Inhibition of lung permeability changes after burn and smoke inhalation by an anti-interleukin-8 antibody in sheep

Sakurai, Hiroyuki; Soejima, Kazutaka; Schmalstieg, Frank C.; Nozaki, Motohiro; Traber, Daniel L.

doi:10.1007/s00595-008-3879-3

Cited by 13 publications

(8 citation statements)

References 21 publications

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“…Thus, the possibility that the AMPK inhibitor Compound C could directly affect these cell types should be considered. Additionally, our in vivo findings confirm that chemokines produced by lung epithelial cells are important in the development of lung inflammation induced by toxic smoke (1,7,11,12). Given that fact that a ROS scavenger can alleviate wood smoke-induced lung injury (5,46), it is likely that ROS is also the trigger to activate the AMPK signaling in vivo.…”

Section: Discussionsupporting

confidence: 77%

“…Particularly, chemokines released from lung cells are believed to be crucial in regulating lung inflammation because they can promote inflammatory cell recruitment into the lung to amplify the inflammation (1). Interleukin-8 (IL-8), a potent chemokine, has been suggested to play a vital role in the initiation and progression of lung inflammation with smoke inhalation (7,8,11,12). However, the molecular mechanisms by which inhaled toxic smoke increases the production of IL-8 from lung cells are totally unknown.…”

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confidence: 98%

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Inflammatory Role of AMP-Activated Protein Kinase Signaling in an Experimental Model of Toxic Smoke Inhalation Injury*

Perng

Chang

Wang

et al. 2013

Critical Care Medicine

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Interleukin-8 induction by wood smoke extract in lung epithelial cells is mediated by novel NADPH oxidase-dependent, reactive oxygen species-sensitive AMP-activated protein kinase signaling with Jun N-terminal kinase and extracellular signal-regulated kinase as the downstream kinases and nuclear factor-κB and signal transducer and activator of transcription protein 3 as the downstream transcription factors. This AMP-activated protein kinase signaling is likely important for inducing lung inflammation with toxic smoke exposure in mice.

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Section: Discussionsupporting

confidence: 77%

mentioning

confidence: 98%

Inflammatory Role of AMP-Activated Protein Kinase Signaling in an Experimental Model of Toxic Smoke Inhalation Injury*

Perng

Chang

Wang

et al. 2013

Critical Care Medicine

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“…1,2 Recent advances in cytokine biology and clinical immunology have led to widespread acceptance of the idea that cytokines can function as systemic mediators. High-mobility group box 1 (HMGB-1, also referred to as amphoterin) is a nuclear protein, 3 which acts as a cytokine once released extracellularly.…”

Section: Introductionmentioning

confidence: 99%

Plasma high-mobility group box 1 as an indicator of surgical stress

et al. 2011

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“…Another important feature of this model is that the hemodynamic stability allows for invasive cardiovascular monitoring for many hours. Evidently, the ovine animal model has substantially contributed to the investigation of combined burn and smoke inhalation injury (19,24,26,27,36). For this study, we have chosen a 24-h period, since our aim was to identify the molecular mechanisms resulting within 1 day after combined burn and smoke inhalation injury.…”

Section: L432 Effects Of Selective Neuronal Nitric Oxide Synthase Inhmentioning

confidence: 99%

Molecular biological effects of selective neuronal nitric oxide synthase inhibition in ovine lung injury

Saunders

Westphal

Enkhbaatar

et al. 2010

American Journal of Physiology-Lung Cellular and Molecular Phys

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Neuronal nitric oxide synthase is critically involved in the pathogenesis of acute lung injury resulting from combined burn and smoke inhalation injury. We hypothesized that 7-nitroindazole, a selective neuronal nitric oxide synthase inhibitor, blocks central molecular mechanisms involved in the pathophysiology of this double-hit insult. Twenty-five adult ewes were surgically prepared and randomly allocated to 1) an uninjured, untreated sham group ( n = 7), 2) an injured control group with no treatment ( n = 7), 3) an injury group treated with 7-nitroindazole from 1-h postinjury to the remainder of the 24-h study period ( n = 7), or 4) a sham-operated group subjected only to 7-nitroindazole to judge the effects in health. The combination injury was associated with twofold increased activity of neuronal nitric oxide synthase and oxidative/nitrosative stress, as indicated by significant increases in plasma nitrate/nitrite concentrations, 3-nitrotyrosine (an indicator of peroxynitrite formation), and malondialdehyde lung tissue content. The presence of systemic inflammation was evidenced by twofold, sixfold, and threefold increases in poly(ADP-ribose) polymerase, IL-8, and myeloperoxidase lung tissue concentrations, respectively (each P < 0.05 vs. sham). These molecular changes were linked to tissue damage, airway obstruction, and pulmonary shunting with deteriorated gas exchange. 7-Nitroindazole blocked, or at least attenuated, all these pathological changes. Our findings suggest 1) that nitric oxide formation derived from increased neuronal nitric oxide synthase activity represents a pivotal reactive agent in the patho-physiology of combined burn and smoke inhalation injury and 2) that selective neuronal nitric oxide synthase inhibition represents a goal-directed approach to attenuate the degree of injury.

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Inhibition of lung permeability changes after burn and smoke inhalation by an anti-interleukin-8 antibody in sheep

Abstract: These findings indicate that the pathogenesis of the increase in microvascular fluid flux seen after the combined injury differs in burned tissue and the lung.

Cited by 13 publications

References 21 publications

Inflammatory Role of AMP-Activated Protein Kinase Signaling in an Experimental Model of Toxic Smoke Inhalation Injury*

Inflammatory Role of AMP-Activated Protein Kinase Signaling in an Experimental Model of Toxic Smoke Inhalation Injury*

Plasma high-mobility group box 1 as an indicator of surgical stress

Molecular biological effects of selective neuronal nitric oxide synthase inhibition in ovine lung injury

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