Regulation by Anti-inflammatory Cytokines (IL-4, IL-10, IL-13, TGFbeta)of Interleukin-8 Production by LPS- And/ or TNFalpha-activated Human Polymorphonuclear Cells

Overview

Journal Mediators Inflamm

Publisher Wiley

Specialties Biochemistry
Pathology

Date 1996 Jan 1

PMID 18475727

Citations 31

Authors

C Marie

C Pitton

C Fitting

J M Cavaillon

Affiliations

Soon will be listed here.

Abstract

The capacity to down-regulate the production of IL-8 by LPS-activated human polymorphonuclear cells (PMN) has been demonstrated for IL-4, IL-10, and TGFbeta. We compared their relative capacities and further extended this property to IL-13. We report a great heterogeneity among individuals related to the responsiveness of PMN to the IL-4 and IL-13 inhibitory effects while their response to the IL-10 effect was homogenous. The inhibitory activities were observed at the transcriptional level. IL-8 induction by TNFalpha was, unlike its induction by LPS, resistant to the inhibitory effects of IL-10, IL-4, IL-13 and TGFbeta. Furthermore, IL-10 and IL-4 inhibitory activity were less effective when TNFalpha was acting synergistically with LPS to induce IL-8 production by PMN. LPS-induced cell-associated IL-8, detected in the PMN cultures, could be marginally inhibited by IL-4 and IL-10. Altogether, our data demonstrate that IL-13 is able to inhibit LPS-induced IL-8 production by human PMN, although IL-10 remains the most active anti-inflammatory cytokine. Despite the capacity of IL-4, IL-10, and IL-13 to limit the production of TNFalpha-induced IL-8 in a whole blood assay, none was able to inhibit this production when studying isolated human polymorphonuclear cells.

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