The role of apoptosis in the pathophysiology of Acute Respiratory Distress Syndrome (ARDS): An up-to-date cell-specific review

Abstract:The acute respiratory distress syndrome (ARDS) is an acute inflammatory process of the lung caused by a direct or indirect insult to the alveolar-capillary membrane. Currently, ARDS is diagnosed based on a combination of clinical and physiological variables. The lack of a specific biomarker for ARDS is arguably one of the most important obstacles to progress in developing novel treatments for ARDS. In this article, we will review the current understanding of some appealing biomarkers that have been measured in human blood, bronchoalveolar lavage fluid (BALF) or exhaled gas that could be used for identifying patients with ARDS, for enrolling ARDS patients into clinical trials, or for better monitoring of patient's management. After a literature search, we identified several biomarkers that are associated with the highest sensitivity and specificity for the diagnosis or outcome prediction of ARDS: receptor for advanced glycation end-products (RAGE), angiopoietin-2 (Ang-2), surfactant protein D (SP-D), inteleukin-8, Fas and Fas ligand, procollagen peptide (PCP) I and III, octane, acetaldehyde, and 3-methylheptane. In general, these are cell-specific for epithelial or endothelial injury or involved in the inflammatory or infectious response. No biomarker or biomarkers have yet been confirmed for the diagnosis of ARDS or prediction of its prognosis.However, it is anticipated that in the near future, using biomarkers for defining ARDS, or for determining those patients who are more likely to benefit from a given therapy will have a major effect on clinical practice.

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“…Apoptosis of epithelial cells occurs in ARDS (57). The Fas and Fas ligand system is the best-studied mechanism regulating epithelial cell death.…”

Section: Fas and Fas Ligandmentioning

confidence: 99%

Biomarkers for the acute respiratory distress syndrome: how to make the diagnosis more precise

García‐Laorden¹,

Lorente²,

Flores³

et al. 2017

Ann. Transl. Med.

102

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“…This is in large part explained by death of type I and type II alveolar epithelial cells [120], along with endothelial cells. ARDS is associated with increased cell death in humans, while inhibitors of apoptosis promote increased survival in rodent models of lung injury [121].…”

Section: Pathogenesis Of Ardsmentioning

confidence: 99%

Advances in Understanding of the Pathogenesis of Acute Respiratory Distress Syndrome

2015

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The clinical syndrome of acute lung injury (ALI) occurs as a result of an initial acute systemic inflammatory response. This can be consequent to a plethora of insults, either direct to the lung or indirect. The insult results in increased epithelial permeability, leading to alveolar flooding with a protein-rich oedema fluid. The resulting loss of gas exchange leads to acute respiratory failure and typically catastrophic illness, termed acute respiratory distress syndrome (ARDS), requiring ventilatory and critical care support. There remains a significant disease burden, with some estimates showing 200,000 cases each year in the USA with a mortality approaching 50%. In addition, there is a significant burden of morbidity in survivors. There are currently no disease-modifying therapies available, and the most effective advances in caring for these patients have been in changes to ventilator strategy as a result of the ARDS network studies nearly 15 years ago. Here, we will give an overview of more recent advances in the understanding of the cellular biology of ALI and highlight areas that may prove fertile for future disease-modifying therapies.

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“…Therefore, the expression level of SOD and catalase were investigated. 20) As shown in Fig. 5A, in the LPS group, MPO activity was obviously increased, whereas the Tyr pretreated groups presented a trend toward lower levels.…”

Section: Effects Of Tyr On Mpo Activity and Antioxidative Enzyme Exprmentioning

confidence: 74%

“…20) Compared with the LPS group, Tyr groups showed a significant decrease in the lung W/D ratio and the total protein concentration in the BALF in a dose-dependent fashion. The results showed that Tyr pretreatment effectively alleviated lung tissue permeability and pulmonary edema in ALI.…”

Section: Discussionmentioning

confidence: 86%

Protective Effects of Tyrosol against LPS-Induced Acute Lung Injury <i>via</i> Inhibiting NF-κB and AP-1 Activation and Activating the HO-1/Nrf2 Pathways

Wang

Xia

Yang

et al. 2017

Biological & Pharmaceutical Bulletin

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Tyrosol (Tyr) is a natural antioxidant that displays anti-oxidant and anti-inflammatory properties. The present study aimed to investigate the effect and mechanism of Tyr on lipopolysaccharide (LPS)-induced acute lung injury (ALI). In a mouse model, we found that pretreatment with Tyr significantly improved survival rate, attenuated lung permeability, ameliorated histopathological alterations, reduced expression of the inflammatory mediators and improved expression of the antioxidant enzyme. Further study revealed that Tyr markedly inhibited nuclear factor-κB (NF-κB) and activator protein-1 (AP-1) activation at both in vivo and in vitro levels. To investigate the underlying mechanism, we examined the impact of Tyr on the heme oxygenase (HO)-1/nuclear factor erythroid-2 related factor 2 (Nrf2) pathway in vivo and in vitro. The results showed that Tyr significantly improved the expression of HO-1 and the activation of Nrf2. This study offers novel evidence to support the efficacy of Tyr against ALI, which helps to clarify the underlying causes of the therapeutic effects behind Tyr.Key words acute lung injury (ALI); tyrosol(Tyr); nuclear factor (NF)-κB; activator protein (AP)-1; heme oxygenase (HO)-1; nuclear factor erythroid-2 related factor 2(Nrf2) Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) are common complications associated with both acute respiratory failure and multiple organ failure. A variety of acute severe illnesses can induce the occurrence of ALI/ARDS, including pneumonia, aspiration of gastric contents, sepsis, and major trauma, and the most major pathogenic condition of ALI/ARDS is sepsis induced by Gram-negative bacteria.

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The role of apoptosis in the pathophysiology of Acute Respiratory Distress Syndrome (ARDS): An up-to-date cell-specific review

Cited by 175 publications

References 78 publications

Biomarkers for the acute respiratory distress syndrome: how to make the diagnosis more precise

Biomarkers for the acute respiratory distress syndrome: how to make the diagnosis more precise

Advances in Understanding of the Pathogenesis of Acute Respiratory Distress Syndrome

Protective Effects of Tyrosol against LPS-Induced Acute Lung Injury <i>via</i> Inhibiting NF-κB and AP-1 Activation and Activating the HO-1/Nrf2 Pathways

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