A murine model of sepsis following smoke inhalation injury

Lange, Matthias; Hamahata, Atsumori; Traber, Daniel L.; Esechie, Aimalohi; Jonkam, Collette; Bansal, Kamna; Nakano, Yoshimitsu; Traber, Lillian D.; Enkhbaatar, Perenlei

doi:10.1016/j.bbrc.2009.12.124

Cited by 29 publications

(29 citation statements)

References 24 publications

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“…Similarly, toxic smoke inhalation also produces different severities of pulmonary inflammation and lung injury in various animal models (4,5,(9)(10)(11)(12)(44)(45)(46)(47)(48), possibly as a result of differences in types of toxic smoke, exposure durations, and methods of smoke delivery. For example, direct delivery of toxic smoke through a tracheotomy tube in large animals may produce more direct damage to the lungs (4,5,(9)(10)(11)(12) as compared with that induced by spontaneous inhalation of toxic smoke inside the exposure chamber in mice (47,48). Additionally, wood smoke contains >100 different toxins, and we believe that the inflammatory responses we observed are consequences resulting from the detrimental effects of many of these toxins but not any specific toxin.…”

Section: Discussionmentioning

confidence: 99%

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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: Discussionmentioning

confidence: 99%

“…•-may react with excess production of nitric oxide, thereby yielding ROS and reactive nitrogen species such as peroxynitrite (48). Indeed, there are also strong data supporting a role for reactive nitrogen species in the inhalation lung injury (51).…”

Section: Discussionmentioning

confidence: 99%

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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“…inhalational injury; burn injury; innate immunology; respiratory infection; acute lung injury BACTERIAL INFECTION IS A MAJOR risk factor for mortality following burn and inhalation injury. Experimental models suggest that direct cell damage, edema, inflammation, and immunologic changes occur in the respiratory tract after these injuries (17,19), and bacterial pneumonia has been linked to mortality in patients with burns and inhalation injury (9). We have previously shown that surface burns affect expression of Toll-like receptors (TLRs) on immune cells and impact systemic immunity with a resulting bias towards immunosuppressive IL-10 production (5,21).…”

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confidence: 99%

Association between early airway damage-associated molecular patterns and subsequent bacterial infection in patients with inhalational and burn injury

Maile

Jones

Pan

et al. 2015

American Journal of Physiology-Lung Cellular and Molecular Phys

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Bacterial infection is a major cause of morbidity affecting outcome following burn and inhalation injury. While experimental burn and inhalation injury animal models have suggested that mediators of cell damage and inflammation increase the risk of infection, few studies have been done on humans. This is a prospective, observational study of patients admitted to the North Carolina Jaycee Burn Center at the University of North Carolina who were intubated and on mechanical ventilation for treatment of burn and inhalational injury. Subjects were enrolled over a 2-yr period and followed till discharge or death. Serial bronchial washings from clinically indicated bronchoscopies were collected and analyzed for markers of tissue injury and inflammation. These include damage-associated molecular patterns (DAMPs) such as hyaluronic acid (HA), double-stranded DNA (dsDNA), heat-shock protein 70 (HSP-70), and high-mobility group protein B-1 (HMGB-1). The study population was comprised of 72 patients who had bacterial cultures obtained for clinical indications. Elevated HA, dsDNA, and IL-10 levels in bronchial washings obtained early (the first 72 h after injury) were significantly associated with positive bacterial respiratory cultures obtained during the first 14 days postinjury. Independent of initial inhalation injury severity and extent of surface burn, elevated levels of HA dsDNA and IL-10 in the central airways obtained early after injury are associated with subsequent positive bacterial respiratory cultures in patients intubated after acute burn/inhalation injury.

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“…The use of endothelial NOS-knocked out subjects in similar sepsis models may shed some light on this issue. 33 Finally, the effects of combined NOS inhibition on survival have not been determined. The ameliorations of physiologic parameters by the treatment may not necessarily be associated with improved overall outcome.…”

Section: Discussionmentioning

confidence: 99%

Effects of Early Neuronal and Delayed Inducible Nitric Oxide Synthase Blockade on Cardiovascular, Renal, and Hepatic Function in Ovine Sepsis

et al. 2010

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A murine model of sepsis following smoke inhalation injury

Cited by 29 publications

References 24 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*

Association between early airway damage-associated molecular patterns and subsequent bacterial infection in patients with inhalational and burn injury

Effects of Early Neuronal and Delayed Inducible Nitric Oxide Synthase Blockade on Cardiovascular, Renal, and Hepatic Function in Ovine Sepsis

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