Simona Mera 1, Doina Ţăţulescu 1, Cristina Cismaru 1, Adriana Slavcovici 1, Virginia Zanc 1, Mirela Flonta 2, D. Cârstina 1
1 Iuliu Haţieganu University of Medicine and Pharmacy, Cluj-Napoca, Romania Clinic of Infectious Diseases, Cluj-Napoca, Romania
Abstract
Aim. Priming and modulation of the immune response in severe infections are driven by bacterial products and endogenous mediators, such as cytokines. We analyzed several proinfl ammatory cytokines in the early sepsis and studied their correlation with aetiology and severity. Methods. In 24 septic patients we analyzed serum levels of IL-6, TNF-alpha, IL-12 and IFN-gamma in the early sepsis. 14 healthy volunteers served as controls. Results. IL-12 and IFN-gamma were undetectable both in controls and patients. Septic patients had a median TNF-alpha concentration of 6 pg/ml at admission that decreased at the following time-points. In controls, TNF-alpha was undetectable. In patients, IL-6 reached a median of 78 pg/ml at admission and diminished subsequently. Patients with severe sepsis had the highest IL-6 levels. TNF-alpha showed similar levels and kinetics for urinary and respiratory sepsis, yet in respiratory sepsis IL-6 increased more prominently. Gram positive sepsis led to higher amounts of TNF-alpha and IL-6 than Gram negative sepsis. Two out of fi ve non-survivors had very high IL-6 at admission that did not follow the later descendent trend. Conclusions. Since we did not detect circulating levels of IL-12 and IFN-gamma, it appears that sepsis does not to elicit an adaptive immune response in its early phases. Th e low levels of TNF-alpha may be due to the short half-life of the molecule. IL-6 release might be infl uenced by the site of infection and aetiology, and it could serve as a potential parameter in monitoring septic patients.