Immunological responses to thermal injury

Sparkes, B. G.

doi:10.1016/s0305-4179(96)00089-7

Cited by 91 publications

(40 citation statements)

References 59 publications

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“…Numerous alterations in the immune system have been detected following thermal injury to both rodents and humans, including suppressed T cell proliferation, impaired natural killer (NK) cell activity, and macrophage dysfunction. The initial inflammatory response to burn injury is often followed by anti-inflammatory cytokine predominances (5,6). Perturbed balances of Th1 to Th2 cytokines, as regulators of innate and adaptive immunities, are believed to contribute to the suppression of antimicrobial immunity that is associated with thermal injury.…”

Section: Introductionmentioning

confidence: 99%

Interferon-?? Production Is Suppressed in Thermally Injured Mice: Decreased Production of Regulatory Cytokines and Corresponding Receptors

Toliver‐Kinsky

Varma²,

Chen³

et al. 2002

Shock

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Thermal injury to 40% or more of the total body surface area poses a significant risk for the development of opportunistic infections that increase complications and mortality. Altered cytokine induction profiles, including suppression of the Th1 cytokines IFN-gamma and IL-12 and elevations in the anti-inflammatory cytokine IL-10, are believed to contribute to burn-associated immunosuppression and the development of sepsis. The specific changes that lead to altered cytokine production following major burns are not known. We examined the effects of burn injuries to 40% of the mouse body surface on IFN-gamma induction in the major IFN-gamma-producing cell types of the spleen. Additionally, effects on key IFN-gamma-regulatory cytokines were examined after bacterial challenge. We report that in vivo induction of IFN-gamma in natural killer lymphocytes is suppressed in burned mice. Splenic IFN-gamma was suppressed at both the mRNA and protein levels. Early suppression was associated with impairments in both the macrophage/dendritic cell and lymphocyte populations, whereas persistent suppression was associated with impaired lymphocyte function and decreased responsiveness to IFN-gamma-inducing factors. IFN-gamma production could be restored by neutralization of the upregulated cytokine IL-10. Induction of the IFN-gamma-inducers IL-15, IL-12, and IL-2 was also impaired after burn injury, whereas IL-18 levels remained unaffected. Exogenous application of these suppressed cytokines to isolated splenocytes did not restore IFN-gamma to sham levels, indicating a loss of responsiveness to these factors. Expression of the IL-2, IL-12, and IL-15 receptors was suppressed after thermal injury. We conclude that burn-associated suppression of IFN-gamma is due to deficient production of inducing factors and their receptors, leading to severe impairments in cellular IFN-gamma induction pathways.

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Section: Introductionmentioning

confidence: 99%

Interferon-?? Production Is Suppressed in Thermally Injured Mice: Decreased Production of Regulatory Cytokines and Corresponding Receptors

Toliver‐Kinsky

Varma²,

Chen³

et al. 2002

Shock

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“…The former is packed with keratinocytes that make up a mechanical barrier whereas the latter contains capillaries and a variety of immune cells including Langerhans cells, dendritic cells, and macrophages. When skin is damaged by burn injuries the mechanical barrier is ruptured resulting in a complex interplay between pro-and anti-inflammatory responses that create an ideal milieu for bacterial invasion (12)(13)(14)(15)(16)(17). The local inflammatory responses include a dynamic response by epithelial cells and keratinocytes, which modulates antimicrobial peptide gene expression (18) and orchestrate the diapedesis of neutrophils.…”

mentioning

confidence: 99%

Deficiency of Mannose-Binding Lectin Greatly Increases Susceptibility to Postburn Infection withPseudomonas aeruginosa

Møller-Kristensen

Ip²,

Shi³

et al. 2006

The Journal of Immunology

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Burn injury disrupts the mechanical and biological barrier that the skin presents against infection by symbionts like the Pseudomonas aeruginosa, a Gram-negative bacteria. A combination of local factors, antimicrobial peptides, and resident effector cells form the initial response to mechanical injury of the skin. This activity is followed by an inflammatory response that includes influx of phagocytes and serum factors, such as complement and mannose-binding lectin (MBL), which is a broad-spectrum pattern recognition molecule that plays a key role in innate immunity. A growing consensus from studies in humans and mice suggests that lack of MBL together with other comorbid factors predisposes the host to infection. In this study we examined whether MBL deficiency increases the risk of P. aeruginosa infection in a burned host. We found that both wild-type and MBL null mice were resistant to a 5% total body surface area burn alone or s.c. infection with P. aeruginosa alone. However, when mice were burned then inoculated s.c. with P. aeruginosa at the burn site, all MBL null mice died by 42 h from septicemia, whereas only one-third of wild-type mice succumbed (p = 0.0005). This result indicates that MBL plays a key role in containing and preventing a systemic spread of P. aeruginosa infection following burn injury and suggests that MBL deficiency in humans maybe a premorbid variable in the predisposition to infection in burn victims.

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“…Fax: +81-4-2991-1613 E-mail: manabu@ndmc.ac.jp induce exaggerated inflammatory reactions in which the activated Kupffer cells and/ or neutrophils are involved [6][7][8][9][10]. In the agonal phase, these severe stresses are often associated with multiple organ dysfunctions due to extremely exaggerated inflammation [11,12].…”

Section: Introductionmentioning

confidence: 99%

Diverse Enhancement of Superoxide Production from Kupffer Cells and Neutrophils after Burn Injury or Septicemia

Masuda

Kinoshita

Ono

et al. 2006

J. Clin. Biochem. Nutr.

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Summary Objective: To investigate the difference in superoxide production from circulating neutrophils and Kupffer cells between in the mice after burn injury and mice suffering from bacterial septicemia.Background: Both severe burn injury and septicemia can result in a critical / fatal outcome for the patients even after initial resuscitation. Analyses of defense mechanisms in the host who survive after severe stress are thereby very important for improvement of intensive care.Method: Either burn injury or inoculations with Peudomonas aeruginosa were subjected to C57BL /6 mice. After 7 days, circulating neutrophils and Kupffer cells were obtained from the mice to examine superoxide or cytokine production.Results: Neither of the mouse groups showed any pathological changes in major organs or any elevations in the serum transaminase or TNF levels at 7 days after burn injury or bacterial inoculation. The burn injured mice showed significantly higher superoxide production from neutrophils by stimulation with phorbor myristate acetate (PMA) or opsonized zymosan (OZ) than that from Kupffer cells. In contrast, the bacterial challenged mice showed a significantly higher superoxide production from Kupffer cells than that from neutrophils. In addition, the burn injured mice showed a significantly higher production of IL-10, namely antiinflammatory cytokine, from the Kupffer cells by LPS stimulation than the bacterial challenged mice while the bacterial challenged mice showed a significantly higher production of IL-12, namely proinflammatory cytokine, from Kupffer cells by LPS stimulation than the burn injured mice.Conclusions: Neutrophils might thus be activated to a greater degree than Kupffer cells in mice after burn injury, while Kupffer cells might be activated more than neutrophils after bacterial septicemia.

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Immunological responses to thermal injury

Cited by 91 publications

References 59 publications

Interferon-?? Production Is Suppressed in Thermally Injured Mice: Decreased Production of Regulatory Cytokines and Corresponding Receptors

Interferon-?? Production Is Suppressed in Thermally Injured Mice: Decreased Production of Regulatory Cytokines and Corresponding Receptors

Deficiency of Mannose-Binding Lectin Greatly Increases Susceptibility to Postburn Infection withPseudomonas aeruginosa

Diverse Enhancement of Superoxide Production from Kupffer Cells and Neutrophils after Burn Injury or Septicemia

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