title: Clinical evaluation of proinflammatory cytokine inhibitors (sTNFR I, sTNFR II, IL-1 ra), anti-inflammatory cytokines (IL-10, IL-13) and activation of neutrophils after burn-induced inflammation.
abstract: The study was aimed at evaluating the involvement of sTNFR I, sTNFR II, IL-1 ra, IL-10, IL-13 and reactive oxygen species (ROS) in systemic inflammatory response syndrome (SIRS) development in severely burned children and at assessing the prognostic value of the immunological markers studied. The study comprised 37 patients (17 burned children and 20 controls). Serum levels of the markers determined by means of ELISA and respiratory burst of neutrophils as well as p55 and p75 tumour necrosis factor-alpha (TNF-alpha) receptor expression using flow cytometry were evaluated twice. The burned children presented significantly higher levels of IL-10 and cytokine inhibitors within the first 6-24 h after injury compared with controls (P < 0.05). The decreased oxygen metabolism of neutrophils and increased TNF-alpha receptor expression were found on admission. Moreover, a significant decrease in initially high sTNFR I, sTNFR II, IL-1 ra, IL-10, IL-13 concentrations (P < 0.05) and reduced expression of TNF-alpha receptors (P < 0.05) were observed after burn therapy, whereas ROS generation evidently augmented (P < 0.05). Four of our children who developed hypovolaemic shock revealed a significantly lower ROS generation and higher concentrations of soluble TNF-alpha receptors and IL-1 ra together with IL-10, IL-13 compared with children with good outcome (P < 0.05). Our results revealed the involvement of both ROS, soluble TNF-alpha receptors and IL-1 ra in the development of SIRS in burned children; their monitoring allows for an assessment of the systemic inflammatory reaction activity. The neutrophil BURSTTEST and IL-1 ra might have been clinically helpful markers of SIRS prognosis.
authors.affiliation: Department of Paediatric Propaedeutics and Bone Metabolic Diseases, Medical University of Łódź, University Clinical Hospital No. 4, Łódź, Poland. jpsikoraster@gmail.com
authors.forename: J P
authors.initials: JP
authors.lastname: Sikora
authors.forename: D
authors.initials: D
authors.lastname: Chlebna-Sokół
authors.forename: E
authors.initials: E
authors.lastname: Andrzejewska
authors.forename: S
authors.initials: S
authors.lastname: Chrul
authors.forename: E
authors.initials: E
authors.lastname: Polakowska
authors.forename: A
authors.initials: A
authors.lastname: Wysocka
authors.forename: A
authors.initials: A
authors.lastname: Sikora
mesh_terms: D015415:Biomarkers / Q000097:blood*; D002056:Burns / Q000097:blood* / Q000150:complications / Q000276:immunology; D002648:Child; D002675:Child, Preschool; D016207:Cytokines / Q000097:blood*; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D005434:Flow Cytometry; D006801:Humans; D007223:Infant; D007249:Inflammation / Q000097:blood / Q000209:etiology / Q000276:immunology; D016753:Interleukin-10; D018793:Interleukin-13; D008297:Male; D009504:Neutrophils / Q000378:metabolism*; D011379:Prognosis; D017382:Reactive Oxygen Species / Q000378:metabolism; D018124:Receptors, Tumor Necrosis Factor / Q000097:blood; D018746:Systemic Inflammatory Response Syndrome / Q000097:blood* / Q000209:etiology / Q000503:physiopathology
chemical_list: D015415:Biomarkers; D016207:Cytokines; D018793:Interleukin-13; D017382:Reactive Oxygen Species; D018124:Receptors, Tumor Necrosis Factor; D016753:Interleukin-10