Stress Increases Vulnerability to Inflammation in the Rat Prefrontal Cortex

Pablos, Rocío M. de; Villarán, Ruth F.; Argüelles, Sandro; Herrera, Antonio J.; Venero, José L.; Ayala, Antonio; Cano, Josefina; Machado, Alberto

doi:10.1523/jneurosci.0802-06.2006

Cited by 193 publications

(190 citation statements)

References 100 publications

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“…CUS fails to suppress the increased expression of IL-1β and TNF-α following infusion of LPS into the prefrontal cortex (de Pablos et al 2006). Even more striking, CUS augments TNF-α, IL-1β , and iNOS protein levels in hippocampus and cortex when LPS is administered peripherally, an effect that is GR-mediated (Munhoz et al 2006).…”

Section: 3mentioning

confidence: 95%

“…Second, a similar question has been raised concerning the effects of dexamethasone on memory consolidation and for this topic there exist many lines of evidence that support the conclusion that like corticosterone, dexamethasone is capable of exerting its effects centrally (Roozendaal 2000). Finally, as reviewed, corticosterone is also capable of increasing inflammation in vivo and antagonism of GR signaling blocks this effect (de Pablos et al 2006;Munhoz et al 2006;Munhoz in prep).…”

Section: Is Gc Enhanced Inflammation Due To a Decrease In Local Gc Exmentioning

confidence: 95%

“…Moreover, CUS following direct LPS infusion into the prefrontal cortex increases components of the MAPK signaling pathway involved in inflammatory pathogenesis including phosphorylated JNK, p38, and ERK (de Pablos et al 2006). These effects of CUS are also GR-mediated.…”

Section: 3mentioning

confidence: 97%

“…The chronic unpredictable stress (CUS) paradigm exposes animals to a different stressor each day and animals subjected to CUS after direct LPS infusion into the prefrontal cortex have markedly increased neuron and astroglia death. This effect of CUS is reversed by blocking GR, suggesting that GC signaling is the critical component of CUS involved (de Pablos et al 2006). These findings are in contrast to the aforementioned protective effects of basal to low-stress levels of corticosterone on LPS toxicity.…”

Section: Just How Anti-inflammatory Are Gcs In the Brain?mentioning

confidence: 99%

“…Furthermore, rats exposed to chronic high stress levels of corticosterone show accelerated and augmented microglial activation and migration of peripheral cells to the injury site (Dinkel et al 2003). Similarly, GCs released during CUS enhance microglial activation following direct LPS injection to the prefrontal cortex (de Pablos et al 2006). These findings implicate chronic stress levels of GCs in enhanced activation of the immune cell response to neurological cytotoxicity.…”

Section: Just How Anti-inflammatory Are Gcs In the Brain?mentioning

confidence: 99%

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An inflammatory review of glucocorticoid actions in the CNS

Sorrells¹,

Sapolsky²

2007

Brain, Behavior, and Immunity

397

283

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In recent years the classic view that glucocorticoids, the adrenal steroids secreted during stress, are universally anti-inflammatory has been challenged at a variety of levels. It was first observed that under some circumstances, acute GC exposure could have pro-inflammatory effects on the peripheral immune response. More recently, chronic exposure to GCs has been found to have pro-inflammatory effects on the specialized immune response to injury in the central nervous system. Here we review the evidence that in some cases, glucocorticoids can increase pro-inflammatory cell migration, cytokine production, and even transcription factor activity in the brain. We consider how these unexpected effects of glucocorticoids can co-exist with their well-established anti-inflammatory properties, as well as the considerable clinical implications of these findings.

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Section: 3mentioning

confidence: 95%

Section: Is Gc Enhanced Inflammation Due To a Decrease In Local Gc Exmentioning

confidence: 95%

Section: 3mentioning

confidence: 97%

Section: Just How Anti-inflammatory Are Gcs In the Brain?mentioning

confidence: 99%

Section: Just How Anti-inflammatory Are Gcs In the Brain?mentioning

confidence: 99%

See 3 more Smart Citations

An inflammatory review of glucocorticoid actions in the CNS

Sorrells¹,

Sapolsky²

2007

Brain, Behavior, and Immunity

397

283

View full text Add to dashboard Cite

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Multiorgan‐on‐a‐chip for realization of gut‐skin axis

Lee

Sung

2022

Biotech & Bioengineering

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The concept of physiological link between the gut and the skin, known as the gutskin axis, has been gaining more evidence recently. Although experimental data from animal and human studies support the existence of the gut-skin axis, in vitro model platforms that can test the hypothesis are lacking. Organ-on-a-chip offers the possibility of connecting different tissues and recapitulating interactions between them. In this study, we report a multiorgan chip that can capture the basic interorgan communication between the gut and the skin. Its modular design enables separate culture and differentiation of the gut and skin tissues, and after assembly the two organs are connected via microfluidic channels than enables perfusion and mass transfer. We showed that the impairment of the gut barrier function exacerbated the adverse effect of fatty acids on skin cells, with decreased viability, increased level of cytokine secretion and human beta defensin-2 (hBD-2), an inflammatory dermal disease marker. Based on these results, we believe that our multiorgan chip can be a novel in vitro platform for recapitulating complex mechanisms underlying the gutskin axis.

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Hypothalamic‐Pituitary‐Adrenal (HPA) Axis and Aging

Gupta

Morley

2014

Comprehensive Physiology

122

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Human aging is associated with increasing frailty and morbidity which can result in significant disability. Dysfunction of the hypothalamic-pituitary-adrenal (HPA) axis may contribute to aging-related diseases like depression, cognitive deficits, and Alzheimer's disease in some older individuals. In addition to neuro-cognitive dysfunction, it has also been associated with declining physical performance possibly due to sarcopenia. This article reviews the pathophysiology of HPA dysfunction with respect to increased basal adrenocorticotropic hormone (ACTH) and cortisol secretion, decreased glucocorticoid (GC) negative feedback at the level of the paraventricular nucleus (PVN) of the hypothalamus, hippocampus (HC), and prefrontal cortex (PFC), and flattening of diurnal pattern of cortisol release. It is possible that the increased cortisol secretion is secondary to peripheral conversion from cortisone. There is a decline in pregnolone secretion and C-19 steroids (DHEA) with aging. There is a small decrease in aldosterone with aging, but a subset of the older population have a genetic predisposition to develop hyperaldosteronism due to the increased ACTH stimulation. The understanding of the HPA axis and aging remains a complex area with conflicting studies leading to controversial interpretations.

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Stress Increases Vulnerability to Inflammation in the Rat Prefrontal Cortex

Cited by 193 publications

References 100 publications

An inflammatory review of glucocorticoid actions in the CNS

An inflammatory review of glucocorticoid actions in the CNS

Multiorgan‐on‐a‐chip for realization of gut‐skin axis

Hypothalamic‐Pituitary‐Adrenal (HPA) Axis and Aging

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