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Low-grade Systemic Inflammation (low-grade + systemic_inflammation)
Selected AbstractsLow-grade systemic inflammation in patients with amyotrophic lateral sclerosisACTA NEUROLOGICA SCANDINAVICA, Issue 6 2009D. Keizman Objective,,, To prospectively determine the intensity of systemic low-grade inflammation in patients with amyotrophic lateral sclerosis (ALS). Patients and methods,,, Patients with ALS and matched healthy controls underwent blood tests for inflammation-sensitive biomarkers: erythrocyte sedimentation rate (ESR), quantitative fibrinogen, wide-range C-reactive protein (wrCRP) concentrations, leukocyte count and neutrophil-to-lymphocyte ratio (NLR). The correlation between these inflammatory biomarkers and disability status of the patients, expressed by the ALS Functional Rating Scale (ALSFRS-R), was evaluated. Results,,, Eighty patients with ALS and 80 matched controls were included. wrCRP, fibrinogen, ESR and NLR values were significantly elevated in patients compared with controls. There was a significant correlation between the ALSFRS-R score and wrCRP, ESR and fibrinogen levels. This correlation persisted on sequential examinations. Conclusions,,, A systemic low-grade inflammation was detected in patients with ALS and correlated with their degree of disability. A heightened systemic inflammatory state is apparently associated with a negative prognosis in ALS. [source] Dysregulation of monocyte oxidative burst in streptococcal endocarditisEUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 10 2001E. Presterl Background Streptococcal subacute endocarditis is characterized by low-grade systemic inflammation. Although structural cardiac defects are pivotal, phagocytic cells, i.e. monocytes and neutrophils, are involved in the induction and the course of bacterial endocarditis. Decreased production of reactive oxygen metabolites was described in long-lasting infections. We hypothesized that the oxidative burst of phagocytes induced by the infecting organism is defective in patients with streptococcal endocarditis. Patients and methods The monocytes and neutrophils of 11 patients with streptococcal native valve endocarditis were challenged with the respective pathogens and two control streptococcal strains, and the oxidative burst was determined by fluorescence-activated cell sorter analysis. These experiments were done before any antibiotic therapy was administered, and repeated at least 12 months after recovery. Eight volunteers served as healthy controls. Results The monocyte response to the respective pathogens was decreased in the patient groups compared to the response to the control streptococci. After cure the monocyte response to the pathogens was not different to the response to the control strains. The monocyte response of the healthy volunteers did not show any differences between the patients' pathogens and the control strains. The neutrophil oxidative burst to the pathogens was similar to that to the control streptococci in both patient and the volunteer group. Conclusion The decreased response of patient monocytes to the pathogens may contribute to the low-grade inflammatory response and to the course of streptococcal endocarditis. [source] Severe periodontitis is associated with systemic inflammation and a dysmetabolic status: a case,control studyJOURNAL OF CLINICAL PERIODONTOLOGY, Issue 11 2007Luigi Nibali Abstract Background and Aim: A cluster of metabolic factors defines a syndrome that predisposes to diabetes and cardiovascular disease. Chronic infections such as periodontitis might alter these individual metabolic factors and the systemic inflammatory burden. The aim of this study was to investigate the association between severe periodontitis and increase in inflammatory and metabolic risk factors for cardiovascular disease. Materials and Methods: We examined 302 patients with severe periodontitis and 183 healthy controls, and we collected a blood sample from each subject in order to investigate differences in inflammatory (leukocyte numbers and differential counts) and metabolic markers (lipids and glucose). Results: After correcting for differences in age, gender, smoking and ethnicity, periodontitis subjects exhibited a low-grade systemic inflammation (increased white cell counts, 1.10±1.02 × 109/l, 95%CI 1.05,1.15, p=0.0001), dyslipidemia [lower high-density lipoprotein cholesterol, 1.14±1.03 mmol/l, 95%CI 1.08,1.20, p<0.0001 and higher low-density lipoprotein cholesterol, 1.12±1.03, 95%CI 1.05,1.19, p<0.0001) and increased non-fasting serum glucose levels (1.04±1.01 mmol/l, 95%CI 1.02,1.06, p=0.01) when compared with controls. The associations were confirmed in a subpopulation of Caucasian non-smokers. A trend for a dose dependent effect of the number of periodontal pockets on the tested inflammatory and metabolic markers was observed. Conclusions: These data suggest a possible link between severe generalized periodontitis, systemic inflammation and a dysmetabolic state in otherwise healthy individuals. [source] Inflammatory effects of nutritional stimuli: further support for the need for a big picture approach to tackling obesity and chronic diseaseOBESITY REVIEWS, Issue 2 2010G. Egger Summary The discovery of a form of low-grade systemic inflammation (called ,metaflammation'), and the close evolutionary link between the immune and metabolic systems, poses questions about the supposed antigens (inducers) of such an immune reaction. Initially, this was thought to be mediated through obesity. However, we have identified a number of lifestyle or environmentally related inducers that may cause metaflammation, even in the absence of obesity. In this paper, the third of a series linking obesity with broad environmental and evolutionary factors, we identify nutritional stimuli with evidence of an involvement in metaflammation. From this we propose that components of certain foods and beverages with which humans have not evolved, are more often the inducers of an inflammatory effect in the body than those with which humans have become more familiar, and to which a neutral, or anti-inflammatory response may be expected to have developed. The implications of such a finding are considered in relation to broader aspects of the environment, economic growth, policy change and current global financial issues. [source] Ghrelin and leptin modulate immunity and liver function in overweight childrenPEDIATRICS INTERNATIONAL, Issue 1 2009Yuki Okamatsu Abstract Background:, The rising prevalence of obesity represents a growing worldwide public health problem. Interactions of adipocytokines and low-grade systemic inflammation presently are considered important in the development of obesity, as well as associated chronic disease including bronchial asthma, obesity-related liver disease and type 2 diabetes mellitus. The purpose of the present study was to investigate metabolic, hormonal, immunologic and inflammatory factors in overweight children and to further clarify possible immunomodulatory effects of obesity-related hormones and cytokines. Methods:, Forty-nine prepubertal overweight children and 49 age-matched controls of normal weight without underlying disease were enrolled. Levels of plasma ghrelin and serum leptin, cytokines (interleukin [IL]-4, IL-10, IL-12, 1L-13), C-reactive protein, immunoglobulin, and insulin were measured, and liver function tests were done to better understand their status in the setting of obesity. Results:, Overweight subjects had significantly higher measures of adiposity (body mass indexI, % body fat) and had significantly higher serum levels of IgG, IgA and IgE than non-obese children (P = 0.038, 0.0043, 0.0034, respectively); the opposite was true for IgM (P = 0.025). The incidence of presumed non-alcoholic fatty liver disease was 28.6% in overweight children. In overweight children, serum leptin levels were associated with liver function index (aspartate aminotransferase/alanine aminotransferase ratio) and serum insulin levels. Some elevated immunoglobulin levels significantly correlated with plasma ghrelin levels and liver function index. Conclusions:, It is possible that appetite-regulating hormones modulate both humoral immunity and liver function. Further studies with a larger number of subjects are needed to clarify the precise mechanisms of this association. [source] Change in waist circumference over 11 years and current waist circumference independently predict elevated CRP in Filipino women,AMERICAN JOURNAL OF HUMAN BIOLOGY, Issue 3 2010Julienne N. Rutherford C-reactive protein, a marker of chronic, low-grade inflammation, is strongly associated with current central adiposity, and has been linked to elevated risk of cardiovascular disease. Less is known about the contribution of longitudinal change in waist circumference to current inflammation. We evaluated the extent to which current waist circumference and change over an 11-year interval contribute independently to low-grade systemic inflammation measured in a group of 1,294 women, 35,69 years, participating in the Cebu Longitudinal Nutrition and Health Survey in the Philippines. Waist circumference was measured at the time of blood draw for CRP analysis in 2005 and during an earlier survey in 1994. A waist circumference delta variable was constructed by subtracting current circumference from past circumference. We used logistic regression models to predict having an elevated plasma CRP concentration (3 mg L,1 < CRP < 10 mg L,1). Waist circumference in 2005 was a strong predictor of elevated CRP (OR 1.10, 95% CI = 1.08, 1.12, P < 0.001). In combined models, increase in circumference over 11 years was a significant and independent predictor of elevated CRP risk (OR = 1.023, 95% CI = 1.00, 1.05, P < 0.05). Considering the average increase over time, the cumulative risk of elevated CRP due to increased central adiposity was 25.7%. However, women who reduced their waist circumference between 1994 and 2005 had greatly reduced risk (6.2%), suggesting that even long-term inflammatory burden can be reversed by weight loss. Although current waist circumference is an important contributor to risk of elevated systemic inflammation in this as in other populations, history of central adiposity may be an independent phenomenon. Am. J. Hum. Biol. 2010. © 2009 Wiley-Liss, Inc. [source] | ||||||||||