LPS induces IL-10 production by human alveolar macrophages via MAPKinases- and Sp1-dependent mechanisms.

Abstract:

BACKGROUND:IL-10 is a cytokine mainly produced by macrophages that plays key roles in tolerance to inhaled antigens and in lung homeostasis. Its regulation in alveolar macrophages (HAM), the resident lung phagocytes, remains however unknown. METHODS:The present study investigated the role of intracellular signalling and transcription factors controlling the production of IL-10 in LPS-activated HAM from normal nonsmoking volunteers. RESULTS:LPS (1-1000 pg/ml) induced in vitro IL-10 production by HAM, both at mRNA and protein levels. LPS also activated the phosphorylation of ERK, p38 and JNK MAPkinases (immunoblots) and Sp-1 nuclear activity (EMSA). Selective inhibitors of MAPKinases (respectively PD98059, SB203580 and SP600125) and of Sp-1 signaling (mithramycin) decreased IL-10 expression in HAM. In addition, whilst not affecting IL-10 mRNA degradation, the three MAPKinase inhibitors completely abolished Sp-1 activation by LPS in HAM. CONCLUSION:These results demonstrate for the first time that expression of IL-10 in lung macrophages stimulated by LPS depends on the concomitant activation of ERK, p38 and JNK MAPKinases, which control downstream signalling to Sp-1 transcription factor. This study further points to Sp-1 as a key signalling pathway for IL-10 expression in the lung.

journal_name

Respir Res

journal_title

Respiratory research

authors

Chanteux H,Guisset AC,Pilette C,Sibille Y

doi

10.1186/1465-9921-8-71

subject

Has Abstract

pub_date

2007-10-04 00:00:00

pages

71

eissn

1465-9921

issn

1465-993X

pii

1465-9921-8-71

journal_volume

8

pub_type

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