Prädiktion eines Fetal Inflammatory Response Syndrome beim frühen vorzeitigen Blasensprung durch Interleukin-6 und TNF-alpha bei nicht-invasiver Probengewinnung

2013 ◽  
Vol 217 (S 01) ◽  
Author(s):  
M Kunze ◽  
CA Morfeld ◽  
M Klar ◽  
F Markfeld-Erol ◽  
R Rasenack ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Interleukin 6 ◽  
Tnf Alpha ◽  
Fetal Inflammatory Response

Fetal Inflammatory Response Syndrom: Leidet die zerebrale Sauerstoffversorgung?

2020 ◽  
Vol 224 (05) ◽  
pp. 243-243
Keyword(s):  
Inflammatory Response ◽  
Interleukin 6 ◽  
Fetal Inflammatory Response

Ein sogenanntes FIRS (fetal inflammatory response syndrome) liegt per Definition vor, wenn in Folge einer systemischen Aktivierung des fetalen Immunsystems im Nabelschnurblut erhöhte Interleukin-6(IL-6)-Spiegel gemessen werden. Die betroffenen Kinder haben ein erhöhtes Komplikations- und Sterberisiko. Beeinträchtigt das FIRS die zerebrale Sauerstoffversorgung von Frühgeborenen innerhalb der ersten Lebensminuten?

Role of umbilical interleukin-6, procalcitonin and C-reactive protein measurement in the dia gnosis of fetal inflammatory response syndrome

2021 ◽  
Vol 86 (2) ◽  
pp. 80-85
Author(s):  
Zbyněk Straňák ◽  
◽  
Ivan Berka ◽  
Jan Širc ◽  
Jan Urbánek ◽  
...  
Keyword(s):  
High Risk ◽  
Inflammatory Response ◽  
Neonatal Mortality ◽  
Interleukin 6 ◽  
C Reactive Protein ◽  
Term Infants ◽  
Mortality And Morbidity ◽  
Reactive Protein ◽  
High Risk Infants ◽  
Fetal Inflammatory Response

Overview Objective: Fetal Inflammatory Response Syndrome (FIRS) is a serious complication accompanied by increased neonatal mortality and morbidity. Early dia­gnosis of FIRS is essential to detect high risk infants. The aim of the study was to evaluate the correlation between interleukin-6 
(IL-6), procalcitonin (PCT), C-reactive protein (CRP) in cord blood and histologically proven funisitis/ chorioamnionitis in high-risk infants after preterm birth. Methods: Blood sampling for the measurement of inflammatory bio­markers was performed immediately after placental delivery and umbilical cutting. Umbilical and placental inflammatory changes were assessed using a recently released scoring system (Amsterdam Placental Workshop Group Consensus). Results: One hundred preterm infants (30.5 ± 2.5 gestational week, birth weight 1,443 ± 566 grams) and 21 health term infants were analyzed. Histologic chorioamnionitis was confirmed in 19% cases and chorioamnionitis with funisitis in 7% cases. Thirty-three infants (33%) fulfilled criteria of FIRS (funistis and/ or umbilical IL-6 > 11 ng/ L). The presence of FIRS correlated significantly with maternal leukocytosis (P < 0.001), preterm premature rupture of membrane (P < 0.001) and preterm uterine contraction (P < 0.0001). In comparison to preterm and healthy term infants we found statistically significant higher levels of umbilical inflammatory bio­markers (IL-6, PCT, CRP) in FIRS group (P < 0.0001). Composite mortality and morbidity (bronchopulmonary dysplasia, intraventricular haemorrhage, periventricular leukomalacia) was higher in FIRS group (28.1 vs 22.4% in preterm group). However, the difference was not statistically significant (P = 0.53). Conclusion: Our study confirmed the correlation of umbilical inflammatory bio­markers levels (IL-6, PCT, CRP) and the presence of FIRS. We did not find significant adverse impact of FIRS on neonatal mortality and morbidity. Nevertheless, our results could be influenced by the size of study group and strict inclusion criteria (only cases after C-section were analyzed). Keywords: fetal inflammatory response syndrome – neonatal mortality – morbidity – interleukin-6 – C-reactive protein – procalcitonin – chorioamnionitis and funisitis

scholarly journals Defective inflammatory response in interleukin 6-deficient mice.

1994 ◽  
Vol 180 (4) ◽  
pp. 1243-1250 ◽  
Author(s):  
E Fattori ◽  
M Cappelletti ◽  
P Costa ◽  
C Sellitto ◽  
L Cantoni ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Interleukin 6 ◽  
Tissue Damage ◽  
Acute Phase Proteins ◽  
Host Responses ◽  
Tnf Alpha ◽  
Wild Type ◽  
Compensatory Mechanisms ◽  
Necrosis Factor Alpha ◽  
Deficient Mice

Systemic and localized inflammation elicit a number of host responses which include fever, cachexia, hypoglycemia, and major changes in the concentration of liver plasma proteins. Interleukin 6 (IL-6) is considered an important mediator of the inflammatory response, together with IL-1 and tumor necrosis factor alpha (TNF-alpha). The purpose of this study was to unequivocally determine the role of IL-6 in these phenomena making use of IL-6-deficient mice that we have recently generated by gene targeting. We report here that in the absence of IL-6, mice are unable to mount a normal inflammatory response to localized tissue damage generated by turpentine injection. The induction of acute phase proteins is dramatically reduced, mice do not lose body weight and only suffer from mild anorexia and hypoglycemia. In contrast, when systemic inflammation is elicited through the injection of bacterial lipopolysaccharide (LPS), these parameters are altered to the same extent both in wild-type and IL-6-deficient mice, demonstrating that under these conditions IL-6 function is dispensable. Moreover, we show that LPS-treated IL-6-deficient mice produce three times more TNF-alpha than wild-type controls, suggesting that increased TNF-alpha production might be one of the compensatory mechanisms through which a normal response to LPS is achieved in the absence of IL-6. We also show that corticosterone is normally induced in IL-6-deficient mice, demonstrating that IL-6 is not required for the activation of the hypothalamic-pituitary-adrenal axis. Our results reinforce the idea that different patterns of cytokines are involved in systemic and localized tissue damage, and identify IL-6 as an essential mediator of the inflammatory response to localized inflammation.

scholarly journals Inhibition of factor XII in septic baboons attenuates the activation of complement and fibrinolytic systems and reduces the release of interleukin-6 and neutrophil elastase

Blood ◽  
1996 ◽  
Vol 87 (6) ◽  
pp. 2337-2344 ◽  
Author(s):  
PM Jansen ◽  
RA Pixley ◽  
M Brouwer ◽  
IW de Jong ◽  
AC Chang ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Plasminogen Activator ◽  
Interleukin 6 ◽  
Lethal Dose ◽  
Contact System ◽  
Tissue Type ◽  
Tnf Alpha ◽  
Factor Xii ◽  
E Coli ◽  
Mediator Systems

In previous studies, we have shown that administration of monoclonal antibody (MoAb) C6B7 against human factor XII to baboons challenged with a lethal dose of Escherichia coli abrogates activation of the contact system and modulates secondary hypotension. To evaluate the contribution of activated contact proteases to the appearance of other inflammatory mediators in this experimental model of sepsis, we studied the effect of administration of MoAb C6B7 on activation of complement and fibrinolytic cascades, stimulation of neutrophil degranulation, and release of the proinflammatory cytokines, tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6). Activation of the complement system, as reflected by circulating C3b/c and C4b/c levels, was significantly reduced in five animals that had received MoAb C6B7 before a lethal dose of E coli as compared with five control animals that had been given a lethal challenge only. Inhibition of contact activation also modulated the fibrinolytic response, since the release of tissue-type plasminogen activator (t-PA) and the appearance of plasmin-alpha2-antiplasmin (PAP) complexes into the circulation was significantly attenuated upon pretreatment with anti-factor XII MoAb. In contrast, plasma levels of plasminogen activator inhibitor (PAI) were modestly enhanced in the treatment group. Degranulation of neutrophils, as assessed by circulating elastase-alpha1-protease inhibitor complexes, and release of IL-6 but not of TNF-alpha was decreased in anti-factor XII-treated animals. Observed differences in the inflammatory response between treatment and control groups were not likely due to different challenges, since the number of E coli that had been infused, as well as circulating levels of endotoxin after the challenge, were similar for both groups. These data suggest that activation of the contact system modulates directly or indirectly various mediator systems involved in the inflammatory response during severe sepsis in nonhuman primates.

Effects of a High-Carb vs. High-Fat Meal on Glycemia, Insulin, Interleukin-6, TNF-Alpha, and Apo-B

Diabetes ◽  
2018 ◽  
Vol 67 (Supplement 1) ◽  
pp. 265-LB ◽  
Author(s):  
HELMUT O. STEINBERG ◽  
FRANKIE B. STENTZ ◽  
NANDITA K. SHANKAR
Keyword(s):  
Interleukin 6 ◽  
Tnf Alpha ◽  
High Fat ◽  
Apo B ◽  
Fat Meal

scholarly journals Toll-like receptor linked cytokine profiles in cerebrospinal fluid discriminate neurological infection from sterile inflammation

2020 ◽  
Vol 2 (2) ◽  
Author(s):  
Simone M Cuff ◽  
Joseph P Merola ◽  
Jason P Twohig ◽  
Matthias Eberl ◽  
William P Gray
Keyword(s):  
Cerebrospinal Fluid ◽  
Clinical Practice ◽  
Inflammatory Response ◽  
Nosocomial Infection ◽  
Pathway Analysis ◽  
Interleukin 6 ◽  
Sterile Inflammation ◽  
Interleukin 17 ◽  
Toll Like Receptor ◽  
Fluid Biomarker

Abstract Rapid determination of an infective aetiology causing neurological inflammation in the cerebrospinal fluid can be challenging in clinical practice. Post-surgical nosocomial infection is difficult to diagnose accurately, as it occurs on a background of altered cerebrospinal fluid composition due to the underlying pathologies and surgical procedures involved. There is additional diagnostic difficulty after external ventricular drain or ventriculoperitoneal shunt surgery, as infection is often caused by pathogens growing as biofilms, which may fail to elicit a significant inflammatory response and are challenging to identify by microbiological culture. Despite much research effort, a single sensitive and specific cerebrospinal fluid biomarker has yet to be defined which reliably distinguishes infective from non-infective inflammation. As a result, many patients with suspected infection are treated empirically with broad-spectrum antibiotics in the absence of definitive diagnostic criteria. To begin to address these issues, we examined cerebrospinal fluid taken at the point of clinical equipoise to diagnose cerebrospinal fluid infection in 14 consecutive neurosurgical patients showing signs of inflammatory complications. Using the guidelines of the Infectious Diseases Society of America, six cases were subsequently characterized as infected and eight as sterile inflammation. Twenty-four contemporaneous patients with idiopathic intracranial hypertension or normal pressure hydrocephalus were included as non-inflamed controls. We measured 182 immune and neurological biomarkers in each sample and used pathway analysis to elucidate the biological underpinnings of any biomarker changes. Increased levels of the inflammatory cytokine interleukin-6 and interleukin-6-related mediators such as oncostatin M were excellent indicators of inflammation. However, interleukin-6 levels alone could not distinguish between bacterially infected and uninfected patients. Within the patient cohort with neurological inflammation, a pattern of raised interleukin-17, interleukin-12p40/p70 and interleukin-23 levels delineated nosocomial bacteriological infection from background neuroinflammation. Pathway analysis showed that the observed immune signatures could be explained through a common generic inflammatory response marked by interleukin-6 in both nosocomial and non-infectious inflammation, overlaid with a toll-like receptor-associated and bacterial peptidoglycan-triggered interleukin-17 pathway response that occurred exclusively during infection. This is the first demonstration of a pathway dependent cerebrospinal fluid biomarker differentiation distinguishing nosocomial infection from background neuroinflammation. It is especially relevant to the commonly encountered pathologies in clinical practice, such as subarachnoid haemorrhage and post-cranial neurosurgery. While requiring confirmation in a larger cohort, the current data indicate the potential utility of cerebrospinal fluid biomarker strategies to identify differential initiation of a common downstream interleukin-6 pathway to diagnose nosocomial infection in this challenging clinical cohort.

Sign in / Sign up

Export Citation Format

Share Document