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

Donato Torre,Agostino Pugliese,Carla Cantamessa,Giovanna Gavazzeni,Gilberto Biondi,Roberto Tambini,Silvana Aristodemo,Antonio Goglio

doi:10.1080/09629350020002912

Abstract

The systemic inflammatory response syndrome (SIRS) is an inflammatory process seen in association with a large number of clinical infective and non-infective conditions. The aim of this study was to investigate the role of anti-inflammatory cytokines such as interleukin-4 (IL-4), interleukin-10 (IL-10), and transforming growth factor-beta (TGF-beta). Serum levels of IL-4, IL-10 and TGF-beta were determined in 45 patients with SIRS: 38 patients had SIRS of infectious origin, whereas seven patients had non-infectious SIRS. Twenty healthy subjects 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 the time of diagnosis and 5 days later. In contrast, serum levels of IL-10 were not increased at the time of diagnosis, but a slight decrease was noted after 5 days. Serum levels of TGF-beta were not increased at time of diagnosis, 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 diagnosis, whereas no significant difference between infectious and non-infectious 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 significant correlation between IL-4 and mortality, and only levels of IL-4 were significantly increased in the SIRS caused by infectious stimuli.

Highlights

The systemic inflammatory response syndrome (SIRS) is an inflammatory process seen in association with a number of clinical infective and non-infective conditions.[1]
It is well known that in terleukin –4 (IL–4), in terleukin –10 (IL–10) and transforming growth factor b (TGF-b) are considered anti-inflammatory cytokines because, when administered to animals with infection or inflammation, they reduce the severity of disease and reduce the production of IL–1 and tumour necrosis factor (TNF).[7]
Serum levels of IL–4, IL–10 and TGF-b were determined in patients with infectious or non-infectious SIRS

Summary

Introduction

The systemic inflammatory response syndrome (SIRS) is an inflammatory process seen in association with a number of clinical infective and non-infective conditions.[1]. Acute-phase response is initiated by tumour necrosis factor (TNF), Il–1, and the IL–8 family, which are grouped together and called proinflammatory cytokines.[6] Successively, acute-phase response is controlled by a simultaneous decrease in proinflammatory mediators and release of endogenous antagonists. It is well known that IL–4, IL–10 and transforming growth factor b (TGF-b) are considered anti-inflammatory cytokines because, when administered to animals with infection or inflammation, they reduce the severity of disease and reduce the production of IL–1 and TNF.[7]

Methods

Results

Conclusion