Determinants of inflammatory markers in a bi-ethnic population

Department of Health Promotion and Education, Loma Linda University, Loma Linda, California 92354, USA.
Ethnicity & disease (Impact Factor: 1). 03/2011; 21(2):142-9.
Source: PubMed


Inflammation is a common pathophysiological pathway for a number of chronic diseases, and is strongly influenced by sociodemographic factors and lifestyle. Less is known about factors that may influence the inflammatory response in individuals of distinct ethnic backgrounds. Therefore, this study examined the relationship between ethnicity and blood levels of inflammatory markers in a sample of non-smoking church-goers.
In a cross-sectional investigation, 508 men and women (> 35 years old, 62% White, 38% Black) participated in the Biopsychosocial Religion and Health substudy of the Adventist Health Study 2. The contribution of socioeconomic status (education level and difficulty meeting expenses for basic needs) and health covariates (exercise, vegetarian or other type of diet, body mass index, and presence of inflammatory conditions) toward serum levels of C-reactive protein (CRP), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-alpha) was assessed with linear regression models. Levels of interleukin-10 (IL-10), an anti-inflammatory marker, were also assessed.
Blacks showed higher levels of CRP and IL-6 than Whites. Controlling for sociodemographic and health variables attenuated the ethnic difference in CRP while IL-6 levels remained higher in Blacks than in Whites (beta = .118; 95% confidence interval = .014-.206; P = .025). Ethnic differences in IL-10 and TNF-alpha were not found. Vegetarian diet was associated with lower CRP levels while exercise frequency was associated with higher IL-10 levels.
Higher susceptibility of Blacks to inflammatory diseases may reflect higher IL-6, which could be important in assessing health disparities among Blacks and Whites. Vegetarian diet and exercise may counteract effects of disparities.

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Available from: Jerry W Lee, Oct 09, 2015
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    • " type 2 diabetes , including heart disease , blindness , amputations , stroke and death ( Konen et al . , 1999 ) . Increasing evidence suggests these conditions and complications are driven by inflammatory processes ) . African Americans also tend to show higher levels of inflammatory markers ( Geronimus et al . , 2006 ; Chyu and Upchurch , 2011 ; Paalani et al . , 2011 ) than do whites . Thus , better understanding factors that protect against inflammatory processes may be particularly useful in identifying risk and protective factors for African American health in young adulthood . Life history theory ( Charnov , 1993 ) provides a broad frame - work for hypothesizing two mechanisms that may relate pa"
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    ABSTRACT: The current investigation was designed to examine the association of parenting during late childhood and early adolescence, a time of rapid physical development, with biological propensity for inflammation. Based on life course theory, it was hypothesized that parenting during this period of rapid growth and development would be associated with biological outcomes and self-reported health assessed in young adulthood. It was expected that association of parenting with health would be mediated either by effects on methylation of a key inflammatory factor, Tumor necrosis factor (TNF), or else by association with a pro-inflammatory shift in the distribution of mononuclear blood cells. Supporting expectations, in a sample of 398 African American youth residing in rural Georgia, followed from age 11 to age 19, parenting at ages 11-13 was associated with youth reports of better health at age 19. We found that parenting was associated with changes in TNF methylation as well as with changes in cell-type composition. However, whereas methylation of TNF was a significant mediator of the association of parenting with young adult health, variation in mononuclear white blood cell types was not a significant mediator of the association of parenting with young adult health. The current research suggests the potential value of examining the health-related effects of parenting in late childhood and early adolescence. Further examination of protection against pro-inflammatory tendencies conferred by parenting appears warranted.
    Frontiers in Psychology 05/2015; 6. DOI:10.3389/fpsyg.2015.00676 · 2.80 Impact Factor
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    • "For example, differences in the individual response to inflammatory stressors may have important downstream effects on initiation and progression of acute and chronic inflammatory diseases. Epidemiological data have revealed race and gender differences in resting levels of inflammatory biomarkers [7,8] and some of these biomarkers are predictors of the subsequent development of cardiometabolic disease [9,10]. Little is known, however, of demographic influences on the response of such biomarkers to inflammatory stresses. "
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    ABSTRACT: Race- and gender-variation in innate immunity may contribute to demographic differences in inflammatory and cardiometabolic disease; yet their influence on dynamic responses during inflammatory stress is poorly understood. Our objective was to examine race and gender influence on the response to experimental endotoxemia. The Genetics of Evoked Responses to Niacin and Endotoxemia (GENE) study was designed to investigate regulation of inflammatory and metabolic responses during low-grade endotoxemia (LPS 1 ng/kg intravenously) in healthy individuals (median age 24, IQR=7) of European (EA; n=193, 47% female) and African ancestry (AA; n=101, 59% female). Baseline clinical, metabolic, and inflammatory biomarkers by race and gender were consistent with epidemiological literature; pre-LPS cytokines (e.g. median (IQR) IL-6, 2.7 (2) vs.2.1 (2) pg/ml, P=0.001) were higher in AA than EA. In contrast, acute cytokine responses during endotoxemia were lower in AA than EA (e.g. median (IQR) peak IL-1RA, 30 (38) vs.43 (45) ng/ml P=0.002) as was the induction of hepatic acute-phase proteins (e.g. median (IQR) peak CRP 12.9 (9) vs.17.4 (12) mg/L P=0.005). Further, baseline levels of cytokines were only weakly correlated with peak inflammatory responses (all rs <0.2) both in AA and in EA. There were less pronounced and less consistent differences in the response by gender, with males having a higher AUC for CRP response compared to females (median (IQR) AUC: 185 (112) vs. 155 (118), P=0.02). We observed lower levels of evoked inflammation in response to endotoxin in AA compared with EA, despite similar or higher baseline levels of inflammatory markers in AA. Our data also suggest that levels of inflammatory biomarkers measured in epidemiological settings might not predict the degree of acute stress-response or risk of diseases characterized by activation of innate immunity. Trial registration FDA registration number NCT00953667
    Journal of Translational Medicine 03/2013; 11(1):63. DOI:10.1186/1479-5876-11-63 · 3.93 Impact Factor
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    • "[18,19] Relative to EAs, it is possible that inflammatory pathways are upregulated in AAs. Previous studies have shown that AAs have higher serum CRP and interleukin-6 (IL-6) concentrations and display heightened oxidative stress and inflammation based on in vitro human umbilical vein endothelial cells (HUVECs) studies [38,39]. It is biologically plausible that MCP-1 may play differential roles in the pathophysiology of DN based on the type of diabetes and ethnic background. "
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    ABSTRACT: Background Monocyte chemoattractant protein-1 (MCP-1) plays important roles in kidney disease susceptibility and atherogenesis in experimental models. Relationships between serum MCP-1 concentration and early nephropathy and subclinical cardiovascular disease (CVD) were assessed in African Americans (AAs) with type 2 diabetes (T2D). Methods Serum MCP-1 concentration, urine albumin:creatinine ratio (ACR), estimated glomerular filtration rate (eGFR), and atherosclerotic calcified plaque (CP) in the coronary and carotid arteries and infrarenal aorta were measured in 479 unrelated AAs with T2D. Generalized linear models were fitted to test for associations between MCP-1 and urine ACR, eGFR, and CP. Results Participants were 57% female, with mean ± SD (median) age 55.6±9.5 (55.0) years, diabetes duration 10.3±8.2 (8.0) years, urine ACR 149.7±566.7 (14.0) mg/g, CKD-EPI eGFR 92.4±23.3 (92.0) ml/min/1.73m2, MCP-1 262.9±239.1 (224.4) pg/ml, coronary artery CP 280.1±633.8 (13.5), carotid artery CP 47.1±132.9 (0), and aorta CP 1616.0±2864.0 (319.0). Adjusting for age, sex, smoking, HbA1c, BMI, and LDL, serum MCP-1 was positively associated with albuminuria (parameter estimate 0.0021, P=0.04) and negatively associated with eGFR (parameter estimate −0.0003, P=0.001). MCP-1 remained associated with eGFR after adjustment for urine ACR. MCP-1 levels did not correlate with the extent of CP in any vascular bed, HbA1c or diabetes duration, but were positively associated with BMI. No interaction between BMI and MCP-1 was detected on nephropathy outcomes. Conclusions Serum MCP-1 levels are associated with eGFR and albuminuria in AAs with T2D. MCP-1 was not associated with subclinical CVD in this population. Inflammation appears to play important roles in development and/or progression of kidney disease in AAs.
    BMC Nephrology 11/2012; 13(1):148. DOI:10.1186/1471-2369-13-148 · 1.69 Impact Factor
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