A combined score of pro- and anti-inflammatory interleukins improves mortality prediction in severe sepsis

Andaluz‐Ojeda, David; Bobillo, Felipe; Iglesias, Verónica; Almansa, Raquel; Rico, Lucía; Gandía, Francisco; Resino, Salvador; Tamayo, Eduardo; Lejarazu, Raúl Ortíz de; Bermejo-Martín, Jesús F.

doi:10.1016/j.cyto.2011.12.002

Cited by 146 publications

(124 citation statements)

References 21 publications

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“…sNGAL is associated with serum IL-6 Serum IL-6, an important inflammatory sepsis cytokine, is used as a prognostic prediction and early biomarker of patients with sepsis (32)(33)(34). In animal experiments, Otto et al (18) explored sNGAL and several pro-and anti-inflammatory cytokines in a CLP mouse model.…”

Section: Discussionmentioning

confidence: 98%

Serum Neutrophil Gelatinase Associated Lipocalin (NGAL) Outperforms Serum Creatinine in Detecting Sepsis-Induced Acute Kidney Injury, Experiments on Bilateral Nephrectomy and Bilateral Ureter Obstruction Mouse Models

Leelahavanichkul

Somparn

Issara-Amphorn

et al. 2016

Shock

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Serum neutrophil gelatinase associated lipocalin (sNGAL), a promising acute kidney injury (AKI) biomarker produced by renal and non-renal tissues, might be affected by sepsis. We evaluated sNGAL in zero glomerular filtration rate models [bilateral ureter obstruction (BUO) and bilateral nephrectomy (BiNx)] with subsequent cecal ligation and puncture (CLP)-induced sepsis in 6 to 8-week-old ICR mice. We found that sNGAL increased earlier than serum creatinine (Scr) in BiNx/BUO with and without CLP. The earliest time-point of increased sNGAL in BiNx+CLP was 1 h after surgery. Scr, but not sNGAL, was lower at 18 h after BiNx/BUO+CLP compared with BiNx/BUO alone. Compared with BUO, BiNx had higher, and equal sNGAL at 1 to 18 h and 36 h, respectively. Additionally, similar NGAL expression in internal organs (heart, lung, liver, and spleen) and survival rates indicated the comparable severity of BiNx and BUO. Serum interleukin (IL)-6 was increased and correlated with sNGAL in BiNx/BUO with and without sepsis. In summary, we demonstrated: sNGAL is an early AKI biomarker, which is not affected by sepsis; sNGAL is mainly produced by extrarenal sources as demonstrated by the comparable sNGAL in BiNx and BUO; the saturation of renal NGAL re-absorption in BUO is demonstrated by lower sNGAL in BUO at 1 to 18 h, but not at 36 h when compared with BiNx; and a correlation of sNGAL and IL-6 implied sNGAL is a good sepsis prognostic biomarker. Therefore, sNGAL is a more beneficial sepsis-AKI biomarker than Scr.

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Section: Discussionmentioning

confidence: 98%

Serum Neutrophil Gelatinase Associated Lipocalin (NGAL) Outperforms Serum Creatinine in Detecting Sepsis-Induced Acute Kidney Injury, Experiments on Bilateral Nephrectomy and Bilateral Ureter Obstruction Mouse Models

Leelahavanichkul

Somparn

Issara-Amphorn

et al. 2016

Shock

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“…Although baseline concentrations of plasma cytokines were similar between trained and untrained mice, the sepsis-associated increase of circulating IL-6 and IL-10 was reduced in trained mice. Clinical studies have shown strong association between higher plasma levels of plasma cytokines IL-6 and IL-10 and the prevalence of multiple organ failure and mortality in sepsis (28)(29)(30). We assume that physical training could induce specific adaptations in diverse cell types and tissues leading to either an initial reduction of cytokine release or a diminished response to the "cytokine storm," which in turn might protect the animals against sepsis-associated organ injury and death.…”

Section: Discussionmentioning

confidence: 99%

Physical Exercise Induces Specific Adaptations Resulting in Reduced Organ Injury and Mortality During Severe Polymicrobial Sepsis

Soßdorf

Fischer

Meyer

et al. 2013

Critical Care Medicine

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“…For the purposes of this analysis, we used quartiles in order to simultaneously compare several markers without losing interpretability by log-transforming the data (Grund and Sabin, 2010). Several other clinical research studies have generated similar aggregate scores to evaluate inflammatory load by establishing 1) a cut-point above and below the 75 th percentile (Andaluz-Ojeda et al, 2012; Correia et al, 2010; Juengst et al 2014), 2) cut-points below the 25 th , between 25 th –75 th percentile, and greater than 75 th percentile (Wakelkamp et al, 2003; Boelen et al, 1995), or 3) quartiles (Kumar et al 2014). …”

Section: Methodsmentioning

confidence: 99%

Variable neuroendocrine–immune dysfunction in individuals with unfavorable outcome after severe traumatic brain injury

Santarsieri

Kumar

Kochanek

et al. 2015

Brain, Behavior, and Immunity

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Bidirectional communication between the immune and neuroendocrine systems is not well understood in the context of traumatic brain injury (TBI). The purpose of this study was to characterize relationships between cerebrospinal fluid (CSF) cortisol and inflammation after TBI, and to determine how these relationships differ by outcome. CSF samples were collected from 91 subjects with severe TBI during days 0–6 post-injury, analyzed for cortisol and inflammatory markers, and compared to healthy controls (n=13 cortisol, n=11 inflammatory markers). Group-based trajectory analysis (TRAJ) delineated subpopulations with similar longitudinal CSF cortisol profiles (high vs. low cortisol). Glasgow Outcome Scale (GOS) scores at 6 months served as the primary outcome measure reflecting global outcome. Inflammatory markers that displayed significant bivariate associations with both GOS and cortisol TRAJ (interleukin [IL]-6, IL-10, soluble Fas [sFas], soluble intracellular adhesion molecule [sICAM]-1, and tumor necrosis factor alpha [TNF]-α) were used to generate a cumulative inflammatory load score (ILS). Subsequent analysis revealed that cortisol TRAJ group membership mediated ILS effects on outcome (indirect effect estimate= −0.253, 95% CI (−0.481, −0.025), p=0.03). Correlational analysis between mean cortisol levels and ILS were examined separately within each cortisol TRAJ group and by outcome. Within the low cortisol TRAJ group, subjects with unfavorable 6-month outcome displayed a negative correlation between ILS and mean cortisol (r=−0.562, p=0.045). Conversely, subjects with unfavorable outcome in the high cortisol TRAJ group displayed a positive correlation between ILS and mean cortisol (r=0.391, p=0.006). Our results suggest that unfavorable outcome after TBI may result from dysfunctional neuroendocrine-immune communication wherein an adequate immune response is not mounted or, alternatively, neuroinflammation is prolonged. Importantly, the nature of neuroendocrine-immune dysfunction differs between cortisol TRAJ groups. These results present a novel biomarker-based index from which to discriminate outcome and emphasize the need for evaluating tailored treatments targeting inflammation early after injury.

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A combined score of pro- and anti-inflammatory interleukins improves mortality prediction in severe sepsis

Cited by 146 publications

References 21 publications

Serum Neutrophil Gelatinase Associated Lipocalin (NGAL) Outperforms Serum Creatinine in Detecting Sepsis-Induced Acute Kidney Injury, Experiments on Bilateral Nephrectomy and Bilateral Ureter Obstruction Mouse Models

Serum Neutrophil Gelatinase Associated Lipocalin (NGAL) Outperforms Serum Creatinine in Detecting Sepsis-Induced Acute Kidney Injury, Experiments on Bilateral Nephrectomy and Bilateral Ureter Obstruction Mouse Models

Physical Exercise Induces Specific Adaptations Resulting in Reduced Organ Injury and Mortality During Severe Polymicrobial Sepsis

Variable neuroendocrine–immune dysfunction in individuals with unfavorable outcome after severe traumatic brain injury

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