scholarly journals Active middle-aged men have lower fasting inflammatory markers but the postprandial inflammatory response is minimal and unaffected by physical activity status

2009 ◽  
Vol 107 (1) ◽  
pp. 63-68 ◽  
Author(s):  
Natalie C. Dixon ◽  
Tina L. Hurst ◽  
Duncan C. S. Talbot ◽  
Rex M. Tyrrell ◽  
Dylan Thompson
Keyword(s):  
Physical Activity ◽  
Inflammatory Markers ◽  
Metabolic Response ◽  
Inflammatory Marker ◽  
Middle Aged ◽  
Mixed Meal ◽  
Reactive Protein ◽  
Fasted State ◽  
Single Use ◽  
Postprandial Inflammation

Physical activity modifies some postprandial responses such as glycemic control, although it is unclear whether this translates into lower postprandial inflammation. Our objective in this study was to determine whether postprandial inflammatory markers are lower in active compared with sedentary middle-aged men. Thirteen active and twelve sedentary middle-aged men consumed a mixed meal on one occasion. Blood was taken via a cannula before and up to 8 h after the meal and with a single-use needle before and 8 h after the meal. Active men had lower fasted IL-6 (0.6 ± 0.2 vs. 1.2 ± 0.3 pg/ml; P = 0.004) and C-reactive protein (1.3 ± 0.3 vs. 2.9 ± 0.6 mg/l; P = 0.04) concentrations than sedentary men. Cannula blood IL-6 concentrations increased by 3.49 pg/ml in the 8 h following the meal ( P < 0.001); however, this increase was minimal (0.36 pg/ml) in blood taken via a single-use needle from the contralateral arm ( P = 0.013). The sedentary group had larger glucose ( P = 0.034), insulin ( P = 0.013), and triacylglycerol ( P = 0.057) responses to the meal. These results provide further evidence that physical activity is associated with lower inflammatory marker concentrations in a fasted state and a lower postprandial metabolic response to a meal. However, this does not translate into lower postprandial inflammatory markers since the only evidence of postprandial inflammation (a large increase in serum IL-6) was actually due to the cannula used for blood sampling.

Physical Activity, Sedentary Time, and Sleep and the Association With Inflammatory Markers and Adiponectin in 8- to 11-Year-Old Danish Children

2016 ◽  
Vol 13 (7) ◽  
pp. 733-739 ◽  
Author(s):  
Mette S. Nielsen ◽  
Jonas S. Quist ◽  
Jean-Philippe Chaput ◽  
Stine-Mathilde Dalskov ◽  
Camilla T. Damsgaard ◽  
...  
Keyword(s):  
Physical Activity ◽  
Sleep Duration ◽  
Inflammatory Markers ◽  
Sedentary Time ◽  
Vigorous Physical Activity ◽  
Movement Behavior ◽  
Inverse Association ◽  
Pubertal Status ◽  
Negatively Associated ◽  
Reactive Protein

Background:Inflammatory markers, adiponectin, and movement/nonmovement behaviors have all been linked to risk factors for cardiovascular disease; however, the association between childhood movement/nonmovement behaviors and inflammatory markers and adiponectin is unknown.Methods:We explored the association between accelerometer determined moderate-to-vigorous physical activity (MVPA), sedentary time, and sleep (7 days/8 nights) and fasting C-reactive protein (CRP), interleukin-6 (IL-6), and adiponectin in 806 school children. A sleep variability score was calculated.Results:MVPA was negatively associated with adiponectin in boys and girls (P < .001) and with CRP and IL-6 in girls (P < .05) independent of sleep duration, sedentary time, age, fat mass index (FMI), and pubertal status. Sedentary time was positively associated with adiponectin in boys and girls (both P < .001), and sleep duration with adiponectin in boys independent of age, FMI, and pubertal status (P < .001); however, these associations disappeared after mutual adjustments for movement behavior. Sleep duration variability was positively associated with CRP in girls independent of all covariates (P < .01).Conclusion:MVPA remained negatively associated with inflammatory markers and adiponectin, and sleep duration variability positively associated with CRP after adjustment for FMI, pubertal status, and other movement behavior. The inverse association between MVPA and adiponectin conflicts with the anti-inflammatory properties of adiponectin.

scholarly journals Association between childhood infection, serum inflammatory markers and intelligence: findings from a population-based prospective birth cohort study

2017 ◽  
Vol 146 (2) ◽  
pp. 256-264 ◽  
Author(s):  
N. MACKINNON ◽  
S. ZAMMIT ◽  
G. LEWIS ◽  
P. B. JONES ◽  
G. M. KHANDAKER
Keyword(s):  
Birth Cohort ◽  
Inflammatory Markers ◽  
Intellectual Development ◽  
Inflammatory Marker ◽  
Population Based ◽  
Birth Cohort Study ◽  
Reactive Protein ◽  
Parents And Children ◽  
High Infection ◽  
Prospective Birth Cohort

SUMMARYA link between infection, inflammation, neurodevelopment and adult illnesses has been proposed. The objective of this study was to examine the association between infection burden during childhood – a critical period of development for the immune and nervous systems – and subsequent systemic inflammatory markers and general intelligence. In the Avon Longitudinal Study of Parents and Children, a prospective birth cohort in England, we examined the association of exposure to infections during childhood, assessed at seven follow-ups between age 1·5 and 7·5 years, with subsequent: (1) serum interleukin 6 and C-reactive protein (CRP) levels at age 9; (2) intelligence quotient (IQ) at age 8. We also examined the relationship between inflammatory markers and IQ. Very high infection burden (90+ percentile) was associated with higher CRP levels, but this relationship was explained by body mass index (adjusted odds ratio (OR) 1·19; 95% confidence interval (CI) 0·95–1·50), maternal occupation (adjusted OR 1·23; 95% CI 0·98–1·55) and atopic disorders (adjusted OR 1·24; 95% CI 0·98–1·55). Higher CRP levels were associated with lower IQ; adjusted β = −0·79 (95% CI −1·31 to −0·27); P = 0·003. There was no strong evidence for an association between infection and IQ. The findings indicate that childhood infections do not have an independent, lasting effect on circulating inflammatory marker levels subsequently in childhood; however, elevated inflammatory markers may be harmful for intellectual development/function.

scholarly journals Calorie Restriction Modulates Inactivity-Induced Changes in the Inflammatory Markers C-Reactive Protein and Pentraxin-3

2008 ◽  
Vol 93 (8) ◽  
pp. 3226-3229 ◽  
Author(s):  
Alessandra Bosutti ◽  
Grazia Malaponte ◽  
Michela Zanetti ◽  
Pietro Castellino ◽  
Martina Heer ◽  
...  
Keyword(s):  
Physical Activity ◽  
Energy Balance ◽  
Inflammatory Response ◽  
Calorie Restriction ◽  
Inflammatory Markers ◽  
Bed Rest ◽  
Energy Restriction ◽  
Pentraxin 3 ◽  
C Reactive Protein ◽  
Reactive Protein

Abstract Context: Energy balance and physical activity potentially influence systemic inflammation. Objective: Our objective was to test the hypothesis that moderate energy restriction may prevent activation of inactivity-induced inflammatory response. Design: Participants were studied four times at the end of 14-d periods of experimental bed rest or controlled ambulation, after receiving eucaloric or hypocaloric diets. Setting: The study was conducted at the clinical research center of the German Space Agency. Subjects: Nine healthy young volunteers participated. Interventions: Energy intake was calibrated to physical activity and decreased by about 20% in hypocaloric conditions. Main Outcome Measures: Changes in body fat by dual-energy x-ray absorptiometry as well as plasma inflammatory markers and cytokine mRNA levels in blood cells were measured. Results: Fat mass did not change significantly in eucaloric conditions and decreased in hypocaloric periods (−1.0 ± 0.3 and −1.0 ± 0.3 kg in ambulatory and bed rest, respectively). Bed rest in eucaloric conditions increased plasma C-reactive protein (CRP) (+143 ± 53%) and both the ratios between plasma IL-6 and IL-10 (4±1 times) and white blood cell IL-6 and IL-10 mRNAs (5 ± 1 times). Energy restriction prevented bed-rest-mediated increases in CRP and the IL-6 to IL-10 ratio. Bed rest increased (P = 0.03) long pentraxin-3 (PTX3) plasma concentration, without significant activity-by-diet interaction. In all conditions (n = 36), CRP and PTX3 were inversely correlated (r = −0.61; P &lt; 0.001). Changes in fat mass, leptin, and IL-6 directly correlated with CRP and inversely correlated with PTX3. IL-10 inversely correlated with CRP and directly correlated with PTX3 (r = 0.52; P &lt; 0.01). Conclusions: Calorie restriction prevents the inflammatory response induced by 14 d of bed rest. We suggest an inverse regulation of CRP and PTX3 in response to changes in energy balance.

Effect of antiplatelet therapy on inflammatory markers in atherothrombotic patients

2010 ◽  
Vol 103 (01) ◽  
pp. 71-82 ◽  
Author(s):  
Joseph Muhlestein
Keyword(s):  
Antiplatelet Therapy ◽  
Inflammatory Markers ◽  
Thrombus Formation ◽  
Inflammatory Marker ◽  
Vascular Inflammation ◽  
Antiplatelet Agents ◽  
Cd40 Ligand ◽  
Reactive Protein ◽  
Atherosclerotic Lesions

SummaryInflammation is central to the pathogenesis and progression of atherosclerosis and thrombosis, the underlying cause of major cardiovascular disease. Platelets, in addition to their role in haemostasis, play a key role in both thrombus formation and inflammation following vascular injury, especially atherosclerotic lesions. An increasing body of evidence suggests that inhibition of platelet function can modulate inflammatory markers, particularly those associated with activated platelets, such as CD40 ligand, P-selectin, and C-reactive protein. The currently available antiplatelet agents aspirin, clopidogrel, prasugrel, abciximab, and eptifibatide have shown varying effects on inflammatory markers. These effects seem to be mostly indirect, i.e. mediated primarily through reduced platelet activation that results in reduced inflammatory marker expression. However, there is some evidence that suggests direct effects (i.e. those independent of platelets) may also play a role in modulating inflammatory markers. Evidence linking inflammation and thrombosis supports the hypothesis that agents with both anti-inflammatory and antiplatelet effects may reduce vascular inflammation and limit acute and long-term thrombotic events. An assessment of the involvement of inflammatory mediators in atherosclerosis may provide further insight into important predictive markers of cardiovascular outcomes that may also serve as potential therapeutic targets. This review examines the evidence for and potential clinical relevance of the effects of antiplatelet therapy on inflammatory markers.

scholarly journals CNS and systemic inflammation underlying neuropsychiatric symptoms and related cognitive decline in older people.

2020 ◽  
Author(s):  
Christopher Clark ◽  
Jonas Richiardi ◽  
Bénédicte Maréchal ◽  
Gene L. Bowman ◽  
Loïc Dayon ◽  
...  
Keyword(s):  
Older People ◽  
Cognitive Decline ◽  
Inflammatory Markers ◽  
Psychiatric Symptoms ◽  
Inflammatory Marker ◽  
Neuropsychiatric Symptoms ◽  
Interferon Γ ◽  
Elderly Subjects ◽  
Csf Biomarkers ◽  
Reactive Protein

Abstract BACKGROUND Neuroinflammation may contribute to psychiatric symptoms in older people, in particular in the context of Alzheimer’s disease (AD). Here, our objective was to determine systemic and central nervous system (CNS) inflammatory signatures associated with neuropsychiatric symptoms (NPS) in older subjects, and investigate their relationships with AD pathology and cognitive decline.METHODS We quantified a panel of inflammatory markers in both cerebrospinal fluid (CSF) and circulating blood serum in elderly subjects with normal cognition or with beginning cognitive decline. We further performed a comprehensive clinical assessment including longitudinal cognitive and neuropsychiatric evaluations and measured CSF biomarkers of core AD pathology. Multivariate analysis selected CSF and serum neuroinflammatory molecules associated with the presence of overall NPS and specific symptoms.RESULTS The presence of NPS was associated with distinct inflammatory markers profiles involving soluble intracellular cell adhesion molecule-1 (sICAM-1), C-reactive protein (CRP), Interleukin (IL) -8 and 10 kDa interferon-γ-induced protein (IP-10) in CSF; and Eotaxin-3, IL-6 and CRP in serum. Further analysis identified specific inflammatory marker signatures associated with anxiety, depression and disinhibition. Presenting NPS was associated with subsequent cognitive decline and this association was mediated by CSF sICAM-1.CONCLUSIONS These results suggest that NPS in older people are associated with distinct systemic and CNS inflammatory processes. Neuroinflammation may explain the link between NPS and more rapid clinical disease progression.

scholarly journals The Relationship Between Neuroticism and Inflammatory Markers: A Twin Study

2014 ◽  
Vol 17 (3) ◽  
pp. 177-182 ◽  
Author(s):  
Arthur A. Sas ◽  
Frühling V. Rijsdijk ◽  
Johan Ormel ◽  
Harold Snieder ◽  
Harriëtte Riese
Keyword(s):  
Inflammatory Markers ◽  
Structural Equation ◽  
Inflammatory Marker ◽  
Genetic Correlations ◽  
Equation Modeling ◽  
Reactive Protein ◽  
Inflammatory Status ◽  
Physical Disorders ◽  
The Relationship ◽  
Important Marker

Introduction: Neuroticism is an important marker of vulnerability for both mental and physical disorders. Its link with multiple etiological pathways has been studied before. Inflammatory markers have been demonstrated to predict similar mental and physical disorders as neuroticism. However, currently no study has focused on the shared genetic background of neuroticism and inflammatory markers. In the present study we will focus on the phenotypic and genetic relationship between neuroticism and three commonly used inflammatory markers: C-reactive protein (CRP), fibrinogen and Immunoglobulin-G (IgG). Material and Methods: The study was conducted in 125 Dutch female twin pairs. For each participant, four different neuroticism scores were available to calculate a neuroticism composite score that was used in the statistical analyses. Blood samples for inflammatory marker determination were taken after an overnight fast. Heritabilities, phenotypic and genetic correlations were estimated using bivariate structural equation modeling. Results: Heritabilities are fair for neuroticism (0.55), CRP (0.52) and fibrinogen (0.67) and moderate for IgG (0.43). No significant phenotypic or genetic correlations were found between neuroticism and the inflammatory markers. Interaction models yielded no moderation of the genetic and environmental pathways in the regulation of inflammatory markers by neuroticism. Conclusion: Substantial heritabilities were observed for all variables. No evidence was found for significant shared (or moderation of) genetic or environmental pathways underlying neuroticism and inflammatory status.

scholarly journals Admission inflammatory markers and isolation of a causative organism in patients with spontaneous spinal infection

2013 ◽  
Vol 95 (8) ◽  
pp. 604-608 ◽  
Author(s):  
PAG Torrie ◽  
A Leonidou ◽  
IJ Harding ◽  
G Wynne Jones ◽  
MJ Hutchinson ◽  
...  
Keyword(s):  
Inflammatory Markers ◽  
Inflammatory Marker ◽  
White Cell Count ◽  
Blood Cultures ◽  
Spinal Infection ◽  
Causative Organism ◽  
Reactive Protein ◽  
Positive Biopsy ◽  
Independent Variable ◽  
Responsible Pathogen

Introduction The purpose of this study was to investigate the significance of the inflammatory markers on admission in the isolation of a causative pathogen in patients with spinal infection. Spinal infection is treated frequently at spinal units and can encompass a broad range of clinical entities. Its diagnosis is often delayed because of the difficulty of identifying the responsible pathogen. Methods Patients with spinal infection treated in our institution over a period of eight years were identified and their notes studied retrospectively. Admission C-reactive protein (CRP), white cell count (WCC) as well as co-morbidities and mode of pathogen identification were recorded. Overall, 96 patients were included in the study. Results The CRP levels on admission were correlated significantly with the overall potential for isolation of a pathogen (p<0.0001) and positive biopsy cultures (p=0.0016). Admission WCC levels were associated significantly with the overall potential for isolation of a pathogen (p=0.0003) and positive biopsy cultures (p=0.0023). Both CRP and WCC levels were significantly negatively correlated with the duration of the preceding symptoms (p=0.0003 and p<0.0001 respectively). Delay in presentation was significantly negatively correlated with organism isolation (p=0.0001). Multivariate analyses identified the delay in presentation as the strongest independent variable for organism isolation (p=0.014) in cases of spontaneous spinal infection when compared with the admission CRP level (p=0.031) and WCC (p=0.056). Conclusions In spontaneous spinal infection, delay in presentation is the strongest independent variable for organism isolation. High inflammatory marker levels on admission are a useful prognostic marker for the overall potential of isolating a causative organism either by blood cultures or by biopsy in patients with negative blood cultures. Furthermore, the admission inflammatory marker levels allow for treating surgeons to counsel their patients of the likelihood of achieving a positive microbiological yield from biopsy.

scholarly journals Interleukin-6, C-reactive protein and interleukin-10 after antidepressant treatment in people with depression: a meta-analysis

2012 ◽  
Vol 42 (10) ◽  
pp. 2015-2026 ◽  
Author(s):  
S. A. Hiles ◽  
A. L. Baker ◽  
T. de Malmanche ◽  
J. Attia
Keyword(s):  
Interleukin 6 ◽  
Inflammatory Markers ◽  
Antidepressant Treatment ◽  
Inflammatory Marker ◽  
Meta Analysis ◽  
Interleukin 10 ◽  
Cochrane Library ◽  
C Reactive Protein ◽  
Cross Sectional ◽  
Reactive Protein

BackgroundCross-sectional studies support an association between depression and inflammatory markers. However, little is known of their relationship in the context of antidepressant treatment. Our aim was to explore via meta-analysis whether antidepressant treatment is associated with a reduction in three inflammatory markers associated with depression.MethodA computerized search of EMBASE, Medline, PsycINFO and Cochrane Library databases was completed using subject headings for depression and either interleukin-6, C-reactive protein or interleukin-10, selecting studies which reported circulating levels of inflammatory markers before and after antidepressant treatment for people with depression. Outcome and moderator variables were coded for analysis, including inflammatory marker change, depression severity change, age, gender ratio, assay brand, treatment response and weight change.ResultsPooled effect sizes showed a significant decrease in interleukin-6 (n=14, d=−0.42, p=0.02), marginally significant decrease in C-reactive protein (n=8, d=−0.57, p=0.05) and a non-significant decrease in interleukin-10 (n=3, d=−0.45, p=0.14) after treatment. High levels of heterogeneity were observed, which may be associated with clinical variations between the studies such as weight gain, anxiety, incomplete remission and other individual differences and co-morbidities.ConclusionsThe findings of this meta-analysis indicate that there may be a normalization of overactive inflammatory processes following antidepressant treatment.

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