Anti-inflammatory response of IL-4, IL-10 and TGF-beta in patients with systemic inflammatory response syndrome

Citation
D. Torre et al., Anti-inflammatory response of IL-4, IL-10 and TGF-beta in patients with systemic inflammatory response syndrome, MEDIAT INFL, 9(3-4), 2000, pp. 193-195
Citations number
11
Categorie Soggetti
Immunology
Journal title
MEDIATORS OF INFLAMMATION
ISSN journal
09629351 → ACNP
Volume
9
Issue
3-4
Year of publication
2000
Pages
193 - 195
Database
ISI
SICI code
0962-9351(2000)9:3-4<193:AROIIA>2.0.ZU;2-4
Abstract
THE systemic inflammatory response syndrome (SIRS) is an inflammatory proce ss seen in association with a large number of clinical infective and noninf ective conditions. The aim of this study was to investigate the role of anti-inflammatory cyto kines such as interleukin-4 (IL-4), interleukin-10 (IL-10), and transformin g growth factor-beta (TGF-beta). Serum levels of IL-4, IL-10 and TGF-beta w ere determined in 45 patients with SIRS: 38 patients had SIRS of infectious origin, whereas seven patients had non-infectious SIRS. Twenty healthy sub jects were used as controls. Serum levels of IL-4, IL-10 and TGF-beta were determined by an immunoenzyme assay. A significant increase of IL-4 was observed in these patients at th e time of diagnosis and 5 days later. In contrast, serum levels of IL-10 we re not increased at the time of diagnosis, but as light decrease was noted after 5 days. Serum levels of TGF-beta were not increased at time of diagno sis, and a slight increase was observed after 5 days. Serum levels of IL-4 were significantly higher in patients with infectious SIRS at the time of d iagnosis, whereas no significant difference between infectious and non-infe ctious SIRS was noted for serum levels of IL-10 and TGF-beta at the time of diagnosis and 5 days later. During SIRS, serum levels of IL-4 were significantly increased with a signi ficant correlation between IL-4 and mortality, and only levels of IL-4 were significantly increased in the SIRS caused by infectious stimuli.