scholarly journals Harsh Parenting and Youth Systemic Inflammation_In Press

2019 ◽  
Author(s):  
Assaf Oshri ◽  
Erinn Duprey ◽  
Sihong Liu ◽  
Katherine Ehrlich
Keyword(s):  
Nervous System ◽  
Systemic Inflammation ◽  
Interleukin 6 ◽  
Family Stress ◽  
Harsh Parenting ◽  
Low Grade ◽  
C Reactive Protein ◽  
Reactive Protein ◽  
The Impact

Objective: The present study aimed to test the role of the autonomic nervous system (ANS) in modulating the impact of family stress, induced by harsh parenting, on youths’ inflammation. First, we examined the direct effect of severity of adverse parenting behaviors on two serum biomarkers of systemic inflammation (C-reactive protein and interleukin-6) among youth. Second, we tested the moderating role of ANS reactivity in response to laboratory-induced stress in the association between harsh parenting and inflammation among these youth. Methods: The sample included 101 low-income children (75.2% African-American) between 9 and 12 years of age (Mage =10.9; SDage = 1.2) who participated in a conflict task with their primary caregiver in a laboratory setting. Heart rate variability reactivity (HRV-R), skin conductance level reactivity (SCL-R), and pre-ejection period reactivity (PEPr-R) were used to index parasympathetic and sympathetic nervous system reactivity. Markers of low-grade inflammation (C-reactive protein and interleukin-6) were obtained from serum. Results: After adjusting for confounding variables, ANS activity moderated the associations between family stress and systemic inflammation. Specifically, elevated HRV-R buffered the effect of family stress on youths’ inflammation, whereas elevated PEPr-R and SCL-R exacerbated the effect. Conclusion: These findings show that self-regulatory capacity and threat sensitivity, as indicated by ANS function, may have an impact on the associations between family stress and systemic inflammation.

C-Reactive Protein, Interleukin 6, and N-Terminal Pro-Brain Natriuretic Peptide Following Cardioversion of Atrial Fibrillation: Is There a Role of Biomarkers in Arrhythmia Recurrence?

Angiology ◽  
2010 ◽  
Vol 62 (4) ◽  
pp. 310-316 ◽  
Author(s):  
Stavroula N. Psychari ◽  
Dionyssios Chatzopoulos ◽  
Efstathios K. Iliodromitis ◽  
Thomas S. Apostolou ◽  
Dimitrios T. Kremastinos
Keyword(s):  
Atrial Fibrillation ◽  
Brain Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Interleukin 6 ◽  
C Reactive Protein ◽  
Reactive Protein

P4679Changes in systemic inflammation and endothelial dysfunction after balloon pulmonary angioplasty

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
W Magon ◽  
J Stepniewski ◽  
K Jonas ◽  
M Waligora ◽  
P Podolec ◽  
...  
Keyword(s):  
Endothelial Dysfunction ◽  
Serum Concentration ◽  
Systemic Inflammation ◽  
Interleukin 6 ◽  
C Reactive Protein ◽  
Pulmonary Hemodynamics ◽  
Endothelin 1 ◽  
Reactive Protein ◽  
Balloon Pulmonary Angioplasty

Abstract Introduction Pulmonary endarterectomy leads to a decrease in systemic inflammation and improvement in endothelial function in patients with chronic thromboembolic pulmonary hypertension (CTEPH). Balloon pulmonary angioplasty (BPA) improves pulmonary hemodynamics in patients with inoperable CTEPH. Aim To assess changes in systemic inflammation and endothelial dysfunction after a single BPA session and after completion of the treatment. Methods We enrolled consecutive, inoperable CTEPH patients who underwent BPA. Interleukin 6, 10 (IL-6, IL-10), and C-reactive protein (hsCRP) constituted markers of systemic inflammation. Endothelin-1 (ET-1) served as a marker of endothelial dysfunction. Serum concentration of selected markers was assessed in every patient before, 24 hours after the first BPA session and 6 months after completion of the BPA treatment. Age- and sex-matched healthy subjects served as a control group. Results We recruited 20 patients with inoperable CTEPH (6 males [30%]), aged 67 [61–74] years in New York Heart Association class III (n=19 [95%]) and II (n=1 [5%]). BPA treatment was completed with a median of 5 [2–8] BPA sessions per patient. Before starting the treatment CTEPH patients, as compared to controls (n=10), had raised serum level of IL-6 (3.82 [2.75 - 6.03] vs. 2.64 [0.88 - 4.75] pg/ml; p=0.04), hsCRP (2.47 [0.93 - 4.27] vs. 1.23 [0.48–3.21] ng/ml; p=0.02) and ET-1 (2.68 [2.24 - 3.64] vs. 1.47 [1.4 - 1.82] pg/ml; p=0.004). There was no difference in IL-10 level. 24 hours after a BPA session we observed an increased level of IL-6, IL-10 and hsCRP. (Tab.) 6 months after completion of the BPA treatment there was a reduced level of IL-6, hsCRP and ET-1 (Tab.) Table 1. Changes (Δ) in serum concentration of analyzed markers 24 hours after a single BPA session and at 6-months assessment after completion of the BPA treatment (n=20) Initial Δ at 24 hours after single BPA p Δ at 6-months follow-up p ET-1 [pg/ml] 2.68 [2.24; 3.64] −0.2 [−0.5; 0.23] 0.21 −0.47 [−0.96; 0.05] 0.004 IL-6 [pg/ml] 3.82 [2.75; 6.03] 3.67 [1.41; 7.16] 0.008 −0.82 [−3.11; 0.54] 0.04 IL-10 [pg/ml] 0.53 [0.44; 0.58] 0.32 [0.21; 0.87] 0.006 −0.11 [−0.33; 0.14] 0.94 hsCRP [ng/ml] 2.47 [0.93; 4.27] 5.4 [3.96; 10.59] 0.008 −0.36 [−0.94; 0.16] 0.02 ET-1, endothelin 1; hsCRP, C-reactive protein; IL-6, interleukin 6; IL-10, interleukin 10. Conclusions Patients with inoperable CTEPH, as compared to healthy controls, exhibit an increased systemic inflammation and endothelial dysfunction, which both improve after completion of the BPA treatment. At short-term follow-up after single BPA session there is an increase in systemic inflammatory response.

scholarly journals The role of systemic inflammation in heart failure

2021 ◽  
Vol 102 (4) ◽  
pp. 510-517
Author(s):  
E V Khazova ◽  
O V Bulashova
Keyword(s):  
Heart Failure ◽  
Cardiovascular Diseases ◽  
Systemic Inflammation ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
C Reactive Protein ◽  
Ventricular Ejection Fraction ◽  
Reactive Protein ◽  
Highly Sensitive

The discussion continues about the role of systemic inflammation in the pathogenesis of cardiovascular diseases of ischemic etiology. This article reviews the information on the role of C-reactive protein in patients with atherosclerosis and heart failure in risk stratification for adverse cardiovascular events, including assessment of factors affecting the basal level of highly sensitive C-reactive protein. Research data (MRFIT, MONICA) have demonstrated a relationship between an increased level of C-reactive protein and the development of coronary heart disease. An increase in the serum level of highly sensitive C-reactive protein is observed in arterial hypertension, dyslipidemia, type 2 diabetes mellitus and insulin resistance, which indicates the involvement of systemic inflammation in these disorders. Currently, the assessment of highly sensitive C-reactive protein is used to determine the risk of developing myocardial infarction and stroke. It has been proven that heart failure patients have a high level of highly sensitive C-reactive protein compared with patients without heart failure. The level of C-reactive protein is referred to as modifiable risk factors for cardiovascular diseases of ischemic origin, since lifestyle changes or taking drugs such as statins, non-steroidal anti-inflammatory drugs, glucocorticoids, etc. reduce the level of highly sensitive C-reactive protein. In patients with heart failure with different left ventricular ejection fraction values, it was found that the regression of the inflammatory response is accompanied by an improvement in prognosis, which confirms the hypothesis of inflammation as a response to stress, which has negative consequences for the cardiovascular system.

scholarly journals The effect of interleukin-1 on C-reactive protein expression in Hep3B cells is exerted at the transcriptional level

1995 ◽  
Vol 310 (1) ◽  
pp. 143-148 ◽  
Author(s):  
D Zhang ◽  
S L Jiang ◽  
D Rzewnicki ◽  
D Samols ◽  
I Kushner
Keyword(s):  
Interleukin 6 ◽  
Interleukin 1 ◽  
Kinetic Studies ◽  
Acute Phase Reactant ◽  
Transcriptional Level ◽  
Mrna Levels ◽  
C Reactive Protein ◽  
Reactive Protein ◽  
Hep3b Cells

The combination of interleukin 6 (IL-6) and interleukin 1 (IL-1) synergistically induces the human acute-phase reactant, C-reactive protein (CRP) in Hep3B cells. While previous studies have indicated that IL-6 induces transcription of CRP, the mode of action of IL-1 has not been clearly defined. It has been suggested that the effect of IL-1 might be post-transcriptional, exerted through the 5′-untranslated region (5′-UTR). To evaluate the role of IL-1 in CRP gene expression, we studied the effects of interleukin-6 (IL-6) and interleukin-1 beta (IL-1 beta) on both the endogenous CRP gene and on transfected CRP-CAT constructs in Hep3B cells. In kinetic studies of the endogenous CRP gene, IL-1 beta alone had no effect on CRP mRNA levels, but when added to IL-6, synergistically enhanced both CRP mRNA levels and transcription, as determined by Northern-blot analyses and nuclear run-on studies. IL-6 alone and the combination of [IL-1 beta + IL-6] each induced increases in mRNA levels roughly comparable with observed increases in transcription. These findings indicate that the effect of IL-1 beta on CRP expression is exerted largely at the transcriptional level in this system. This conclusion was confirmed by studies in Hep3B cells transiently transfected with CRP-CAT constructs, each containing 157 bp of the CRP 5′-flanking region but differing in the length of the 5′-UTR from 104 bp to 3 bp. All constructs responded in the same way; IL-6, but not IL-1 beta, induced significant chloramphenicol acetyltransferase (CAT) expression which was synergistically enhanced 2- to 3-fold by IL-1 beta. These results indicate that IL-1 beta stimulates transcriptional events in the presence of IL-6 and that the upstream 157 bases of the CRP promoter contain elements capable of both IL-6 induction and the synergistic effect of IL-1 beta on transcription.

Systemic inflammatory response syndrome without systemic inflammation in acutely ill patients admitted to hospital in a medical emergency

1999 ◽  
Vol 96 (3) ◽  
pp. 287-295 ◽  
Author(s):  
Annika TAKALA ◽  
Irma JOUSELA ◽  
Klaus T. OLKKOLA ◽  
Sten-Erik JANSSON ◽  
Marjatta LEIRISALO-REPO ◽  
...  
Keyword(s):  
Systemic Inflammatory Response Syndrome ◽  
Inflammatory Response ◽  
Systemic Inflammation ◽  
Interleukin 6 ◽  
Systemic Inflammatory Response ◽  
Composite Score ◽  
C Reactive Protein ◽  
Cd11b Expression ◽  
Reactive Protein ◽  
Markers Of Inflammation

Criteria of the systemic inflammatory response syndrome (SIRS) are known to include patients without systemic inflammation. Our aim was to explore additional markers of inflammation that would distinguish SIRS patients with systemic inflammation from patients without inflammation. The study included 100 acutely ill patients with SIRS. Peripheral blood neutrophil and monocyte CD11b expression, serum interleukin-6, interleukin-1β, tumour necrosis factor-α and C-reactive protein were determined, and severity of inflammation was evaluated by systemic inflammation composite score based on CD11b expression, C-reactive protein and cytokine levels. Levels of CD11b expression, C-reactive protein and interleukin-6 were higher in sepsis patients than in SIRS patients who met two criteria (SIRS2 group) or three criteria of SIRS (SIRS3 group). The systemic inflammation composite score of SIRS2 patients (median 1.5; range 0–8, n = 56) was lower than that of SIRS3 patients (3.5; range 0–9, n = 14, P = 0.013) and that of sepsis patients (5.0; range 3–10, n = 19, P< 0.001). The systemic inflammation composite score was 0 in 13/94 patients. In 81 patients in whom systemic inflammation composite scores exceeded 1, interleukin-6 was increased in 64 (79.0%), C-reactive protein in 59 (72.8%) and CD11b in 50 (61.7%). None of these markers, when used alone, identified all patients but at least one marker was positive in each patient. Quantifying phagocyte CD11b expression and serum interleukin-6 and C-reactive protein concurrently provides a means to discriminate SIRS patients with systemic inflammation from patients without systemic inflammation.

scholarly journals PROGNOSTIC INDICES AND MARKERS OF SYSTEMIC INFLAMMATION IN PATIENTS WITH COPD AND CAD

2017 ◽  
pp. 81-85
Author(s):  
G. L. IGNATOVA ◽  
V. N. ANTONOV
Keyword(s):  
Systemic Inflammation ◽  
Prognostic Markers ◽  
Functional Disorders ◽  
Inflammation Markers ◽  
C Reactive Protein ◽  
Reactive Protein ◽  
Male Patients ◽  
The Impact ◽  
The Relationship

The article discusses the problem of COPD combined with CAD, determination of inflammatory markers and the prognostic BODE, DOSE and ADO indices. The aim of the study was to evaluate the effect of PCV13 immunization on clinical and functional manifestations of systemic inflammation in patients with COPD and CAD, as well as the relationship with the prognostic markers. Material and methods: The study included 36 male patients with COPD and 36 patients with COPD and CAD, FC II-III stable angina who were treated at Regional Clinical Hospital _4 in Chelyabinsk during the period 2015--2016. Conclusions: 1. Patients with COPD combined with CAD had statistically significant clinical and functional disorders manifested by an increase in the degree of dyspnea and reduction in FEV1. 2. In patients with COPD concomitant with CAD, against the background of the comorbidities, the levels of systemic inflammation markers — C-reactive protein, fibrinogen and procalcitonin — were more overt than in patients only with COPD. 3. Monitoring changes in procalcitonin levels could be used as an additional highly informative method for estimating the probability of the presence of bacterial inflammation and effectiveness of therapy. 4. The prognostic BODE, DOSE and ADO indices tend to decrease unidirectionally under the impact of vaccination with pneumococcal conjugate vaccine. 5. PCV13 can reduce the level of systemic inflammation within 1 year after its application.

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