Biomarkers in acute lung injury

Mokrá, Daniela; Kosutova, Petra

doi:10.1016/j.resp.2014.10.006

Cited by 214 publications

(130 citation statements)

References 72 publications

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“…The concentrations of cytokines such as TNF-α, IL-6, and IFN-γ were increased in the LPS group compared with the control group and the LPS+Fb group at the same time points, which was consistent with previous results [34]. Isolated fibrocytes were administered to mice with ALI, and the concentrations of TNF-α, IL-6, and IFN-γ were determined.…”

Section: Discussionsupporting

confidence: 90%

Fibrocytes Ameliorate Acute Lung Injury by Decreasing Inflammatory Cytokine and Chemokine Levels and Reducing Neutrophil Accumulation in the Lung

Tai

Ding

et al. 2017

Cell Physiol Biochem

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Background/Aims: Acute lung injury (ALI) remains a severe disease that threatens human life around the world. To decrease the mortality of ALI and improve ALI treatment efficacy, the development of more ALI treatments is urgently needed. Whether fibrocytes directly participate in ALI has not been studied. Therefore, a mouse model of ALI was induced with lipopolysaccharide (LPS). Methods: Fibrocytes were harvested from peripheral blood mononuclear cells of bleomycin mice and identified by using flow cytometry to detect the expression of molecular makers. The fibrocytes were injected for the treatment of acute lung injury mice. The curative effects were evaluated by using ELISA to determine the cytokines (including TNF-α, IL-6 and IFN-γ) concentrations in bronchoalveolar lavage fluid (BALF) supernatant. Results: The concentrations of cytokines such as tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and interferon-γ (IFN-γ) were increased in mice with ALI induced with LPS. The concentrations of TNF-α, IL-6, and IFN-γ as well as their mRNA and protein expression levels were decreased by administration of fibrocytes. The effect of fibrocytes in ameliorating ALI was time dependent. LPS treatment induced an increase in myeloperoxidase (MPO) activity, whereas the fibrocyte treatment caused inhibition of MPO activity as well as expression of the neutrophil-chemoattractant chemokine macrophage inflammatory protein 2 (MIP-2). Conclusion: Taken together, these data suggest that fibrocytes ameliorated ALI by suppressing inflammatory cytokines and chemokines as well as by decreasing the accumulation of neutrophils in the lung.

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Section: Discussionsupporting

confidence: 90%

Fibrocytes Ameliorate Acute Lung Injury by Decreasing Inflammatory Cytokine and Chemokine Levels and Reducing Neutrophil Accumulation in the Lung

Tai

Ding

et al. 2017

Cell Physiol Biochem

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“…In our present study, SEC or SMC post-intake effectively attenuated pulmonary edema in those mice, which was evidenced by lower W/D weight ratios. Neutrophils could be activated by inflammatory insult, like LPS, and migrate to the site of injury, where they undergo defensive actions via degranulation, phagocytosis and ROS generation [20]. Furthermore, activated neutrophils act as signaling indicators to promote inflammatory response and enhance the production of additional cytokines in local and/or systemic levels [21].…”

Section: Discussionmentioning

confidence: 99%

Post-Intake of S-Ethyl Cysteine and S-Methyl Cysteine Improved LPS-Induced Acute Lung Injury in Mice

Hsia

Yin

2016

Nutrients

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The effects of S-ethyl cysteine (SEC) and S-methyl cysteine (SMC) on lipopolysaccharide (LPS)-induced acute lung injury in mice were examined. Eight hours after LPS challenge, SEC or SMC was supplied in drinking water at 0.5% or 1% for 3 days. LPS increased lung myeloperoxidase activity, neutrophil counts and edema. SEC or SMC post-intake attenuated these events. SEC or SMC suppressed LPS-induced lung expression of cyclooxygenase-2, nuclear factor-κB and mitogen-activated protein kinase, and lowered the generation of tumor necrosis factor-alpha, monocyte chemoattractant protein-1 and prostaglandin E2. LPS enhanced the expression of p47phox, gp91phox, Bax and cleaved caspase-3, and increased the production of reactive oxygen species in the lung. SEC or SMC post-intake reversed these alterations. These findings suggest that these agents could protect the lung through their anti-inflammatory, anti-oxidative and anti-apoptotic activities.

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“…This might represent an immense step forward in evaluating the patient's evolution under current or experimental therapy. 19 Among recently proposed markers, endocan aka endothelial cell-specific molecule-1 has considerable potential. This soluble 50 kDa dermatan sulfate proteoglycan is secreted by both pulmonary and kidney vascular endothelial cells.…”

Section: Biomarkers Of Ards: Looking Beyond the Lung?mentioning

confidence: 99%

Biomarkers in critical illness: have we made progress?

Honoré¹,

Jacobs²,

Hendrickx³

et al. 2016

IJNRD

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Biomarkers have emerged as exemplary key players in translational medicine. Many have been assessed for timely recognition, early treatment, and adequate follow-up for a variety of pathologies. Biomarker sensitivity has improved considerably over the last years but specificity remains poor, in particular when two "marker-sensitive" conditions overlap in one patient. Biomarker research holds an enormous potential for diagnostic and prognostic purposes in postoperative and critically ill patients who present varying degrees of inflammation, infection, and concomitant (sub)acute organ dysfunction or failure. Despite a remarkable progress in development and testing, biomarkers are not yet ready for routine use at the bedside.

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Biomarkers in acute lung injury

Cited by 214 publications

References 72 publications

Fibrocytes Ameliorate Acute Lung Injury by Decreasing Inflammatory Cytokine and Chemokine Levels and Reducing Neutrophil Accumulation in the Lung

Fibrocytes Ameliorate Acute Lung Injury by Decreasing Inflammatory Cytokine and Chemokine Levels and Reducing Neutrophil Accumulation in the Lung

Post-Intake of S-Ethyl Cysteine and S-Methyl Cysteine Improved LPS-Induced Acute Lung Injury in Mice

Biomarkers in critical illness: have we made progress?

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