Interleukin-10 controls human peripheral PMN activation triggered by lipopolysaccharide.

Abstract:

:Large amounts of anti-inflammatory mediators, such as interleukin (IL)-10, are produced and found early in the course of sepsis. We explore the role of IL-10 on neutrophil (PMN) activation/function using an in vitro model. Isolated human PMN were pre-incubated with lipopolysaccharide (LPS) and/or IL-10 for 18h. Subsequently, a second LPS exposure was performed and CD11b and CD66b up-regulation, and the reactive oxygen species (ROS) generation were measured 2h later. We found that IL-10 prevented PMN activation and the secretion of TNF-α and IL-8 induced by the first LPS contact. In the absence of IL-10, a second LPS exposure induced additive effects that were prevented by IL-10. Only ROS generation was highly affected by the blockade of PMN-secreted TNF-α or IL-8. Additionally, IL-10 prevented other possible mechanisms of LPS priming. Therefore, IL-10 modulates PMN activation preventing autocrine activating loops and priming mechanisms, rendering PMN less responsive to a second LPS exposure.

journal_name

Cytokine

journal_title

Cytokine

authors

Martire-Greco D,Rodriguez-Rodrigues N,Landoni VI,Rearte B,Isturiz MA,Fernández GC

doi

10.1016/j.cyto.2013.03.025

subject

Has Abstract

pub_date

2013-06-01 00:00:00

pages

426-32

issue

3

eissn

1043-4666

issn

1096-0023

pii

S1043-4666(13)00144-0

journal_volume

62

pub_type

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