Identification of Oxidative Stress and Toll-like Receptor 4 Signaling as a Key Pathway of Acute Lung Injury

Imai, Yumiko; Kuba, Keiji; Neely, G. Gregory; Yaghubian-Malhami, Rubina; Perkmann, Thomas; Loo, Geert; Ermolaeva, Maria A.; Veldhuizen, Ruud A. W.; Leung, Connie Y. H.; Wang, Hongliang; Liu, Haolin; Sun, Yang; Pasparakis, Manolis; Köpf, Manfred; Mech, Christin; Bavari, Sina; Peiris, Malik; Slutsky, Arthur S.; Akira, Shizuo; Hultqvist, Malin; Holmdahl, Rikard; Nicholls, John M.; Jiang, Chengyu; Binder, Christoph J.; Penninger, Josef

doi:10.1016/j.cell.2008.02.043

Cited by 1,214 publications

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“…Lipid peroxidation can impair cellular membrane function, eventually leading to release of intracellular content 50 (Figure 2). Moreover, sensing of lipid peroxidation products by the PRR Toll-like receptor 4 (TLR4), tissue damage, as demonstrated in the pathogenesis of Influenza virus infection 51 . Inhibition of lipid peroxidation by peroxidase 4 (GPX4) 28,52 , relies on glutathione supply by a NRF2-regulated pathway involving, SLC7A11, which together with SLC3A2 encode the cystine/glutamate antiporter, GCLC and GCLM that encode the γ-glutamylcysteine synthetase (γGCS) and GSS that encodes the glutathione synthetase 28,52 .…”

Section: Damage Responses and Tissue Damage Controlmentioning

confidence: 99%

Disease tolerance and immunity in host protection against infection

2017

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The immune system has most likely evolved to limit the negative impact exerted by pathogens on host homeostasis. This defense strategy relies on the concerted action of innate and adaptive components of the immune system, which sense and target pathogens for containment, destruction or expulsion. Resistance to infection refers to these immune functions, which reduce the pathogen load of an infected host as the means to preserve homeostasis. Immune-driven resistance to infection is coupled to an additional, and arguably as important, defense strategy that limits the extent of dysfunction imposed to host parenchyma tissues during infection, without exerting a direct negative impact on pathogens.This defense strategy, called disease tolerance, relies on tissue damage control mechanisms that prevent the deleterious effects of pathogens, while uncoupling immunedriven resistance mechanisms from immunopathology and disease. Here we provide a unifying view of resistance and disease tolerance within the framework of immunity to infection.

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Section: Damage Responses and Tissue Damage Controlmentioning

confidence: 99%

Disease tolerance and immunity in host protection against infection

2017

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“…These molecules include high-mobility group box-1 (HMGB1), matrix fragments and oxidized phospholipids [51], and provide alternative pathways by which nonbacterial products could further augment lung injury [52].…”

Section: Epithelial Cell Responses To Mechanical Stretchmentioning

confidence: 99%

Role of the pulmonary epithelium and inflammatory signals in acute lung injury

Manicone¹

2009

Expert Review of Clinical Immunology

118

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Acute lung injury (ALI) is a clinical disease marked by respiratory failure due to disruption of the epithelial and endothelial barrier, flooding of the alveolar compartment with protein-rich fluid and recruitment of neutrophils into the alveolar space. ALI affects approximately 200,000 patients annually in the USA and results in approximately 75,000 deaths. It is associated with prolonged mechanical ventilation, intensive medical care, high morbidity and mortality, and rising healthcare costs. Owing to its impact on public health, great strides have been made towards understanding the pathobiology of ALI to affect outcome. This review will focus on the role of the epithelial cell in the pathogenesis and resolution of ALI and the role of various inflammatory mediators in ALI. Keywordsβ2-agonist; acute lung injury; acute respiratory distress syndrome; chemokine; cytokine; epithelial cell; inflammation; methylprednisolone; neutrophil; salbutamol; steroid; ventilator-induced lung injuryAcute lung injury/acute respiratory distress syndrome (ALI/ARDS) was first described in 1967 by Ashbaugh and colleagues in a group of 12 patients who shared a constellation of clinical symptoms including acute respiratory distress, hypoxemia refractory to supplemental oxygen, decreased lung compliance and diffuse pulmonary infiltrates [1]. Since this first description, the clinical criteria have evolved to include acute onset of respiratory distress, bilateral pulmonary infiltrates seen on chest radiographs, absence of left-sided heart failure and hypoxemia, with the severity of hypoxemia distinguishing ALI and ARDS (Box 1) [2]. Extrapolating from recent epidemiologic studies using these criteria, ALI affects about 200,000 patients annually in the USA and results in approximately 75,000 deaths [3]. This disease, which can be caused by common events such as pneumonia, sepsis and trauma, results in high morbidity, mortality and healthcare expenditures associated with prolonged mechanical ventilation and intensive care. Because of its impact on public health and patient outcomes, great strides have been made towards understanding the pathobiology of ALI.When defined broadly to include all processes related to defense against microbes, other environmental insults and injury, a wide variety of cell types and proteins participate in inflammation and immunity. Leukocytes are the paradigmatic inflammatory cell type, but they are not the only cells that function in defense and immunity. The epithelial lining of all tissues forms a continuous barrier to the environment and is the first line of defense against infectious agents and toxins. Though specialized to serve distinct functions among tissues, epithelial cells respond similarly to injury and infection, and regulate leukocyte influx through the production of proinflammatory cytokines, chemokines and other factors that modulate chemokine gradients and effect leukocyte migration. This review will focus on the role of the pulmonary epithelium and inflammatory mediators in ALI. More s...

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“…Lipid peroxidation can impair membrane functions and promote tissue damage, compromising disease tolerance, as illustrated for influenza virus infection in mice 64 . Presumably effector mechanisms that restrain lipid peroxidation, such as for example mediated by glutathione peroxidase 4 (GPX4) 65 or by the lipophilic antioxidant bilirubin 66 (reviewed in 67 ), should promote tissue damage control and in turn disease tolerance, but this remains to be established.…”

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confidence: 99%

Tissue damage control in disease tolerance

Soares

Gozzelino

Weis

2014

Trends in Immunology

159

174

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The deposited article is a prost-print version.This publication hasn't any creative commons license associated.This deposit is composed by the main article, and it hasn't any supplementary materials associated.Immune-driven resistance mechanisms are the prevailing host defense strategy against infection. By contrast, disease tolerance mechanisms limit disease severity by preventing tissue damage or ameliorating tissue function without interfering with pathogen load. We propose here that tissue damage control underlies many of the protective effects of disease tolerance. We explore the mechanisms of cellular adaptation that underlie tissue damage control in response to infection as well as sterile inflammation, integrating both stress and damage responses. Finally, we discuss the potential impact of targeting these mechanisms in the treatment of disease.Fundação para a Ciência e Tecnologia grants: (PTDC/SAU-TOX/116627/2010, HMSP-ICT/0022/2010, SFRH/BPD/44256/2008); European Commission 7th Framework grant: (ERC-2011-AdG. 294709-DAMAGECONTROL); Deutsche Forschungsgemeinschaft grant: (DFG WE 4971/3-1).info:eu-repo/semantics/publishedVersio

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Identification of Oxidative Stress and Toll-like Receptor 4 Signaling as a Key Pathway of Acute Lung Injury

Cited by 1,214 publications

References 50 publications

Disease tolerance and immunity in host protection against infection

Disease tolerance and immunity in host protection against infection

Role of the pulmonary epithelium and inflammatory signals in acute lung injury

Tissue damage control in disease tolerance

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