Immunoparalysis: Clinical and immunological associations in SIRS and severe sepsis patients

Επιστημονική δημοσίευση - Άρθρο Περιοδικού uoadl:3003655 42 Αναγνώσεις

Μονάδα:
Ερευνητικό υλικό ΕΚΠΑ
Τίτλος:
Immunoparalysis: Clinical and immunological associations in SIRS and severe sepsis patients
Γλώσσες Τεκμηρίου:
Αγγλικά
Περίληψη:
Introduction This study was designed to identify changes in the monocytic membrane marker HLA-DR and heat shock proteins (HSPs) in relation to T-regulatory cells (T-regs) and other immunological marker changes in patients with systemic inflammatory response syndrome (SIRS) or sepsis/septic shock. Methods Healthy volunteers, intensive care unit (ICU) patients with SIRS due to head injury and ICU patients with severe sepsis/septic shock were enrolled in the current study. Determination of CD14+/HLA-DR+ cells, intracellular heat-shock proteins and other immunological parameters were performed by flow cytometry and RT-PCR techniques as appropriate. Univariate and multivariate analysis examined associations of CD14/HLA-DR, HSPs, T-regs and suppressor of cytokine signalling (SOCS) proteins with SIRS, sepsis and outcome. Results Fifty patients (37 with severe sepsis and 13 with SIRS) were enrolled, together with 20 healthy volunteers used as a control group. Compared to healthy individuals, patients with SIRS and severe sepsis showed progressive decline of their CD14/HLA-DR expression (0% to 7.7% to 50% within each study subpopulation, p < 0.001). Mean fluorescent intensity (MFI) levels of HSP70 and HSP90 on monocytes and polymorphonuclear cells were significantly higher in SIRS patients compared to controls and fell significantly in severe sepsis/septic shock patients (p < 0.05 for all comparisons). There was no statistically significant difference between subgroups for levels of T-regulatory cells or relative copies of Suppressor of Cytokine Signalling 3 (SOCS3) proteins. In univariate models percent of CD14/HLA-DR was associated with mortality (OR: 1.8 95%CI 1.02–3.2, p = 0.05), while in multivariate models after adjusting for CD14/HLA-DR only younger age and lower Acute Physiology and Chronic Health Evaluation II (APACHE II) scores were associated with increased chances of survival (beta −0.05, OR 0.9, 95% CI 0.9–0.99, p = 0.038 for age and beta −0.11, OR 0.89, 95% CI 0.8–0.99, p = 0.037 for APACHE II score). Conclusions Significant associations with SIRS and sepsis were found for CD14/HLA-DR expression and monocyte and polymorphonuclear cell levels of HSP70 and 90. The role of these biomarkers in assessing the prognosis of sepsis needs to be further explored and validated in prospective studies. © 2017 Elsevier Ltd
Έτος δημοσίευσης:
2017
Συγγραφείς:
Papadopoulos, P.
Pistiki, A.
Theodorakopoulou, M.
Christodoulopoulou, T.
Damoraki, G.
Goukos, D.
Briassouli, E.
Dimopoulou, I.
Armaganidis, A.
Nanas, S.
Briassoulis, G.
Tsiodras, S.
Περιοδικό:
Cytokine
Εκδότης:
INSTAP Academic Press
Τόμος:
92
Σελίδες:
83-92
Λέξεις-κλειδιά:
CD14 antigen; heat shock protein 70; heat shock protein 90; HLA DR antigen; interleukin 10; interleukin 17; lactate dehydrogenase; suppressor of cytokine signaling; heat shock protein 70; heat shock protein 90; HLA DR antigen; lipopolysaccharide receptor; SOCS3 protein, human; suppressor of cytokine signaling 3, adult; Article; clinical article; controlled study; disease severity; female; head injury; human; immune response; intensive care unit; lactate dehydrogenase blood level; lower respiratory tract infection; male; monocyte; phosphate blood level; polymorphonuclear cell; protein blood level; protein expression; regulatory T lymphocyte; sepsis; systemic inflammatory response syndrome; aged; disease free survival; immunology; middle aged; mortality; pathology; septic shock; survival rate, Aged; Disease-Free Survival; Female; HLA-DR Antigens; HSP70 Heat-Shock Proteins; HSP90 Heat-Shock Proteins; Humans; Lipopolysaccharide Receptors; Male; Middle Aged; Monocytes; Shock, Septic; Suppressor of Cytokine Signaling 3 Protein; Survival Rate; T-Lymphocytes, Regulatory
Επίσημο URL (Εκδότης):
DOI:
10.1016/j.cyto.2017.01.012
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