Serum Lipopolysaccharide-Binding Protein is Associated with Chronic Inflammation and Metabolic Syndrome in Hemodialysis Patients

Abstract

Background: In hemodialysis (HD) patients, impaired gut barrier and alteration in microbiota in the gut is thought to increase the risk of bacterial translocation and chronic inflammation. Lipopolysaccharide-binding protein (LBP) is an acute-phase reactant that mediates immune responses triggered by microbial products. Our aim is to investigate the relationship between circulating levels of LBP, and various metabolic and inflammatory markers in HD patients. Besides, we also aim to determine its relationship among ­patients with different body mass index. Patients and Methods: A total of 123 HD patients were stratified into three ­tertiles, according to serum LBP level. The LBP and inflammatory markers were determined using immunoassay methods. A bioimpedance spectroscopy device was used for body composition measurement. Results: The serum levels of the two proinflammatory markers, high-sensitivity C-reactive protein (hsCRP) and interleukin (IL)-6, were significantly higher in patients in the upper tertile when compared with the rest of the tertiles. In HD patients, a significant positive correlation was found between serum LBP levels and CRP, IL-6, soluble CD14 (sCD14), and fasting blood glucose levels. Patients with metabolic syndrome and pre-existing cardiovascular disease had higher LBP levels than those without metabolic syndrome. Besides, obese patients were also associated with higher serum LBP levels. Multivariate regression analyses showed that IL-6 level was the strongest correlate of LBP level, followed by hsCRP level and sCD14. Conclusions: Our study suggested that elevated plasma LBP was associated with metabolic syndrome and obesity. In addition, increased LBP level was correlated positively to markers of inflammation, and sCD14 levels.

Glycosylation deficiency of lipopolysaccharide-binding protein and corticosteroid-binding globulin associated with activity and response to treatment for rheumatoid arthritis

“…This is in agreement with previous studies which proposed LBP as a sensitive serum biomarker to evaluate RA course in active RA patients, considering that LBP was significantly correlated with RA disease activity parameters [28][29][30]. Concerning its post translational modification, LBP hold four known sites of N-glycosylation whose function remains unexplained [66,73]. We observed in ERA a significant decrease of glycosylated LBP level compared to controls, which was, as observed for CBG, reverted after 12 months-period of treatment.…”

“…LBP is an acute-phase protein which binds LPS, a glycolipid present on the membrane of Gram-negative bacteria. Therefore, LBP appears to be directly involved in the recognition of pathogenic bacteria, delivers endotoxin and enhances LPS-mediated cytokine induction [66,67]. Indeed, the complex between LPS and LBP binds to CD14 receptor promoting the production of cytokines through the activation of TLR4 signalling [68,69].…”

Serum sCD14, PGLYRP2 and FGA as potential biomarkers for multidrug‐resistant tuberculosis based on data‐independent acquisition and targeted proteomics

“…Based on the interaction and correlation analysis, we discovered the possible pro‐inflammatory effects of MTB proteins on the body and weakened host's protective immune response against MTB. There was a positive correlation between the protein abundance of sCD14 and LBP, which has been observed in chronic inflammation patients as well 29 . The sCD14 abundance also showed a low‐positive correlation to restriction endonuclease S subunit.…”

“…There was a positive correlation between the protein abundance of sCD14 and LBP, which has been observed in chronic inflammation patients as well. 29 The sCD14 abundance also showed a low-positive correlation to restriction endonuclease S subunit. Compared with the DS-TB group, the abundance of restriction endonuclease S subunit tended to be up-regulated in the MDR-TB group, indicating that the virulent MTB complex could strongly resist the host immune response during infection.…”

From Farm to Pharmacy: Strawberry-Enabled Oral Delivery of Protein Drugs

“…In each case, we compared several intestinal and systemic health outcomes in pelargonidin-treated subjects to control animals receiving saline gavages (17). Treated mice did not lose weight during the study (Fig 5i) nor did they experience elevated blood levels of the intestinal inflammation markers lipopolysaccharide binding protein (33) (LBP, Fig 5j), intestinal fatty acid binding protein (34,35) (I-FABP, Fig 5k), or procalcitonin (35) (PCT, Fig 5l). Further, gene expression analysis of mice's small intestinal epithelia revealed no significant changes in the expression of the pore-forming tight junction protein Claudin 2 (8) (CLDN2, Fig 5m) or the barrier-forming proteins Claudin 3 (CLDN3, Fig 5n), Zonula Occludens 1 (ZO-1, Fig 5p) (36).…”