Angiopoietin-2 associations with the underlying infection and sepsis severity

Lymperopoulou, Korina; Velissaris, Dimitrios; Kotsaki, Antigone; Antypa, E.; Georgiadou, Sara; Τσαγανός, Θωμάς; Koulenti, Despoina; Paggalou, Evgenia; Damoraki, Georgia; Karagiannidis, Napoleon; Orfanos, Stylianos E.

doi:10.1016/j.cyto.2015.01.022

Cited by 29 publications

(31 citation statements)

References 26 publications

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“…Despite the amount of attention Angiopoietin-2 has recently received, not only as a proangiogenic factor, but also as an important inflammatory mediator, 50 a surrogate marker for the degree of pulmonary endothelial inflammation, 51 and a predictor of development of multiorgan failure 52 and ARDS, 26 we were not able to identify an association between the severity of lung injury and its levels in our experiments. We found some levels of Angiopoietin-2 to be constitutionally expressed in the sham animals, and its levels did not change significantly in the presence of infection and significant lung injury, suggesting that in mice this molecule perhaps has non-homologous function compared to its human counterpart, or its role in ARDS may not have been reflected in this particular disease model.…”

Section: Discussionmentioning

confidence: 59%

Valproic acid mitigates the inflammatory response and prevents acute respiratory distress syndrome in a murine model of Escherichia coli pneumonia at the expense of bacterial clearance

Kasotakis

Galvan

King

et al. 2017

Journal of Trauma and Acute Care Surgery

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Background Histone deacetylase inhibitors (HDACI) are members of a family of epigenetic modifying agents with broad anti-inflammatory properties. These anti-inflammatory properties may have important therapeutic implications in Acute Respiratory Distress Syndrome (ARDS). However, administration of HDACI may create an immunosuppressive environment conducive to bacterial growth. Accordingly, the aim of the current study is to investigate the effect of HDACI Valproic Acid (VPA) on host inflammatory response and bacterial burden in a murine model of E. coli pneumonia-induced ARDS. Methods ARDS was induced in male C57BL6 mice (n=24) by endotracheal instillation of 3×106 E. coli. VPA (250mg/kg) was administered 30 min after E.coli instillation in the intervention group. Blood samples were collected at 3 and 6 hours, and animals were sacrificed at 6 hours. Bronchoalveolar lavage (BAL) was performed and tissue specimens were harvested. Cytokine levels were measured in blood and BAL, and so was transalveolar protein transit. Cell counts, and colony forming units were quantified in BAL fluid. Results VPA reduced neutrophil influx into the lungs and local tissue destruction through decreased myeloperoxidase activity. It also ameliorated the pulmonary and systemic inflammatory response. This led to greater bacterial proliferation in the pulmonary parenchyma. Conclusions Administration of VPA in a clinically relevant bacterial model of murine ARDS mitigates the host inflammatory response, essentially preventing ARDS, but creates an immunosuppressive environment that favors bacterial overgrowth.

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Section: Discussionmentioning

confidence: 59%

Valproic acid mitigates the inflammatory response and prevents acute respiratory distress syndrome in a murine model of Escherichia coli pneumonia at the expense of bacterial clearance

Kasotakis

Galvan

King

et al. 2017

Journal of Trauma and Acute Care Surgery

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“…Addition of specific biomarkers may possibly improve the accuracy of CURB-65/CRB-65. The use of Ang-2 for risk evaluation in sepsis, sepsis-induced ARDS, and other critical illness has been controversially discussed (7,(16)(17)(18)(19)(35)(36)(37). An NHLBI ARDS Network study reported that plasma Ang-2 levels measured in 931 subjects with acute lung injury did not have prognostic value for mortality in the subgroup of infection-related ALI (n = 653) (35).…”

Section: Discussionmentioning

confidence: 99%

“…In patients with sepsis, Ang-2 serum levels were higher than in healthy volunteers and even further increased in patients with sepsis-associated lung injury (7). Previous studies support usage of Ang-2 as a biomarker for risk evaluation in sepsis and acute respiratory distress syndrome (ARDS) (16)(17)(18)(19). However, little is known about the expression and function of Ang-1 and Ang-2 in the pulmonary circulation, and the role of Ang-1 and Ang-2 in pneumonia has not been investigated so far.…”

mentioning

confidence: 97%

Prognostic and Pathogenic Role of Angiopoietin-1 and -2 in Pneumonia

Gutbier

Neuhauß

Reppe

et al. 2018

Am J Respir Crit Care Med

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“…Accumulating evidence shows a significant association of circulating Angpt2 level with inflammatory response [6]. Angpt2 not only promote a significant increase in neutrophil accumulation, migration and adherence to the endothelium [3,28], but also Angpt2 boosts vascular leakage [3] and sensitizes the lymphatic vasculature to inflammatory stimuli [29].…”

Section: Discussionmentioning

confidence: 99%

“…Conversely, Angpt2 inhibits the protective Angpt1/Tie-2 signaling and contributes to angiogenic and inflammatory response to other growth factors and cytokines, thereby disturbing endothelium and vessel permeability [5]. Accumulating evidence suggests that the increase in circulating level of Angpt2 reflects systemic inflammation, but might not be specific for any organ [6–9]. …”

Section: Introductionmentioning

confidence: 99%

The interaction between fluid status and angiopoietin-2 in adverse renal outcomes of chronic kidney disease

et al. 2017

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BackgroundFluid overload is not only the characteristic but also an important complication in chronic kidney disease (CKD) patients. Angiopoietin-2 (Angpt2) disturbs endothelium and vessel permeability, which may induce fluid overload. The aim of this study is to examine the interaction between fluid status and Angpt2 in adverse renal outcomes of CKD.MethodsThis cohort study enrolled 290 patients with CKD stages 3–5 from January 2011 to December 2011 and followed up until December 2015. Fluid status was presented as overhydration (OH) value measured by body composition monitor, while OH>1.1L was defined as fluid overload. Renal outcomes were defined as commencing dialysis and rapid renal function decline (the slope of estimated glomerular filtration rate < -5 ml/min/1.73 m2/y).ResultsDuring a mean follow-up of 38.6±18.3 months, 125 (43.1%) patients progressed to commencing dialysis and 99(34.7%) patients presented rapid renal function decline. All patients were stratified by OH of 1.1L and the median of circulating Angpt2. These patients with both OH>1.1L and high circulating Angpt2 were more likely to reach commencing dialysis compared to other groups. The risks for commencing dialysis and rapid renal function decline were significantly higher in patients with OH>1.1L and high circulating Angpt2 level compared to those with OH≦1.1L and low circulating Angpt2 (2.14, 1.21–3.78, P = 0.009; 4.96, 1.45–16.97, P = 0.01). There was a significant interaction between OH level and circulating Angpt2 in entering dialysis (P-interaction = 0.02).ConclusionsFluid overload and Angpt2 might have a synergistic effect on adverse renal outcomes in CKD patients.

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Angiopoietin-2 associations with the underlying infection and sepsis severity

Cited by 29 publications

References 26 publications

Valproic acid mitigates the inflammatory response and prevents acute respiratory distress syndrome in a murine model of Escherichia coli pneumonia at the expense of bacterial clearance

Valproic acid mitigates the inflammatory response and prevents acute respiratory distress syndrome in a murine model of Escherichia coli pneumonia at the expense of bacterial clearance

Prognostic and Pathogenic Role of Angiopoietin-1 and -2 in Pneumonia

The interaction between fluid status and angiopoietin-2 in adverse renal outcomes of chronic kidney disease

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