The international surgical journal with global reach

This is the Scientific Surgery Archive, which contains all randomized clinical trials in surgery that have been identified by searching the top 50 English language medical journal issues since January 1998. Compiled by Jonothan J. Earnshaw, former Editor-in-Chief, BJS

Interleukin 13 and inflammatory markers in human sepsis. BJS 2004; 91: 762-768.

Published: 22nd March 2004

Authors: N. Collighan, P. V. Giannoudis, O. Kourgeraki, S. L. Perry, P. J. Guillou, M. C. Bellamy et al.

Background

Interleukin (IL) 13 is an anti‐inflammatory cytokine that reduces inflammatory cytokine production, and enhances monocyte survival and MHC class II and CD23 expression. The only report of IL‐13 in human sepsis noted no increase in IL‐13 concentration, in contrast to animal data. This study further examined the expression of IL‐13 in relation to human sepsis.

Method

In a prospective observational study of 31 patients (24 men) with sepsis or septic shock, high‐sensitivity enzyme‐linked immunoabsorbent assay (ELISA) was used to quantify levels of tumour necrosis factor (TNF) α on admission, and on days 1, 3, 5 and 7 thereafter. IL‐13 and IL‐2 were assayed by standard ELISA, and HLA‐DR on CD14‐positive monocytes was measured by flow cytometry.

Results

Twenty‐three patients developed septic shock. Monocyte HLA‐DR levels showed greater depression and a slower recovery in shocked than non‐shocked patients. The serum IL‐13 concentration was significantly higher in the shocked group from admission to day 3, but subsequently decreased to levels similar to those in the non‐shocked group. IL‐13 concentrations were higher in non‐survivors. The TNF‐α concentration was higher in those with septic shock than in those without. The TNF‐α level correlated with IL‐13 concentration (rS = 0·61, P = 0·002). The IL‐13/TNF‐α ratio was greater in patients with shock than those with sepsis only (P = 0·017). IL‐2 was undetectable.

Conclusion

In human sepsis and septic shock, IL‐13 correlated with TNF‐α expression, but its effect on HLA‐DR class II molecules remains unclear. Copyright © 2004 British Journal of Surgery Society Ltd. Published by John Wiley & Sons, Ltd.

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