Chronic Pathophysiologic Elevation of Corticosterone After Thermal Injury or Thermal Injury and Burn Wound Infection Adversely Affects Body Mass, Lymphocyte Numbers, and Outcome

Hawes, A S; Richardson, Richard P.; Antonacci, Anthony C.; Calvano, Steve E.

doi:10.1097/00004630-199501000-00002

Cited by 17 publications

(12 citation statements)

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“…Our studies collectively suggest that diminished intestinal T cell function and increased intestinal permeability are likely to contribute to increased bacterial translocation after EtOH and burn injury (6,11,29). Bacterial translocation has been observed after burn injury in a number of previous studies (4,7,16,23,24,27,47). Furthermore, these studies support the concept that intestine-derived factors including bacteria and their products play significant roles in initiating/exacerbating multiple organ dysfunction in acutely injured patients as well as in patients with EtOH intoxication (5,8,15,20,32).…”

supporting

confidence: 57%

“…It is sufficient to state that the above studies collectively suggest that Cort levels tightly control immune cell functions. Thus any change in Cort levels as low as reported by Faunce et al (18) or as high as has been shown in many injury conditions (1,21,23,27,30,33,39,42) is likely to affect the immune response.…”

Section: Discussionmentioning

confidence: 75%

“…Several lines of evidence suggest that EtOH intoxication and burn injury independently activate the hypothalamic-pituitaryadrenal (HPA) axis (8,21,23,27,33,38,39,50). Corticosterone (Cort), which is the glucocorticoid end product of the HPA axis in rodents, plays an important role in influencing the immune system.…”

mentioning

confidence: 99%

“…Corticosterone (Cort), which is the glucocorticoid end product of the HPA axis in rodents, plays an important role in influencing the immune system. There is evidence that elevated levels of Cort suppress macrophage and T cell functions (1,2,21,23,42,46,49,50). In contrast, other studies suggest adrenal insufficiency to be the cause of impaired host ability to clear infectious agents (8,18,38).…”

mentioning

confidence: 99%

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Corticosterone suppresses mesenteric lymph node T cells by inhibiting p38/ERK pathway and promotes bacterial translocation after alcohol and burn injury

Li¹,

Rana²,

Kovacs³

et al. 2005

American Journal of Physiology-Regulatory, Integrative and Comp

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supporting

confidence: 57%

Section: Discussionmentioning

confidence: 75%

mentioning

confidence: 99%

mentioning

confidence: 99%

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Corticosterone suppresses mesenteric lymph node T cells by inhibiting p38/ERK pathway and promotes bacterial translocation after alcohol and burn injury

Li¹,

Rana²,

Kovacs³

et al. 2005

American Journal of Physiology-Regulatory, Integrative and Comp

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“…20]. In addition, they are known to be elevated after stresses such as alcohol exposure and traumatic injury, especially burns [21][22][23]. Given a body of literature that suggests that glucocorticoids serve to direct and maintain proper immune function under both normal circumstances [for review see ref .…”

Section: Introductionmentioning

confidence: 99%

Glucocorticoids protect against suppression of T cell responses in a murine model of acute ethanol exposure and thermal injury by regulating IL-6

Faunce

Gregory

Kovacs

1998

Journal of Leukocyte Biology

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Previous reports by this laboratory demonstrated that acute alcohol exposure combined with a 15% body surface area dorsal scald injury results in significant reductions in delayed-type hypersensitivity (DTH) and splenocyte proliferative responses compared to either insult alone. Previous studies by this lab have also shown that these defects are mediated, in part, by increased production of interleukin-6 (IL-6). Because both alcohol exposure and thermal injury are known to modulate glucocorticoid (CORT) levels, and CORT regulates IL-6 gene expression, the relationship between circulating CORT and IL-6 production in burn ؉ ethanol mice was examined . At 24 and 48 h post-burn, a positive correlation existed between circulating CORT levels and measurements of cellular immune function. Administration of exogenous CORT to burn ؉ ethanol-treated mice resulted in significant restoration (to 60% of control) of DTH and splenocyte proliferative responses. This restoration was concomitant with a down-regulation of circulating and macrophage-derived IL-6. The specificity of CORT in modulating these responses was tested by assessing cellular immune function and IL-6 levels after glucocorticoid receptor blockade with RU486. Taken together, these data strongly suggest that under normal circumstances CORT protects burned mice from severe immune dysfunction, a protection that is not afforded to burn ؉ ethanol-treated mice. Furthermore, the immune dysfunction observed in burn ؉ ethanol mice may be due to a lack of glucocorticoid attenuation of IL-6. J. Leukoc. Biol. 64: 724-732; 1998.

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Immune deficiency following thermal trauma is associated with apoptotic cell death

et al. 1995

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Thermal injury-associated specific immune deficiency occurs despite indicators of systemic activation of the lymphoid compartment. We investigated the possibility that postburn immune failure and T cell activation are casually related through activation-induced (apoptotic) cell death. The relationship between the cellular immune response and cell mortality was examined in cultures of peripheral blood mononuclear cells (PBMC) from 14 immunosuppressed patients with extensive burns (35-90% total body surface area). Impaired cellular immunity coincided with significantly reduced cell viability as ascertained by propidium iodide staining and dye reduction assays. Following stimulation with the mitogenic lectin, phytohemagglutinin (PHA), the majority of DNA in patient cultures was fragmented, suggesting the occurrence of apoptotic cell death. Even without stimulation a portion of patient cells was apoptotic as indicated by oligonucleosomal bands on agarose gel electrophoresis. Exogenous interleukin-2 or phorbol ester markedly reduced constitutive as well as PHA-induced DNA fragmentation. In situ demonstration of DNA strand breaks in freshly isolated patient PBMC, by a TdT-based labeling technique, confirmed that a larger fraction (up to 60%) of circulating lymphocytes was undergoing apoptosis on the periphery. These novel observations suggest that apoptosis may play a major role in thermal injury-related cellular immunodeficiency.

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Chronic Pathophysiologic Elevation of Corticosterone After Thermal Injury or Thermal Injury and Burn Wound Infection Adversely Affects Body Mass, Lymphocyte Numbers, and Outcome

Cited by 17 publications

References 0 publications

Corticosterone suppresses mesenteric lymph node T cells by inhibiting p38/ERK pathway and promotes bacterial translocation after alcohol and burn injury

Corticosterone suppresses mesenteric lymph node T cells by inhibiting p38/ERK pathway and promotes bacterial translocation after alcohol and burn injury

Glucocorticoids protect against suppression of T cell responses in a murine model of acute ethanol exposure and thermal injury by regulating IL-6

Immune deficiency following thermal trauma is associated with apoptotic cell death

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