Identification of <i>DDX58</i> and <i>CXCL10</i> as Potential Biomarkers in Acute Respiratory Distress Syndrome

Xie, Yongpeng; Liu, Kexi; Luo, Jiye; Liu, Suxia; Zheng, Hui; Cao, Lijuan; Li, Xiaomin

doi:10.1089/dna.2019.4968

Cited by 12 publications

(9 citation statements)

References 26 publications

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“…The expression of the three ligands of CXCR3 (CXCL9, CXCL10, and CXCL11) is significantly increased in various diseases such as interstitial cystitis, ulcerative colitis, and myositis [21], and previous studies found that blocking CXCL10 can reduce the degree of the damage of these diseases. Our previous research also found that CXCL10 gene expression is significantly increased in mechanically ventilated patients with ARDS [6], and this conclusion was also confirmed in this clinical study. The higher the MP, the higher the CXCL10 and CXCR3 expression.…”

Section: Discussionsupporting

confidence: 89%

“…However, it is not yet clear which signaling pathways or effect molecules are involved in the energy-biological injury during mechanical ventilation in ARDS patients. Therefore, according to our previous work [6], the role of mast cell chemotaxis mediated by CXCL10 and its receptor CXCR3 was further explored in vivo on patients and animal experiments.…”

Section: Introductionmentioning

confidence: 99%

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High Expression of CXCL10/CXCR3 in Ventilator-Induced Lung Injury Caused by High Mechanical Power

Xie

Zheng

Mou

et al. 2022

BioMed Research International

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Background. The energy delivered by a ventilator to the respiratory system in one minute is defined as mechanical power (MP). However, the effect of ventilator-induced lung injury (VILI) in patients suffering from acute respiratory distress syndrome (ARDS) is still unknown. Our previous studies revealed that CXCL10 may be a potential biomarker of lung injury in ARDS. Therefore, the aim of this study was to compare the lung injury of rats and patients under different MP conditions to explore the involvement of CXCL10 and its receptor CXCR3 in VILI. Methods. Patients were divided into the high mechanical power group (HMPp group) and low mechanical power group (LMPp group), while rats were assigned to the high mechanical power group (HMPr group), medium mechanical power group (MMPr group), and low mechanical power group (LMPr group). CXCL10 and CXCR3 plasma content in ARDS patients and rats under ventilation at different MP was measured, as well as their protein and mRNA expression in rat lungs. Results. CXCL10 and CXCR3 content in the plasma of ARDS patients in the HMPp was significantly higher than that in the LMPp. The increase of MP during mechanical ventilation in the rats gradually increased lung damage, and CXCL10 and CXCR3 levels in rat plasma gradually increased with the increase of MP. CXCL10 and CXCR3 protein and mRNA expression in the HMPr group and MMPr group was significantly higher than that in the LMPr group ( P < 0.05 ). More mast cells were present in the trachea, bronchus, blood vessels, and lymphatic system in the rat lungs of the HMPr group, and the number of mast cells in the HMPr group ( 13.32 ± 3.27 ) was significantly higher than that in the LMPr group ( 3.25 ± 0.29 ) ( P < 0.05 ). Conclusion. The higher the MP, the more severe the lung injury, and the higher the CXCL10/CXCR3 expression. Therefore, CXCL10/CXCR3 might participate in VILI by mediating mast cell chemotaxis.

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Section: Discussionsupporting

confidence: 89%

Section: Introductionmentioning

confidence: 99%

High Expression of CXCL10/CXCR3 in Ventilator-Induced Lung Injury Caused by High Mechanical Power

Xie

Zheng

Mou

et al. 2022

BioMed Research International

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“…IFN-γ-induced chemoattractant CXCL10 was one of the primary cytokines elevated in cases and was a suggestive marker for disease severity. Previous studies have also shown increased levels of CXCL10 along with CCL7 (MCP-3) in COVID-19, and CXCL10 was a suggested biomarker for ARDS with protein DDX58 39,40 . As IL-6 blockade has been effective for managing cytokine release syndrome, IL-6 has also been investigated as a therapeutic target for COVID-19 37 .…”

Section: Discussionmentioning

confidence: 89%

Comparing biomarkers for COVID-19 disease with commonly associated preexisting conditions and complications

Huang

2020

Preprint

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Severe coronavirus disease 2019 (COVID-19) has been associated with certain preexisting health conditions and can cause respiratory failure along with other multi-organ injuries. However, the mechanism of these relationships is unclear, and prognostic biomarkers for the disease and its systemic complications are lacking. This study aims to examine the plasma protein profile of COVID-19 patients and evaluate overlapping protein modules with biomarkers of common comorbidities. Blood samples were collected from COVID-19 cases (n=307) and negative controls (n=78) among patients with acute respiratory distress. Proteins were measured by proximity extension assay utilizing next-generation sequencing technology. Its associations to COVID-19 disease characteristics were compared to that of preexisting conditions and established biomarkers for myocardial infarction (MI), stroke, hypertension, diabetes, smoking, and chronic kidney disease. Several proteins were differentially expressed in COVID-19, including multiple pro-inflammatory cytokines such as IFN-gamma, CXCL10, and CCL7/MCP-3. Elevated IL-6 was associated with increased severity, while baseline IL1RL1/ST2 levels were associated with a worse prognosis. Network analysis identified several protein modules associated with COVID-19 disease characteristics overlapping with processes of preexisting hypertension and impaired kidney function. BNP and NTpro-BNP, markers for MI and stroke, increased with disease progression and were positively associated with severity. MMP12 was similarly elevated and has been previously linked to smoking and inflammation in emphysema, along with increased cardiovascular disease risk. In conclusion, this study provides an overview of the systemic effects of COVID-19 and candidate biomarkers for clinical assessment of disease progression and the risk of systemic complications.

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“…TNF signaling pathway is one of the critical pathways in the development and maintenance of in ammation [29] and it has been found to provoke the release of in ammatory cytokines in ALI and mediate the following innate immune response and in ammatory process [30]. Previous study demonstrated that TNF is initiated by TNF-α receptor 1 (TNFR1), its activation induces the increased expression of nuclear factor kappa B (NF-kB) [31].…”

Section: Discussionmentioning

confidence: 99%

Mechanism of 1,25(OH)2D3 in the Treatment of Acute Lung Injury Based on UHPLC/Q-TOF MS-Based Metabolomics and Network Pharmacology

Shi

Chen

Zhang

et al. 2020

Preprint

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Abstract Background: Sepsis-induced acute lung injury (ALI), a high morbidity and mortality disease, still has no effective therapies. 1,25(OH)2D3 is one of the indispensable nutrients in our body. The regulation mechanism of 1,25(OH)2D3 in inflammation has been recognized gradually. Network pharmacology was used wildly to broaden the understanding of diseases and advance drug discovery. In this study, we used network pharmacology and metabolomics to generate the potential mechanism of 1,25(OH)2D3 on acute lung injury.Methods: We used metabolomics and network pharmacology to elucidate the therapeutic mechanism of 1,25(OH)2D3 on acute lung injury. Serum samples, collected from mice with LPS-induced acute lung injury, were detected by UHPLC/Q-TOF MS to evaluate the differential metabolites from multiple metabolic pathways. Meanwhile, the H＆E staining, ELISA and QPCR were used to estimate the efficacy of 1,25(OH)2D3 on acute lung injury. Results: The results of animal experiments showed that 1,25(OH)2D3 could mitigate severe pulmonary edema and inflammatory infiltration caused by LPS, and the treatment of 1,25(OH)2D3 reduced the levels of inflammatory cytokines, interacted 25 related proteins and TNF signaling pathway, Toll-like receptor signaling pathway, PI3K-Akt signaling pathway.Conclusions: The integrated methods coupled with UHPLC/Q-TOF MS and network pharmacology provided a new way to study the potential mechanism of 1,25(OH)2D3 on acute lung injury, which may provide a possible solution for patients with clinical acute lung injury.

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Identification of DDX58 and CXCL10 as Potential Biomarkers in Acute Respiratory Distress Syndrome

Cited by 12 publications

References 26 publications

High Expression of CXCL10/CXCR3 in Ventilator-Induced Lung Injury Caused by High Mechanical Power

High Expression of CXCL10/CXCR3 in Ventilator-Induced Lung Injury Caused by High Mechanical Power

Comparing biomarkers for COVID-19 disease with commonly associated preexisting conditions and complications

Mechanism of 1,25(OH)2D3 in the Treatment of Acute Lung Injury Based on UHPLC/Q-TOF MS-Based Metabolomics and Network Pharmacology

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