN ␥ levels (Landmann et al. 1997). Moreover, in a study of depressed patients who exhibited immune suppression before treatment, the TCA clomipramine increased the production of IL-1 ␤ , IL-2, and IL-3 (Weizman et al. 1994).In experimental animals, TCAs as well as selective serotonin reuptake inhibitors (SSRIs) produce mainly immune suppression and anti-inflammatory effects. For example, antidepressant treatment in vivo inhibited the increased acute phase response in olfactory bulbectomized rats, a useful animal model of depression (Song and Leonard 1994), reduced the production of interleukin-1 (IL-1) and IL-2 in a chronic mild stress model of depression (Kubera et al. 1996), inhibited immune activation in rats with experimental allergic neuritis (Zhu et al. 1994), and produced anti-inflammatory ...

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Section: Discussionsupporting

confidence: 92%

Section: Discussionmentioning

confidence: 99%

Section: Antidepressants Produce Various Immunomodulatory Effects Asmentioning

confidence: 99%

mentioning

confidence: 99%

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Effects of Antidepressant Drugs on the Behavioral and Physiological Responses to Lipopolysaccharide (LPS) in Rodents

Yirmiya

Pollak

Barak

et al. 2001

Neuropsychopharmacology

203

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“…In the head kidneys of tilapia lymphocytes, monocytes, plasma cells and eranulocytes have been identified (Sailendri and M uthukkaruppan 1975). Rcccnt research in mammals points to the largely paracrine nature of immuno-endocrine interactions, emphasizing the role of cell-cell com munication al all levels of organization including the adrenals (Gonzalez-Hernandez et al 1994;Tildcrs et al 1994). The unique organization of the adrenal hom o logue in fish may therefore provide an excellent opportunity to study archetypal immuno-endocrine in teractions by in vitro experiments, a suggestion sub stantiated by the data of Schreck and Bradford (1990).…”

Section: Introductionmentioning

confidence: 99%

Bacterial lipopolysaccharide (LPS) and interleukin 1 (IL-1) exert multiple physiological effects in the tilapia Oreochromis mossambicus (Teleostei)

et al. 1995

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Temporal and spatial patterns ofc-fos mRNA induced by intravenous interleukin-1: A cascade of non-neuronal cellular activation at the blood-brain barrier

1998

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Brain cells responsive to a peripheral immune challenge, identified by in situ hybridization of c-fos mRNA following intravenous administration of the proinflammatory cytokine interleukin-1beta (IL-1) or sterile saline, were investigated at 0.5, 1, and 3 hours postinjection in rats. Doses of IL-1 ranged from 0.05 to 10 microg/kg; induction of c-fos mRNA occurred at > or = 0.5 pg/kg. The majority of IL-1-induced c-fos mRNA-positive cells were non-neuronal cells located in barrier regions of the brain. The cells became radiolabeled in two separate but related spatiotemporal patterns. The first pattern, occurring at 0.5 hour, was characterized by c-fos mRNA labeling of cells of the outer meninges (mainly arachnoid), blood vessels (arteries, veins, and capillaries), and choroid plexus. This activation pattern disappeared at 1 hour. At 3 hours, a second activation pattern appeared in cells located just inside the now quiescent barrier cells. In addition, the circumventricular organs each showed characteristic spatiotemporal labeling patterns resulting from successive activation of specific cell types, with a general spread of activation directed away from the circumventricular organs over time. At 3 hours post IL-1, c-fos and glial fibrillary acidic protein (GFAP) mRNAs showed colocalization in the arcuate nucleus/median eminence/glia limitans region. We propose that the first wave of activation is elicited by blood-borne immune signals, but the second wave is caused by molecules generated within the first set of activated cells. The transduced signal appears to propagate to neighboring receptive cells by extracellular diffusion. In this manner, blood-brain barrier cells can transduce peripheral IL-1 signals in widespread areas of the brain, although the circumventricular organs may be the most effective loci for signal transduction.

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Activation of the hypothalamus-pituitary-adrenal axis by bacterial endotoxins: Routes and intermediate signals

Cited by 263 publications

References 126 publications

Effects of Antidepressant Drugs on the Behavioral and Physiological Responses to Lipopolysaccharide (LPS) in Rodents

Effects of Antidepressant Drugs on the Behavioral and Physiological Responses to Lipopolysaccharide (LPS) in Rodents

Bacterial lipopolysaccharide (LPS) and interleukin 1 (IL-1) exert multiple physiological effects in the tilapia Oreochromis mossambicus (Teleostei)

Temporal and spatial patterns ofc-fos mRNA induced by intravenous interleukin-1: A cascade of non-neuronal cellular activation at the blood-brain barrier

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