Pathophysiologic glucocorticoid elevations promote bacterial translocation after thermal injury

Jones, William G.; Minei, Joseph P.; Richardson, Richard P.; Fahey, Thomas J.; Calvano, Steve E.; Antonacci, Anthony C.; Shires, G. Tom

doi:10.1128/iai.58.10.3257-3261.1990

Cited by 21 publications

(2 citation statements)

References 12 publications

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“…recently found Fas antigen expression in parenchymal rat liver cells became significantly elevated after stimulation with LPS, but this was not true of non‐parenchymal liver cells. Together with reports that endogenous GCs contribute to the translocation of enteric bacteria to the blood circulation, 46,47 these findings thus suggest that such ‘bacterial translocation’, which is frequently evoked by psychophysical stress, 47–49 might be involved in the up‐regulation of Fas antigen on hepatocytes.…”

Section: Involvement Of the Hpa Axis In Brain–liver Interactionsupporting

confidence: 61%

Does stress exacerbate liver diseases?

Chida¹,

Sudo

Kubo

2006

J of Gastro and Hepatol

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Although anecdotal comments on detrimental effects of psychosocial stress on liver diseases can be found even in the early literature, only recently has scientific evidence been reported. The present article reviewed such evidence to demonstrate how stress exacerbates liver diseases. A search of the literature from the last two decades was performed using MEDLINE by pairing 'psychological stress' with 'liver' or 'hepatitis.' Additional research was conducted by screening the bibliographies of articles retrieved in the MEDLINE search. The search results showed that the principal effectors of the activated hypothalamic-pituitary-adrenal (HPA) axis, glucocorticoids, can exert a facilitative effect on the hepatic inflammatory response and even increase the risk of developing hepatocellular carcinoma. For certain liver diseases, defective HPA axis activation, which probably contributed to the exacerbation of the liver disease, has been reported. The efferent sympathetic/adrenomedullary system mainly contributes to the stress-induced exacerbation of liver diseases via its neurotransmitters, the catecholamines. In contrast, the efferent parasympathetic nervous system elicits an inhibitory effect on the development of hepatic inflammation. In conclusion, the pathophysiological interaction between stress and the liver appears to be regulated by the complex, dynamic networks of both the endocrine and autonomic nervous systems, which implies a further need for basic research into the involved mechanisms and for clinical evidence to apply psychosocial support to patients with chronic liver diseases.

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Section: Involvement Of the Hpa Axis In Brain–liver Interactionsupporting

confidence: 61%

Does stress exacerbate liver diseases?

Chida¹,

Sudo

Kubo

2006

J of Gastro and Hepatol

View full text Add to dashboard Cite

show abstract

“…Müschen and colleagues40 recently showed the expression of Fas antigen in the parenchymal rat liver cells, but not in the nonparenchymal liver cells, to become significantly elevated after stimulation with lipopolysaccharide. Together with the reports that GC contributes to the translocation of enteric bacteria to the blood,41, 42 these findings suggest that such bacterial translocation, which is frequently evoked by various types of stressor stimuli,43–45 might be involved in the up‐regulated Fas antigen on parenchymal liver cells.…”

Section: Discussionsupporting

confidence: 66%

Electric foot shock stress-induced exacerbation of α-galactosylceramide-triggered apoptosis in mouse liver

et al. 2004

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Recently, liver natural killer T (NKT) cells, which are specifically stimulated by ␣-galactosylceramide (␣-GalCer), were found to play a critical role in intrahepatic immunity to several infections and certain hepatic disorders. However, the role of psychophysical stress on NKT cell-dependent liver injury induced by ␣-GalCer still remains to be elucidated. In this study, we employed inescapable electric foot shock as the mode of psychophysical stress and evaluated its effect on ␣-GalCer-induced hepatitis. Pre-exposure of 12 hours of foot shock stress before ␣-GalCer administration significantly enhanced ␣-GalCer-triggered increase in serum alanine aminotransferase levels, followed by increases in both liver caspase-3 activity and terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL)-positive hepatocytes, thus indicating that the liver NKT cell-dependent apoptotic response was exacerbated by stress. Foot shock stress also significantly increased both the number of liver NKT cells and Fas expression levels on hepatocytes. Pretreatment with RU-486, a glucocorticoid (GC) receptor antagonist, completely reversed such stress-induced enhancement of the ␣-GalCer-triggered serum alanine aminotransferase and hepatocyte Fas antigen responses. In contrast, such a reversal effect was not found in the mice pretreated with naloxone, a -opioid receptor antagonist, which thus suggests that an elevation of endogenous GCs, but not ␤-endorphin, as responsible for such stress-induced aggravation in mouse hepatitis models. A ccumulating evidence shows that gut function bidirectionally interacts with brain function by way of a mechanism that is regulated by the complex networks of the endocrine and autonomic nerve systems. [1][2][3] Researchers have preferentially called this interaction the brain-gut axis. Interestingly, some recent works on the brain-gut axis have further expanded this notion into the novel view that such a bidirectional interaction also exists between the brain and liver. It has been reported that intracisternal injection of thyrotropin-releasing hormone in the medulla, in particular in the left dorsal vagal complex, induces stimulation of hepatic blood flow 4,5 and hepatic proliferation, 6 and consequently protects against experimental liver injury 7 through vagal and cholinergic nerve pathways. Furthermore, corticotropin-releasing factor injected intracisternally has been also shown to elicit an inhibition of hepatic blood flow 8 and exacerbate experimental liver injury 9 through sympathetic and noraderenergic nerve pathways. In addition to these animal studies, some early clinical studies also revealed that emotional stress such as that induced by hypnotic suggestion of "fear" and "anxiety" decreases hepatic blood flow 10 and that the severity of psychosocial stress was significantly correlated with the exaggeration of inflammatory and fibrosing changes in alcoholic liver injury. 11 Taken together, these findings suggest the presence of the close communication between the liver and the br...

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Pathophysiologic Glucocorticoid Levels and Survival of Translocating Bacteria

et al. 1991

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Burn wound sepsis in rats results in sustained corticosterone elevations and the prolonged presence of translocated bacteria in the mesenteric lymph nodes (MLNs). To determine if survival of bacteria in the MLNs may be influenced by pathophysiologic corticosterone levels, MLNs were quantitatively analyzed from rats randomized to the following groups: burn wound sepsis (BI); BI with adrenocortical response attenuated by cyclosporine (cyclosporine/BI); or cyclosporine/BI with corticosterone replacement (cyclosporine/BI + P). Although rates of bacterial translocation were similar, corticosterone levels were significantly different among the three groups and correlated with the number of lymphocytes and the number of enteric bacteria present per gram of MLN. Thus, pathophysiologic elevations of corticosterone levels during sepsis may exert an effect that allows survival of translocated bacteria in the MLNs of rats, perhaps due to glucocorticoid-associated alterations in regional immunity.

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Pathophysiologic glucocorticoid elevations promote bacterial translocation after thermal injury

Cited by 21 publications

References 12 publications

Does stress exacerbate liver diseases?

Does stress exacerbate liver diseases?

Electric foot shock stress-induced exacerbation of α-galactosylceramide-triggered apoptosis in mouse liver

Pathophysiologic Glucocorticoid Levels and Survival of Translocating Bacteria

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