Circulating IL-1ra and IL-10 levels are increased but do not predict the development of acute respiratory distress syndrome in at-risk patients.

Parsons, Polly E.; Moss, Marc; Vannice, James L.; Moore, E. E.; Moore, F. A.; Repine, John E.

doi:10.1164/ajrccm.155.4.9105096

Cited by 77 publications

(38 citation statements)

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“…In contrast, initially high circulating levels of the proinflammatory cytokines IL-6 and monocyte chemotactic protein 1 (MCP1) and the main antiinflammatory cytokine IL-10 decreased over time. Serum levels of IL-5 and IL-8 were higher in nonsurvivors than in survivors, whereas both too-low and too-high levels of IL-6 as well as IL-10 were associated with a higher risk of organ failure and death (37)(38)(39). This U-shaped relationship is in agreement with the deleterious consequences of both the overwhelming proinflammatory response and the prolonged periods of immune suppression present in critical illness (reviewed in ref.…”

Section: Figuresupporting

confidence: 56%

Intensive insulin therapy protects the endothelium of critically ill patients

Langouche

Vanhorebeek²,

Vlasselaers³

et al. 2005

Journal of Clinical Investigation

425

245

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The vascular endothelium controls vasomotor tone and microvascular flow and regulates trafficking of nutrients and biologically active molecules. When endothelial activation is excessive, compromised microcirculation and subsequent cellular hypoxia contribute to the risk of organ failure. We hypothesized that strict blood glucose control with insulin during critical illness protects the endothelium, mediating prevention of organ failure and death. In this preplanned subanalysis of a large, randomized controlled study, intensive insulin therapy lowered circulating levels of ICAM-1 and tended to reduce E-selectin levels in patients with prolonged critical illness, which reflects reduced endothelial activation. This effect was not brought about by altered levels of endothelial stimuli, such as cytokines or VEGF, or by upregulation of eNOS. In contrast, prevention of hyperglycemia by intensive insulin therapy suppressed iNOS gene expression in postmortem liver and skeletal muscle, possibly in part via reduced NF-κB activation, and lowered the elevated circulating NO levels in both survivors and nonsurvivors. These effects on the endothelium statistically explained a significant part of the improved patient outcome with intensive insulin therapy. In conclusion, maintaining normoglycemia with intensive insulin therapy during critical illness protects the endothelium, likely in part via inhibition of excessive iNOS-induced NO release, and thereby contributes to prevention of organ failure and death.

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Section: Figuresupporting

confidence: 56%

Intensive insulin therapy protects the endothelium of critically ill patients

Langouche

Vanhorebeek²,

Vlasselaers³

et al. 2005

Journal of Clinical Investigation

425

245

View full text Add to dashboard Cite

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“…For instance, Aisiku et al reported that plasma IL-10, IL-6 and IL-8 were associated with development of ARDS in patients with severe traumatic brain injury [35]. Contradictorily, Parsons et al reported that circulating IL-1ra and IL-10 levels were increased but not related to the development of ARDS in at-risk patients [36]. In contrast to the high level of peripheral IL-10, the secretory IL-10 from BALF-derived macrophages was significantly repressed due to up-regulation of miR-211-5p, therefore the resolution of the local inflammation was seriously delayed.…”

Section: Discussionmentioning

confidence: 99%

NF-κB-Induced MicroRNA-211 Inhibits Interleukin-10 in Macrophages of Rats with Lipopolysaccharide-Induced Acute Respiratory Distress Syndrome

Wang

Chen

et al. 2018

Cell Physiol Biochem

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Background/Aims: The present study addressed the potential involvement of microRNAs in acute respiratory distress syndrome (ARDS)-related inflammation and elucidates the underlying molecular mechanism. Methods: ARDS rat model was established by lipopolysaccharide, with compromised gas exchange capacity and lung edema. The inflammatory cells from bronchoalveolar lavage fluid (BALF) were profiled with automatic blood cell analyzer. The relative fluorescence intensity of BALF-derived macrophages was analyzed by flow cytometry. The relative microRNA expression was determined using microarray and Taqman assay. The secretory interleukin (IL)-10 was measured by enzyme-linked immunosorbent assay. Luciferase reporter assay was performed to determine the regulatory effects of miR-211 and NF-κB on IL-10 and miR-211 expressions, respectively. Chromatin immunoprecipitation (ChIP) was conducted to detect the direct binding of NK-κB on miR-211 promoter. The protein level was determined by Western blot. Results: The provoked acute inflammation was characterized with increased total cells, macrophages, neutrophils and lymphocytes. The relative expression of miR-211 was aberrantly up-regulated in BALF-derived macrophages from ARDS rats, which was accompanied with reduction of secretory IL-10. We further demonstrated that miR-211 inhibited IL-10 expression by binding to its 3’-UTR. The expression of miR-211 was modulated by NF-κB. Conclusion: Here we elucidated a crucial role of NF-κB/miR-211/IL-10 signaling axis in ARDS-related inflammation.

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“…Lower levels of IL-10 were found in patients with ARDS compared with critically ill non-ARDS patients [15]. Among ARDS patients, high plasma IL-10 but low bronchoalveolar lavage concentration of IL-10 correlated with increased mortality [16,17].…”

mentioning

confidence: 89%

Interleukin-10 polymorphism in position -1082 and acute respiratory distress syndrome

Gong

Thompson

Williams

et al. 2006

European Respiratory Journal

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The GG genotype of the interleukin (IL)-10 promoter polymorphism in position -1082 (-1082GG) has been associated with increased IL-10 production. The current authors hypothesised that the -1082GG genotype is associated with the development of, and outcomes in, acute respiratory distress syndrome (ARDS).A nested case-control study was conducted in 211 Caucasian cases of ARDS and 429 controls who were admitted to an intensive care unit with sepsis, trauma, aspiration or massive transfusions. Cases were followed for organ failure and 60-day mortality.The -1082GG genotype was associated with the development of ARDS, but only in the presence of a significant interaction between the -1082GG genotype and age. Among patients with ARDS, the -1082GG genotype was associated with decreased severity of illness on admission, lower daily organ dysfunction scores and lower 60-day mortality.In conclusion, the high interleukin-10-producing -1082GG genotype may be associated with variable odds for acute respiratory distress syndrome development depending on age. Among those with acute respiratory distress syndrome, the -1082GG genotype is associated with lower mortality and organ failure. Further studies are needed to confirm these findings.

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Circulating IL-1ra and IL-10 levels are increased but do not predict the development of acute respiratory distress syndrome in at-risk patients.

Cited by 77 publications

References 0 publications

Intensive insulin therapy protects the endothelium of critically ill patients

Intensive insulin therapy protects the endothelium of critically ill patients

NF-κB-Induced MicroRNA-211 Inhibits Interleukin-10 in Macrophages of Rats with Lipopolysaccharide-Induced Acute Respiratory Distress Syndrome

Interleukin-10 polymorphism in position -1082 and acute respiratory distress syndrome

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