Smoke Inhalation Enhances Early Alveolar Leukocyte Responsiveness to Endotoxin

Wright, Mary Jo; Murphy, Joseph

doi:10.1097/01.ta.0000171588.25618.87

Cited by 29 publications

(16 citation statements)

References 26 publications

(41 reference statements)

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“…Similar to the current study, Wright and Murphy noted a dramatic decline in both alveolar polymorphonuclear leucocyte and macrophage numbers from smoke-injured lungs of burn patients 4 days after the injury. 27 According to Wright and Joseph, the alveolar cell counts from burn-injured patients who were uncomplicated with inhalation injury were significantly higher and comparable in number to the alveolar cell numbers from smoke-injured lungs on the same day. 27 According to another recent clinical report by Davis et al, nonsurvivors of severe burns and smoke inhalation injuries had fewer total white blood cells in their broncoalveolar lavage fluid when compared with survivors.…”

Section: Discussionmentioning

confidence: 94%

“…27 According to Wright and Joseph, the alveolar cell counts from burn-injured patients who were uncomplicated with inhalation injury were significantly higher and comparable in number to the alveolar cell numbers from smoke-injured lungs on the same day. 27 According to another recent clinical report by Davis et al, nonsurvivors of severe burns and smoke inhalation injuries had fewer total white blood cells in their broncoalveolar lavage fluid when compared with survivors. They considered this finding to be suggestive of impaired leucocyte migration in the setting of immunoparalysis in patients who have these injuries.…”

Section: Discussionmentioning

confidence: 94%

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Destructive Pulmonary Effects of Smoke Inhalation and Simultaneous Alterations in Circulating IL-6, TNF-α, and IFN-γ Levels at Different Burn Depths

Abali

Karakayalı

Özdemir

et al. 2013

Journal of Burn Care & Research

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The current study sought to examine the interactions between inflammatory and immune events in the lung and circulating interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), and interferon-γ (IFN-γ) levels at different burn depths with concomitant smoke inhalation in the rat model. Forty-eight female Sprague-Dawley rats were divided into six groups: S, sham; P, partial-thickness burns; F, full-thickness burns; I, inhalation; Pi, partial-thickness burns + inhalation; and Fi, full-thickness burns + inhalation. Blood samples and lung biopsies were obtained 24 hours later. Blood levels of IL-6, TNF-α, and IF-γ were measured with enzyme-linked immunosorbent assay. The proportions of CD3+ lymphocytes and CD68+ macrophages in the biopsies were studied immunohistochemically. The most severe inflammatory changes, except the neutrophil sequestration, were observed in the Fi group. A dense amount of neutrophils was observed in the F group. Edema and massive alveolar bleeding were seen in the I, Pi, and Fi groups. The amount of CD3+ lymphocytes were dense in the P, F, and Pi groups. The amount of CD68+ macrophages were significantly dense in Pi, F, I, and Fi groups. IL-6, TNF-α, and IF-γ increased in all groups when compared to the S group. The highest IL-6 level was seen in the Fi group. TNF-α significantly increased in the F, Pi, I, and Fi groups. Increase in IFN-γ levels in the Pi and Fi groups was significantly higher than in the P and F groups. In concomitant smoke inhalation and skin burns, pulmonary damage and systemic inflammatory response are related and may be evaluated by blood levels of IL-6, TNF-α, and IFN-γ cytokines.

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Section: Discussionmentioning

confidence: 94%

Section: Discussionmentioning

confidence: 94%

Destructive Pulmonary Effects of Smoke Inhalation and Simultaneous Alterations in Circulating IL-6, TNF-α, and IFN-γ Levels at Different Burn Depths

Abali

Karakayalı

Özdemir

et al. 2013

Journal of Burn Care & Research

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“…Hales et al were not able to prove any influence of TNF-α in smoke-induced microvascular lung injury in sheep, but found an increase of TNF-α in lymph fluid of the lung after injection of endotoxin 25. Some other authors27 28 were also able to demonstrate an increase of TNF-α in burn disease in men, but this might have been due to bacterial superinfections 20 26…”

Section: Discussionmentioning

confidence: 96%

“…Within the first 24 h after combustion gas inhalation, the morphological changes of the alveolar epithelia were only discreet, but functionally relevant with a deterioration of the alveolar clearance and of the barrier function leading to an increased permeability for proteins 12. The main pathway for the development of these changes seemed to be the accumulation of activated neutrophils and macrophages 14 20 21…”

Section: Discussionmentioning

confidence: 99%

“…Thus, microscopically no reactive inflammatory cell infiltrates were found in our cases. Moreover, it is possible that not only the inhalation of heat and combustion gas, but additional factors like endotoxins20 25 26 may be necessary to increase TNF-α expression in the lung. Since ICAM-1 becomes activated via TNF-α, the absence of ICAM-1 expression in our cases is plausible, as it should become manifest only at a later stage of the inflammatory process.…”

Section: Discussionmentioning

confidence: 99%

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Putative role of TNF-α, interleukin-8 and ICAM-1 as indicators of an early inflammatory reaction after burn: a morphological and immunohistochemical study of lung tissue of fire victims

Boehm¹,

Fischer

Bohnert

2010

J Clin Pathol

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In burn victims with short survival times of ≤1 h after fire exposure, the immunohistochemical expression profiles of TNF-α, IL-8 and ICAM-1 in the lungs were not altered enough to prove an instant inflammatory reaction in these cases. Nevertheless, the positive reaction of TNF-α in erythrocytes of burn victims may indicate the beginning of a non-specific immune response to fire-induced inhalation trauma.

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Alveolar Macrophage Chemokine Secretion Mediates Neutrophilic Lung Injury in Nox2-Deficient Mice

et al. 2018

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Acute lung injury (ALI), developing as a component of the systemic inflammatory response syndrome (SIRS), leads to significant morbidity and mortality. Reactive oxygen species (ROS), produced in part by the neutrophil NADPH oxidase 2 (Nox2), have been implicated in the pathogenesis of ALI. Previous studies in our laboratory demonstrated the development of pulmonary inflammation in Nox2-deficient (gp91phox-/y) mice that was absent in WT mice in a murine model of SIRS. Given this finding, we hypothesized that Nox2 in a resident cell in the lung, specifically the alveolar macrophage, has an essential anti-inflammatory role. Using a murine model of SIRS, we examined whole-lung digests and bronchoalveolar lavage fluid (BALf) from WT and gp91phox-/y mice. Both genotypes demonstrated neutrophil sequestration in the lung during SIRS, but neutrophil migration into the alveolar space was only present in the gp91phox-/y mice. Macrophage inflammatory protein (MIP)-1α gene expression and protein secretion were higher in whole-lung digest from uninjected gp91phox-/y mice compared to the WT mice. Gene expression of MIP-1α, MCP-1, and MIP-2 was upregulated in alveolar macrophages obtained from gp91phox-/y mice at baseline compared with WT mice. Further, ex vivo analysis of alveolar macrophages, but not bone marrow-derived macrophages or peritoneal macrophages, demonstrated higher gene expression of MIP-1α and MIP-2. Moreover, isolated lung polymorphonuclear neutrophils migrate to BALf obtained from gp91phox-/y mice, further providing evidence of a cell-specific anti-inflammatory role for Nox2 in alveolar macrophages. We speculate that Nox2 represses the development of inflammatory lung injury by modulating chemokine expression by the alveolar macrophage.

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Smoke Inhalation Enhances Early Alveolar Leukocyte Responsiveness to Endotoxin

Abstract: Smoke inhalation induces a massive influx of alveolar leukocytes that are primed for an early, enhanced LPS-activated cytokine response compared with alveolar leukocytes isolated after burn injury alone or normal controls.

Cited by 29 publications

References 26 publications

Destructive Pulmonary Effects of Smoke Inhalation and Simultaneous Alterations in Circulating IL-6, TNF-α, and IFN-γ Levels at Different Burn Depths

Destructive Pulmonary Effects of Smoke Inhalation and Simultaneous Alterations in Circulating IL-6, TNF-α, and IFN-γ Levels at Different Burn Depths

Putative role of TNF-α, interleukin-8 and ICAM-1 as indicators of an early inflammatory reaction after burn: a morphological and immunohistochemical study of lung tissue of fire victims

Alveolar Macrophage Chemokine Secretion Mediates Neutrophilic Lung Injury in Nox2-Deficient Mice

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