La brûlure : une pathologie inflammatoire

Ravat, François; Payre, J.; Peslages, P.; Fontaine, M; Sens, N.

doi:10.1016/j.patbio.2009.12.001

Cited by 25 publications

(11 citation statements)

References 87 publications

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“…7 The central element is the macrophage cell and the biochemical cytokines TNF-α and interleukin-6 (IL-6). 7 Macrophages are major producers of proinflammatory mediators (ie, prostaglandin E2, reactive nitrogen intermediates, IL-6, TNF-α). 5 Furthermore, thermal injury increases the production of these mediators by macrophages.…”

Section: Cellular Mechanismsmentioning

confidence: 99%

“…8 TNF-α is responsible in part for inducing apoptosis of various cell elements. 7 In addition, proapoptotic factors show increased expression including Bax, Bcl-xl, and caspase-3 activity. Furthermore, epidermal burn injury often triggers significant apoptosis of organ cells, which may be caused by a severe burn-induced systemic inflammatory reaction.…”

Section: Cellular Mechanismsmentioning

confidence: 99%

“…7 However, of these proinflammatory cytokines, only IL-6 has consistently been shown to be elevated systemically post-burn. 5 In experimental animal models with third degree burns of either 20 or 40%, serum IL-6 levels peaked during the first hours after injury and were proportionate to the size of area burned.…”

Section: Cellular Mechanismsmentioning

confidence: 99%

“…7 This phase depends on T lymphocytes of helper Th-2 and three principal mediators: the cytokines IL-4/IL-10 and TGF. 7 This phase has become known as the counter anti-inflammatory response syndrome. 7 …”

Section: Cellular Mechanismsmentioning

confidence: 99%

See 3 more Smart Citations

Burns

Nielson

Duethman

Howard

et al. 2017

Journal of Burn Care & Research

246

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As a result of many years of research, the intricate cellular mechanisms of burn injury are slowly becoming clear. Yet, knowledge of these cellular mechanisms and a multitude of resulting studies have often failed to translate into improved clinical treatment for burn injuries. Perhaps the most valuable information to date is the years of clinical experience and observations in the management and treatment of patients, which has contributed to a gradual improvement in reported outcomes of mortality. This review provides a discussion of the cellular mechanisms and pathways involved in burn injury, resultant systemic effects on organ systems, current management and treatment, and potential therapies that we may see implemented in the future.

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Section: Cellular Mechanismsmentioning

confidence: 99%

Section: Cellular Mechanismsmentioning

confidence: 99%

Section: Cellular Mechanismsmentioning

confidence: 99%

Section: Cellular Mechanismsmentioning

confidence: 99%

See 2 more Smart Citations

Burns

Nielson

Duethman

Howard

et al. 2017

Journal of Burn Care & Research

246

View full text Add to dashboard Cite

show abstract

“…По оценкам Всемирной организации здравоохранения, в мире ежегодно регистрируют 265 000 случаев смерти от ожогов. Высокая летальность при термической травме (ТТ) обусловлена быстрым развитием полиорганной недостаточности в связи с интенсивной болевой импульсацией, гиповолемией и гемоконцентрацией, гипоксией, эндогенной интоксикацией, эскалацией процессов свободнорадикального окисления и изменением иммунного статуса организма [11][12][13].…”

Section: экспериментальная медицинаunclassified

Effect of erythropoietin on the content of lipid peroxidation products in lymphocytes in experimental thermal injury

2015

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Aim. To investigate the effect of different concentrations of erythropoietin on the content of lipid peroxidation products in lymphocytes isolated from the blood of rats with thermal injury. Methods. The study was performed on 22 white male rats. Thermal injury of IIIA degree on 4% of body surface area was simulated by immersion in water at a temperature of 98-99 °C. After 24 hours, blood lymphocytes were isolated and the content of the primary (diene conjugates), secondary (ketodienes and conjugated trienes) and final products (Schiff bases) of lipid peroxidation were determined spectrophotometrically. Erythropoietin was added to lymphocytes at concentrations of 0.01; 0.1 and 1 IU/ml. Results. It was found that 24 hours after thermal injury there were the accumulation of primary, secondary and final products of lipid peroxidation in isopropanol fraction of lipid extracts of peripheral blood lymphocytes. Addition of erythropoietin to the rat lymphocytes resulted in a controversial change in the content of lipid peroxidation products: an increase in the heptane fraction, decrease - in the isopropanol fraction of lipid extract of lymphocytes. In the heptane fraction erythropoietin (at concentrations of 0.01, 0.1, and 1 IU/ml) increased the content of primary, end (at a concentration of 0.1 IU/ml) and secondary (at a concentration of 1 IU/ml) lipid peroxidation products. In isopropanol fraction erythropoietin reduced the content of primary (at concentrations of 0.01, 0.1, and 1 IU/ml), final (at concentrations of 0.01 and 0.1 IU/ml) and secondary (at concentrations of 0.01 and 1 IU/ml) products of lipid peroxidation. Conclusion. It was found that there is an accumulation of lipid peroxidation products in the isopropanol fraction of lipid extract of lymphocytes isolated from peripheral blood of rats with thermal injury; erythropoietin application at concentrations of 0.01; 0.1 and 1 IU/ml increases the content of lipid peroxidation products in heptane fraction and decrease in the isopropanol fraction of lipid extract of lymphocytes.

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DAMP-Controlled and Uncontrolled Responses to Trauma: Wound Healing and Polytrauma

Land

2020

Damage-Associated Molecular Patterns in Human Diseases

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La brûlure : une pathologie inflammatoire

Cited by 25 publications

References 87 publications

Burns

Burns

Effect of erythropoietin on the content of lipid peroxidation products in lymphocytes in experimental thermal injury

DAMP-Controlled and Uncontrolled Responses to Trauma: Wound Healing and Polytrauma

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