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Mediators of Inflammation
Volume 2018, Article ID 7028267, 11 pages
https://doi.org/10.1155/2018/7028267
Research Article

Selected Biomarkers Correlate with the Origin and Severity of Sepsis

1Department of Infectious Diseases, First Faculty of Medicine, Charles University and Military University Hospital Prague, U Vojenské nemocnice 1200, 169 02 Praha 6, Czech Republic
2Department of Infectious Diseases, Third Faculty of Medicine, Charles University and Na Bulovce Hospital, Budínova 2, 180 81 Praha 8, Czech Republic
3Department of Anesthesiology and Intensive Care Medicine, University Hospital of Ostrava, 17. listopadu, 708 52 Ostrava, Czech Republic
4Department of Clinical Sciences, Division of Infection Medicine, Lund University, Sölvegatan 19, 221 00 Lund, Sweden

Correspondence should be addressed to Ondřej Beran; zc.inuc.1fl@nareb.jerdno

Received 22 December 2017; Accepted 14 February 2018; Published 27 March 2018

Academic Editor: Maja Surbatovic

Copyright © 2018 Michal Holub et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

The microbial etiology and source of sepsis influence the inflammatory response. Therefore, the plasma levels of cytokines (IL-6, IL-8, and IL-10), chemokines (CCL2/MCP-1, MIP-1β), heparin-binding protein (HBP), soluble CD14 (sCD14), and cortisol were analyzed in blood from septic patients obtained during the first 96 hours of intensive care unit hospitalization. The etiology was established in 56 out of a total of 62 patients enrolled in the study. Plasma concentrations of MCP-1, sCD14, IL-6, and IL-10 were significantly higher in patients with community-acquired pneumonia (CAP; ) and infective endocarditis (IE; ) compared to those with bacterial meningitis (BM; ). Next, cortisol levels were higher in IE patients than in those with BM and CAP, and at one time point, cortisol was also higher in patients with gram-negative sepsis when compared to those with gram-positive infections. Furthermore, cortisol and MCP-1 levels correlated positively with the daily measured SOFA score. In addition, HBP levels were significantly higher in patients with IE than in those with BM. Our findings suggest that MCP-1, sCD14, IL-6, IL-10, cortisol, and HBP are modulated by the source of sepsis and that elevated MCP-1 and cortisol plasma levels are associated with sepsis-induced organ dysfunction.