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1.
Association between physical activity and inflammatory markers in community-dwelling, middle-aged adults.
Cho, SMJ, Lee, H, Shim, JS, Jeon, JY, Kim, HC
Applied physiology, nutrition, and metabolism = Physiologie appliquee, nutrition et metabolisme. 2021;(7):828-836
Abstract
Physical activity has been known to deter inflammatory process; yet, the evidence is scarce in healthy, middle-aged population. We assessed the association between physical activity and inflammatory biomarkers, including high sensitivity (hs) C-reactive protein, interleukin (IL)-1α, -1β, and -6, tumor necrosis factor (TNF) -α and -β, and monocyte chemotactic protein (MCP) -1 and -3. Functional and leisure-time physical activity was assessed by the International Physical Activity Questionnaire. Inflammatory biomarkers were measured by multiplex enzyme-linked immunosorbent assay. Compared with highly physically active participants based on total metabolic equivalent of task, the most sedentary group had significantly higher odds ratio and [95% confidence interval] for ≥75th percentile of TNF-α (1.64 [1.10-2.44]), TNF-β (1.50 [1.09-2.07]), IL-1β (2.14 [1.49-3.09]), hsIL-1β (1.72 [1.15-2.58]), IL-6 (1.84 [1.24-1.73]), hsIL-6 (2.05 [1.35-3.12]), and MCP-1 (1.91 [1.28-2.87]) levels. Results for IL-1α and MCP-3 were inconsistent, as the least active group had lower odds for above the median IL-1α (0.65 [0.49-0.95]) and MCP-3 (0.71 [0.54-0.93]) yet higher odds for ≥75th percentile IL-1α (2.36 [1.63-3.42]) and MCP-3 (2.44 [1.63-3.64]) levels. Based on duration of moderate-to-vigorous physical activity, sedentary participants had significantly higher odds for above median (1.40 [1.13-1.73]) and ≥75th percentile (1.33 [1.00-1.77]) IL-1β compared with those fulfilling the guideline recommendation. Subgroup analyses showed minimal sex differences. Routine inflammatory assessment may help to achieve primordial prevention of cardiovascular and metabolic diseases. Novelty: Healthy, middle-aged adults with physically active lifestyle were generally at lower odds for elevated inflammatory status. The associations persisted regardless of sex, age, comorbidities, adiposity, and diet.
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Rapid Advancement in Enteral Nutrition Does Not Affect Systemic Inflammation and Insulin Homeostasis Following Pediatric Cardiopulmonary Bypass Surgery.
Floh, AA, Herridge, J, Fan, CS, Manlhiot, C, McCrindle, BW, Van Arsdell, G, Balmer-Minnes, D, Schwartz, SM
Pediatric critical care medicine : a journal of the Society of Critical Care Medicine and the World Federation of Pediatric Intensive and Critical Care Societies. 2020;(7):e441-e448
Abstract
OBJECTIVES To determine impact of enteral nutrition delivery on the relationship among inflammation, insulin resistance, and outcomes following pediatric cardiopulmonary bypass surgery. DESIGN Pilot, randomized study analyzed according to intention-to-treat analysis. SETTING Pediatric cardiac ICU. PATIENTS Infants (≤ 6 mo) undergoing cardiopulmonary bypass. INTERVENTIONS Patients randomly assigned to receive rapid escalation to enteral nutrition reaching goal feeds by 27 hours or standard feeding practice reaching goal feeds by 63 hours. Feeds were initiated on the first postoperative day. MEASUREMENTS AND MAIN RESULTS Fifty patients were randomized equally to study arms. Patients were a median (interquartile range) of 16 days old (7-110 d old), undergoing biventricular surgery (88%) with a median cardiopulmonary bypass time of 125 minutes (105-159 min). Serial blood samples were drawn before and after cardiopulmonary bypass, cardiac ICU admission, and every 12 hours (up to 96 hr) for glucose, insulin, and cytokines (interleukin-1α, interleukin-6, interleukin-8, interleukin-10, and tumor necrosis factor-α) levels. Glucose-insulin ratio was calculated to quantify insulin resistance. Patient characteristics, time to enteral nutrition initiation, enteral nutrition interruptions, and insulin administration were similar across intervention arms. FF reached goal feeds at similar intervals as standard feeding (39 hr [30-60 hr] vs 60 hr [21-78 hr]; p = 0.75). No difference in cytokine, insulin, or glucose-insulin ratio was noted between groups. Higher inflammation was associated with increased glucose-insulin ratio and higher risk of adverse events. In multivariable models of interleukin-8, FF was associated with increased glucose-insulin ratio (estimate of effect [95% CI], 0.152 [0.033-0.272]; p = 0.013). Although higher interleukin-8 was associated with an elevated risk of adverse event, this relationship was possibly mitigated by FF (odds ratio [95% CI], 0.086 [0.002-1.638]; p = 0.13). CONCLUSIONS A FF strategy was not associated with changes to early enteral nutrition delivery. Inflammation, insulin resistance, and morbidity were similar, but FF may modify the relationship between inflammation and adverse event. Multicenter nutrition studies are possible and necessary in this vulnerable population.
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3.
The Dietary Inflammatory Index and Chronic Lymphocytic Leukaemia in the MCC Spain Study.
Flores, JC, Gracia-Lavedan, E, Benavente, Y, Amiano, P, Romaguera, D, Costas, L, Robles, C, Gonzalez-Barca, E, de la Banda, E, Alonso, E, et al
Nutrients. 2019;(1)
Abstract
Chronic inflammation plays a role in the development of chronic lymphocytic leukaemia (CLL), and diet might modulate chronic inflammation. This study aims to evaluate the association between the dietary inflammatory index (DII®) and CLL. A total of 366 CLL cases and 1643 controls of the Spanish multicase-control (MCC) Spain study were included. The inflammatory potential of the diet was assessed using the energy-adjusted dietary inflammatory index (E-DII) based on 30 items from a validated semi-quantitative food frequency questionnaire. Odds ratios (OR) and 95% confidence intervals (CI) were estimated using logistic regression models controlling for potential confounders. Overall, a modest, non-statistically significant, positive association was observed between CLL and E-DII scores (OR for a one-unit increase in E-DII: 1.05 (CI 95%: 0.99, 1.12), p-value = 0.09 and by tertiles: ORT2vsT1: 1.20 (CI 95%: 0.90, 1.59); OR T3vsT1: 1.21 (CI 95%: 0.90, 1.62), p trend = 0.21). These results were independent from disease severity (p-het: 0.70), time from diagnosis (p-het: 0.67) and CLL treatment received (p-het: 0.56). No interactions were detected. In conclusion, the consumption of a diet with high pro-inflammatory components was not significantly associated with CLL. Changes towards a more pro-inflammatory dietary pattern in younger generations not included here warrant future research.
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Subcutaneous Adipose Tissue and Systemic Inflammation Are Associated With Peripheral but Not Hepatic Insulin Resistance in Humans.
van der Kolk, BW, Kalafati, M, Adriaens, M, van Greevenbroek, MMJ, Vogelzangs, N, Saris, WHM, Astrup, A, Valsesia, A, Langin, D, van der Kallen, CJH, et al
Diabetes. 2019;(12):2247-2258
Abstract
Obesity-related insulin resistance (IR) may develop in multiple organs, representing various etiologies for cardiometabolic diseases. We identified abdominal subcutaneous adipose tissue (ScAT) transcriptome profiles in liver or muscle IR by means of RNA sequencing in overweight or obese participants of the Diet, Obesity, and Genes (DiOGenes) (NCT00390637, ClinicalTrials.gov) cohort (n = 368). Tissue-specific IR phenotypes were derived from a 5-point oral glucose tolerance test. Hepatic and muscle IR were characterized by distinct abdominal ScAT transcriptome profiles. Genes related to extracellular remodeling were upregulated in individuals with primarily hepatic IR, while genes related to inflammation were upregulated in individuals with primarily muscle IR. In line with this, in two independent cohorts, the Cohort on Diabetes and Atherosclerosis Maastricht (CODAM) (n = 325) and the Maastricht Study (n = 685), an increased systemic low-grade inflammation profile was specifically related to muscle IR but not to liver IR. We propose that increased ScAT inflammatory gene expression may translate into an increased systemic inflammatory profile, linking ScAT inflammation to the muscle IR phenotype. These distinct IR phenotypes may provide leads for more personalized prevention of cardiometabolic diseases.
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Associations of serum indolepropionic acid, a gut microbiota metabolite, with type 2 diabetes and low-grade inflammation in high-risk individuals.
Tuomainen, M, Lindström, J, Lehtonen, M, Auriola, S, Pihlajamäki, J, Peltonen, M, Tuomilehto, J, Uusitupa, M, de Mello, VD, Hanhineva, K
Nutrition & diabetes. 2018;(1):35
Abstract
We recently reported using non-targeted metabolic profiling that serum indolepropionic acid (IPA), a microbial metabolite of tryptophan, was associated with a lower likelihood of developing type 2 diabetes (T2D). In the present study, we established a targeted quantitative method using liquid chromatography with mass spectrometric detection (HPLC-QQQ-MS/MS) and measured the serum concentrations of IPA in all the participants from the Finnish Diabetes Prevention Study (DPS), who had fasting serum samples available from the 1-year study follow-up (n = 209 lifestyle intervention and n = 206 control group). Higher IPA at 1-year study was inversely associated with the incidence of T2D (OR [CI]: 0.86 [0.73-0.99], P = 0.04) and tended to be directly associated with insulin secretion (β = 0.10, P = 0.06) during the mean 7-year follow-up. Moreover, IPA correlated positively with dietary fiber intake (g/day: r = 0.24, P = 1 × 10-6) and negatively with hsCRP concentrations at both sampling (r = - 0.22, P = 0.0001) and study follow-up (β = - 0.19, P = 0.001). Thus, we suggest that the putative effect of IPA on lowering T2D risk might be mediated by the interplay between dietary fiber intake and inflammation or by direct effect of IPA on β-cell function.
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The effect of fasting status on lipids, lipoproteins, and inflammatory biomarkers assessed after hospitalization for an acute coronary syndrome: Insights from PROVE IT-TIMI 22.
Steen, DL, Umez-Eronini, AA, Guo, J, Khan, N, Cannon, CP
Clinical cardiology. 2018;(1):68-73
Abstract
BACKGROUND For decades, fasting for 8 to 12 hours has been recommended for measurement of lipid profiles. The effect of fasting on low-density lipoprotein cholesterol (LDL-C) and triglycerides (TG) has been described in healthy cohorts and those with stable disease states. Recently, guidelines suggested that fasting may not be necessary due to its small effect on lipid measures. Little is known, however, regarding whether the impact of fasting is altered in the setting of an acute coronary syndrome (ACS). HYPOTHESIS We hypothesized that the post-ACS period would minimally effect the impact of fasting status on lipid measurements. METHODS We evaluated the association of fasting on lipid and other biomarkers at the randomization visit, which occurred at a median of 7 days after the onset of an ACS, as well as during follow-up, in a cohort of 4177 subjects from the Pravastatin or Atorvastatin Evaluation and Infection Therapy-Thrombolysis In Myocardial Infarction 22 (PROVE IT-TIMI 22) trial. RESULTS Fasting samples were independently associated with a higher LDL-C of 4.1 mg/dL and apolipoprotein-B 100 of 2.6 mg/dL as well as a lower TG of 21.0 mg/dL and high-sensitivity C-reactive protein of 0.48 mg/dL. The relative difference was 3.8% for LDL-C and -11.3% for TG. Fasting did not change total cholesterol, high-density lipoprotein cholesterol, apolipoprotein A-I, lipoprotein(a), or apolipoprotein C-III. CONCLUSIONS Although fasting does impact lipid measurements, the effect on LDL-C is small (about 4 mg/dL), both early after ACS and during follow-up. These data provide support for recent guidelines that no longer advocate for fasting lipid samples, including in the setting of ACS.
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LpA-II:B:C:D:E: a new immunochemically-defined acute phase lipoprotein in humans.
Bagdade, JD, Jilma, B, Hudgins, LC, Alaupovic, P, McCurdy, CE
Lipids in health and disease. 2018;(1):127
Abstract
BACKGROUND Previous studies of lipoproteins in patients with sepsis have been performed on density fractions isolated by conventional ultracentrifugation that are heterogeneous and provide no information about the cargo of apoproteins present in the immunochemically distinct subclasses that populate the density classes. Since apoproteins are now known to have important roles in host defense, we have separated these subclasses according to their apoprotein content and characterized their changes during experimental endotoxemia in human volunteers. METHODS We have studied apoB- and apoA containing lipoprotein subclasses in twelve healthy male volunteers before and for 8 h after a single dose of endotoxin (ET; 2 μg/kg) to stimulate inflammation. RESULTS After endotoxin, TG, TC, apoB and the apoB-containing lipoprotein cholesterol-rich subclass LpB and two of the three triglyceride-rich subclasses (TGRLP Lp:B:C, LpB:C:E+ LpB:E) all declined. In contrast, the third TGRLP, LpA-II:B:C:D:E ("complex particle"), after reaching a nadir at 4 h rose 49% above baseline, p = .006 at 8 h and became the dominant particle in the TGRLP pool. This increment exceeds the threshold of > 25% change required for designation as an acute phase protein. Simultaneous decreases in LpA-I:A-II and LpB:C:E + LpB:E suggest that these subclasses undergo post-translational modification and contribute to the formation of new LpA-II:B:C:D:E particles. CONCLUSIONS We have identified a new acute phase lipoprotein whose apoprotein constituents have metabolic and immunoregulatory properties applicable to host defense that make it well constituted to engage in the APR.
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Inflammation and micronutrient biomarkers predict clinical HIV treatment failure and incident active TB in HIV-infected adults: a case-control study.
Shivakoti, R, Gupte, N, Tripathy, S, Poongulali, S, Kanyama, C, Berendes, S, Cardoso, SW, Santos, BR, La Rosa, A, Mwelase, N, et al
BMC medicine. 2018;(1):161
Abstract
BACKGROUND Various individual biomarkers of inflammation and micronutrient status, often correlated with each other, are associated with adverse treatment outcomes in human immunodeficiency virus (HIV)-infected adults. The objective of this study was to conduct exploratory factor analysis (EFA) on multiple inflammation and micronutrient biomarkers to identify biomarker groupings (factors) and determine their association with HIV clinical treatment failure (CTF) and incident active tuberculosis (TB). METHODS Within a multicountry randomized trial of antiretroviral therapy (ART) efficacy (PEARLS) among HIV-infected adults, we nested a case-control study (n = 290; 124 cases, 166 controls) to identify underlying factors, based on EFA of 23 baseline (pre-ART) biomarkers of inflammation and micronutrient status. The EFA biomarker groupings results were used in Cox proportional hazards models to study the association with CTF (primary analysis where cases were incident World Health Organization stage 3, 4 or death by 96 weeks of ART) or incident active TB (secondary analysis). RESULTS In the primary analysis, based on eigenvalues> 1 in the EFA, three factors were extracted: (1) carotenoids), (2) other nutrients, and (3) inflammation. In multivariable-adjusted models, there was an increased hazard of CTF (adjusted hazard ratio (aHR) 1.47, 95% confidence interval (CI)1.17-1.84) per unit increase of inflammation factor score. In the secondary incident active TB case-control analysis, higher scores of the high carotenoids and low interleukin-18 factor was protective against incident active TB (aHR 0.48, 95% CI 0.26-0.87). CONCLUSION Factors identified through EFA were associated with adverse outcomes in HIV-infected individuals. Strategies focused on reducing adverse HIV outcomes through therapeutic interventions that target the underlying factor (e.g., inflammation) rather than focusing on an individual observed biomarker might be more effective and warrant further investigation.
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IL-1 Inhibition and Vascular Function in CKD.
Nowak, KL, Chonchol, M, Ikizler, TA, Farmer-Bailey, H, Salas, N, Chaudhry, R, Wang, W, Smits, G, Tengesdal, I, Dinarello, CA, et al
Journal of the American Society of Nephrology : JASN. 2017;(3):971-980
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Abstract
Vascular endothelial dysfunction and increased arterial stiffness contribute to increased cardiovascular risk in patients with CKD who exhibit chronic systemic inflammation. Because chronic inflammation contributes to vascular dysfunction, blocking inflammation may reduce cardiovascular risk in patients with CKD. In a two-site, double-blind trial, we randomized 42 adult patients with stage 3-4 CKD who were already receiving optimal background therapy to receive either IL-1 trap rilonacept or placebo for 12 weeks. Coprimary end points included change in brachial artery flow-mediated dilation (FMDBA) and aortic pulse-wave velocity (aPWV) after 4, 8, and 12 weeks. Exploratory end points included change in high-sensitivity C-reactive protein (hsCRP), FMDBA after acute ascorbic acid infusion, and vascular endothelial cell protein expression of NADPH oxidase. Participants were 63±11 (mean±SD) years of age and 24% were women; mean eGFR was 38±13 ml/min per 1.73 m2 Compared with placebo, rilonacept improved FMDBA (baseline: 3.36%±2.06% [mean±SD], 12 weeks: 2.45%±2.29% with placebo and baseline: 3.75%±3.12%, 12 weeks: 4.86%±3.20% with rilonacept; P<0.01), without changing aPWV (P=0.56). Rilonacept also reduced hsCRP levels (median [interquartile range]) (baseline: 4.60 [1.90-8.22] mg/L, 12 weeks: 2.16 [0.92-7.38] mg/L; P<0.01) and endothelial cell NADPH oxidase expression (P<0.05). Acute infusion of ascorbic acid to inhibit superoxide production associated with a nonsignificant trend toward increased FMDBA in the placebo group (P=0.07) but not the rilonacept group (P=0.56). Rilonacept was well tolerated (five adverse events versus two with placebo). In conclusion, treatment with an IL-1 trap improved FMDBA without changing aPWV and reduced systemic inflammation in patients with CKD.
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Cystatin C: A Marker for Inflammation and Renal Function Among HIV-infected Children and Adolescents.
Deyà-Martínez, À, Fortuny, C, Soler-Palacín, P, Neth, O, Sánchez, E, Martín-Nalda, A, Falcón-Neyra, L, Vila, A, Valls, A, Noguera-Julian, A
The Pediatric infectious disease journal. 2016;(2):196-200
Abstract
BACKGROUND Renal disease is a leading cause of morbidity in HIV-infected adults in the highly active antiretroviral therapy (HAART) era. Cystatin C has been proposed as a more sensitive marker of renal function, but it may be affected by ongoing inflammation. We aimed to study the cystatin C levels in a cohort of HIV-infected pediatric patients at 3 Spanish centers. METHODS This is a multicenter cross-sectional observational study. Renal function was assessed by means of first morning urine protein/creatinine and albumin/creatinine ratios and creatinine-estimated glomerular filtration rates (GFRs), together with the following inflammation markers: cystatin C, reactive C protein, β-2-microglobulin and 25(OH)-vitamin D levels. A control group of healthy children and adolescents was used. RESULTS Eighty-three patients (51 females, median age: 13.3 years; 32 males, median age: 13.6 years) and 44 controls (24 females, median age: 12.2 years; 20 males, median age: 10.9 years) were included. Among the former, mean CD4 cell count was 860/mm, 29(35%) patients had a previous AIDS diagnosis, 73(88%) were on HAART and HIV viremia was undetectable in 61(73%). No differences in cystatin C levels were observed between the 2 groups. In HIV-infected patients, cystatin C levels correlated with GFR (r = -0.27; P = 0.01), age at first HAART (r = -0.21; P = 0.05), and β-2-microglobulin (r = 0.569; P < 0.01). In multivariate analysis, lower GFR (P = 0.014) and higher β-2-microglobulin levels (P = 0.001) remained as independent risk factors for higher cystatin C values. CONCLUSIONS Cystatin C values were associated with GFR and β-2-microglobulin. Cystatin C may be useful as a marker of renal function in HIV-infected pediatric patients, independently of ongoing inflammation or viremia.