Predictive value of low interleukin-33 in critically ill patients

Krychtiuk, Konstantin A.; Stojković, Stefan; Lenz, Max; Brekalo, Mira; Huber, Kurt; Wojta, Johann; Gisslinger, Heinz; Demyanets, Svitlana; Speidl, Walter S.

doi:10.1016/j.cyto.2017.09.017

Cited by 25 publications

(20 citation statements)

References 38 publications

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“…We showed previously the intracellular expression of IL‐33 in human cardiac myocytes and fibroblasts, and the release of IL‐33 during necrosis of these cells . Moreover, the “decoy” receptor for IL‐33, sST2, was shown to have predictive value in patients with coronary artery disease and HF as well as in critically ill patients . In our study presented here, we found that fluvastatin is able to reduce secretion of sST2 from human cardiac myocytes.…”

Section: Discussionsupporting

confidence: 65%

“…27 Moreover, the "decoy" receptor for IL-33, sST2, was shown to have predictive value in patients with coronary artery disease and HF 16,[49][50][51] as well as in critically ill patients. 52 In our study presented here, we found that fluvastatin is able to reduce secretion of sST2 from human cardiac myocytes. Interestingly, a recent report showed that sST2 levels were attenuated after 12 months of atorvastatin treatment in patients with HIV.…”

Section: Discussionsupporting

confidence: 52%

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Cardioprotective cytokine interleukin‐33 is up‐regulated by statins in human cardiac tissue

Pentz

Kaun

Thaler

et al. 2018

J Cellular Molecular Medi

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Interleukin (IL)‐33 is a member of the IL‐1 family and is able to act cardioprotective. The aim of this study was to investigate the regulation of IL‐33 by 3‐hydroxy‐3‐methylglutaryl‐coenzyme‐A (HMG‐CoA) reductase inhibitors (statins) and bisphosphonates (BPs) in human cardiac tissue. The lipophilic fluvastatin, simvastatin, atorvastatin, and lovastatin as well as the nitrogenous BPs alendronate and ibandronate, but not hydrophilic pravastatin increased IL‐33 mRNA and intracellular IL‐33 protein levels in both human adult cardiac myocytes (HACM) and fibroblasts (HACF). Additionally, fluvastatin reduced soluble ST2 secretion from HACM. IL‐33 was also up‐regulated by the general inhibitor of prenylation perillic acid, a RhoA kinase inhibitor Y‐27632, and by latrunculin B, but statin‐induced IL‐33 expression was inhibited by mevalonate, geranylgeranyl pyrophosphate (GGPP) and RhoA activator U‐46619. The IL‐33 promoter was 2.3‐fold more accessible in statin‐treated HACM compared to untreated cells (P = 0.037). In explanted hearts of statin‐treated patients IL‐33 protein was up‐regulated as compared with the hearts of non‐statin‐treated patients (P = 0.048). As IL‐33 was previously shown to exert cardioprotective effects, one could speculate that such up‐regulation of IL‐33 expression in human cardiac cells, which might happen mainly through protein geranylgeranylation, could be a novel mechanism contributing to known cardioprotective effects of statins and BPs.

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Section: Discussionsupporting

confidence: 65%

Section: Discussionsupporting

confidence: 52%

Cardioprotective cytokine interleukin‐33 is up‐regulated by statins in human cardiac tissue

Pentz

Kaun

Thaler

et al. 2018

J Cellular Molecular Medi

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“…The current study demonstrated that IL-33 was increased in septicemic mice and exerted great predictive value for septicemia risk in the early phase. However, previous studies have shown that non-detectable levels of IL-33 and soluble ST2 levels above the median dramatically increased the 30-day mortality risk in critically ill patients (29), and that serum ST2 levels correlate with sepsis severity (30). These data suggest dual predictive value of IL-33 and ST2 in patients, dependent on the phase and severity of infection.…”

Section: Discussionmentioning

confidence: 87%

Role of Interleukin-33 in Staphylococcus epidermidis-Induced Septicemia

et al. 2020

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Interleukin (IL)-33 is a member of the IL-1 family, which plays an important role in inflammatory response. In this study, we evaluated the effect of IL-33 on septicemia and the underlying mechanisms by establishing a Staphylococcus epidermidis (S. epidermidis)-induced septicemic mouse model. The expression of IL-33, IL-1α, IL-1β, IL-6, IL-17A, IL-22, and PGE2 were measured by double antibody sandwich enzyme-linked immunosorbent assay, and bacterial colony formation in peripheral blood and kidneys were counted postinfection. The percentages of neutrophils, eosinophils, and inflammatory monocytes were evaluated by flow cytometry, and tissue damage was assessed by hematoxylin and eosin (H&E) staining. The survival of septicemic mice was monitored daily. IL-33 expression was significantly augmented following S. epidermidis infection. High IL-33 expression significantly decreased the survival of model mice, and aggravated the damage of lung, liver, and kidney tissues. However, administration of ST2 (receptor for IL-33) to the S. epidermidis-infected mice blocked the IL-33 signaling pathway, which elevated PGE2, IL-17A, and IL-22, and promoted healing of organ damage. In addition, ST2 suppressed the mobilization of inflammatory monocytes, but promoted the accumulation of neutrophils and eosinophils in S. epidermidis-infected mice. Inhibition of PGE2, IL-17A, and IL-22 facilitated the development of septicemia and organ damage in S. epidermidis-infected mice, as well as reducing their survival. Our findings reveal that IL-33 aggravates organ damage in septicemic mice by inhibiting PGE2, IL-17A, and IL-22 production.

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“…Concentrations of these molecules on Day 5 of hospital stay enabled us to characterize the host response in the acute phase of the disease. The soluble form of ST2, which is one of the mechanisms of IL-33 down regulation, has been identified as a reliable biomarker of poor prognosis in cardiovascular diseases, acute respiratory distress syndrome (ARDS) and other inflammatory conditions [25,26]. Furthermore, while IL-33 plays an important role in tissue repair and restores tissue homeostasis in infectious and chronic inflammatory diseases, persistently high sST2 levels is often implicated in the emergence of tissue fibrosis.…”

Section: Discussionmentioning

confidence: 99%

IL-33 and ST2 as predictors of disease severity in children with viral acute lower respiratory infection

et al. 2020

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A B S T R A C TBackground: Mechanisms influencing severity of acute lower respiratory infection (ALRI) in children are not established. We aimed to assess the role of inflammatory markers and respiratory viruses in ALRI severity. Methods: Concentrations of interleukin(IL)-33, soluble suppression of tumorigenicity (sST)2, IL-1ß, tumor necrosis factor α, IL-4, IL-6 and IL-8 and types of respiratory viruses were evaluated in children at the first and fifth days after hospital admission. Disease severity was defined as need for mechanical ventilation. Results: Seventy-nine children < 5 years-old were included; 33(41.8%) received mechanical ventilation. No associations between virus type, viral load or co-detections and severity of disease were observed. Detection of IL-33 and sST2 in nasopharyngeal aspirates (NPA) on admission were associated with higher risk for mechanical ventilation (RR = 2.89 and RR = 4.57, respectively). IL-6 and IL-8 concentrations were higher on Day 5 in mechanically ventilated children. IL-6 NPA concentrations decreased from Day 1 to Day 5 in children who did not receive mechanical ventilation. Increase in sST2 NPA concentrations from Day 1 to Day 5 was associated with longer hospital length of stay (p < 0.01). Conclusions: An exacerbated local activation of the IL-33/ST2 axis and persistently high sST2 concentrations over time were associated with severity of viral ALRI in children.

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Predictive value of low interleukin-33 in critically ill patients

Cited by 25 publications

References 38 publications

Cardioprotective cytokine interleukin‐33 is up‐regulated by statins in human cardiac tissue

Cardioprotective cytokine interleukin‐33 is up‐regulated by statins in human cardiac tissue

Role of Interleukin-33 in Staphylococcus epidermidis-Induced Septicemia

IL-33 and ST2 as predictors of disease severity in children with viral acute lower respiratory infection

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