Response of rat fasciculata-reticularis cells in primary culture to bacterial lipopolysaccharide

Salamanca, Andrés Bordalí; Garcı́a, R.

doi:10.1016/j.micinf.2005.02.016

Cited by 8 publications

(5 citation statements)

References 53 publications

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“…In this sense, the expression of Toll-like receptors 4 and 2 in human adrenal cells (Bornstein et al 2004) and a direct effect of LPS on corticosterone production in rat fasciculata-reticularis cells have been demonstrated (Enriquez de Salamanca & Garcia 2005). According to these results the observed effects of LPS on the adrenal cortex could be attributed to LPS alone, or to a combination of LPS with enhanced cytokine production and/or ACTH release resulting from LPS injection as was also suggested (Beishuizen & Thijs 2003).…”

Section: Discussionmentioning

confidence: 68%

Induction of nitric oxide synthase and heme oxygenase activities by endotoxin in the rat adrenal cortex: involvement of both signaling systems in the modulation of ACTH-dependent steroid production

Grion¹,

Repetto²,

Pomeraniec³

et al. 2007

Journal of Endocrinology

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The present study was designed to investigate the effect of lipopolysaccharide (LPS) on the expression levels and activities of the nitric oxide synthase (NOS) and heme oxygenase (HO) systems in the rat adrenal gland. Both enzymatic activities were significantly increased in this tissue after in vivo treatment with LPS. The concurrent induction of the HO-1, NOS-1, and NOS-2 gene products was also detected as both mRNAs and protein levels were augmented by this treatment in a time-dependent way. A significant interaction between both signaling systems was also demonstrated as in vivo blockage of NOS activity with N(G)-nitro-L-arginine methyl ester (L-NAME) resulted in a significant reduction in HO expression and activity levels, while an increase in NOS activity was observed when HO was inhibited by Sn-protoporphyrin IX (Sn-PPIX). As both NOS and HO activities have been previously involved in the modulation of adrenal steroidogenesis, we investigated the participation of these signaling systems in the adrenal response to LPS. Our results showed that acute stimulation of steroid production by ACTH was significantly increased when either NOS or HO activities were inhibited. We conclude that adrenal NOS and HO can be induced by a non-lethal dose of endotoxin supporting a modulatory role for these activities in the adrenal response to immune challenges.

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Section: Discussionmentioning

confidence: 68%

Induction of nitric oxide synthase and heme oxygenase activities by endotoxin in the rat adrenal cortex: involvement of both signaling systems in the modulation of ACTH-dependent steroid production

Grion¹,

Repetto²,

Pomeraniec³

et al. 2007

Journal of Endocrinology

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“…Although there is little published data on the adrenal MC2R and how LPS may affect it, there is some suggestion that LPS may directly influence the MC2R-mediated GC response. LPS can suppress the ACTH-induced GC response in fasciculata reticularis and glomerulosa cells 27 28 . Prior exposure to LPS can induce endotoxin tolerance in the adrenal, with the corticosterone response to LPS or ACTH being suppressed in primary fasciculata reticularis cells from rats that had previously been given LPS 29 .…”

Section: Discussionmentioning

confidence: 99%

“…Activation of protein kinase A ensues and leads to phosphorylation of cAMP response element protein, activating the transcription of steroidogenic acute regulatory protein (StAR) and other genes involved in steroidogenesis 31 32 . There is some evidence LPS can interact with this mechanism, modifying the binding of ACTH to the cell membrane and modifying the ACTH signal transduction pathway, suppressing ACTH-induced cAMP production in primary culture 27 . However, it is unlikely the differences we see between controls and neonatally overfed are due to a direct action of LPS at the level of the adrenal.…”

Section: Discussionmentioning

confidence: 99%

Overfeeding during a critical postnatal period exacerbates hypothalamic-pituitary-adrenal axis responses to immune challenge: a role for adrenal melanocortin 2 receptors

Cai

Ziko

Barwood

et al. 2016

Sci Rep

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Early life diet can critically program hypothalamic-pituitary-adrenal (HPA) axis function. We have previously shown rats that are overfed as neonates have exacerbated pro-inflammatory responses to immune challenge with lipopolysaccharide (LPS), in part by altering HPA axis responses, but how this occurs is unknown. Here we examined neonatal overfeeding-induced changes in gene expression in each step of the HPA axis. We saw no differences in glucocorticoid or mineralocorticoid receptor expression in key regions responsible for glucocorticoid negative feedback to the brain and no differences in expression of key HPA axis regulatory genes in the paraventricular nucleus of the hypothalamus or pituitary. On the other hand, expression of the adrenal melanocortin 2 receptor (MC2R) is elevated after LPS in control rats, but significantly less so in the neonatally overfed. The in vitro adrenal response to ACTH is also dampened in these rats, while the in vivo response to ACTH does not resolve as efficiently as it does in controls. These data suggest neonatal diet affects the efficiency of the adrenally-mediated response to LPS, potentially influencing how neonatally overfed rats combat bacterial infection.

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“…Second, LPS‐induced leukocyte influx would initially provide a further source of proinflammatory cytokines to enhance steroidogenesis, but these cells also produce defensins (corticostatins), which antagonize the actions of ACTH (55). Third, tolerance develops to LPS in the adrenal gland within 24 hours of treatment due to down‐regulation of TLR4 (56); in addition, ACTH receptor expression is reduced (57), and the downstream up‐regulation of the steroidogenic enzymes CYP11A1 (the rate‐limiting enzyme), HSD3β, and CYP21, but not of steroid acute regulatory protein (StAR) or CYP11B1, is consequently impaired (56). Interestingly, LPS causes only a small reduction in the ability of dcAMP to increase CORT synthesis and does not affect the response to pregnenolone (55), suggesting that the loss of functional ACTH receptors is a key factor in the impairment of steroidogenesis.…”

Section: Discussionmentioning

confidence: 99%

Targeting the annexin 1‐formyl peptide receptor 2/ALX pathway affords protection against bacterial LPS‐induced pathologic changes in the murine adrenal cortex

et al. 2015

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Hypothalamo-pituitary-adrenocortical dysfunction contributes to morbidity and mortality in a high proportion of patients with sepsis. Here, we provide new insights into the underlying adrenal pathology. Using a murine model of endotoxemia (LPS injection), we demonstrate that adrenal insufficiency is triggered early in the disease. LPS induced a local inflammatory response in the adrenal gland within 4 hours of administration, coupled with increased expression of mRNAs for annexin A1 (AnxA1) and the formyl peptide receptors [(Fprs) 1, 2, and 3], a loss of lipid droplets in cortical cells (index of availability of cholesterol, the substrate for steroidogenesis), and a failure to mount a steroidogenic response to ACTH. Deletion of AnxA1 or Fpr2/3 in mice prevented lipid droplet loss, but not leukocyte infiltration. LPS increased adrenal myeloid differentiation primary response gene 88 and TLR2 mRNA expression, but not lymphocyte antigen 96 or TLR4. By contrast, neutrophil depletion prevented leukocyte infiltration and increased AnxA1, Fpr1, and Fpr3 mRNAs but had no impact on lipid droplet loss. Our novel data demonstrate that AnxA1 and Fpr2 have a critical role in the manifestation of adrenal insufficiency in this model, through regulation of cholesterol ester storage, suggesting that pharmacologic interventions targeting the AnxA1/FPR/ALX pathway may provide a new approach for the maintenance of adrenal steroidogenesis in sepsis.

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Response of rat fasciculata-reticularis cells in primary culture to bacterial lipopolysaccharide

Cited by 8 publications

References 53 publications

Induction of nitric oxide synthase and heme oxygenase activities by endotoxin in the rat adrenal cortex: involvement of both signaling systems in the modulation of ACTH-dependent steroid production

Induction of nitric oxide synthase and heme oxygenase activities by endotoxin in the rat adrenal cortex: involvement of both signaling systems in the modulation of ACTH-dependent steroid production

Overfeeding during a critical postnatal period exacerbates hypothalamic-pituitary-adrenal axis responses to immune challenge: a role for adrenal melanocortin 2 receptors

Targeting the annexin 1‐formyl peptide receptor 2/ALX pathway affords protection against bacterial LPS‐induced pathologic changes in the murine adrenal cortex

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