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Impaired Stat3 activation following localized inflammatory stimulus in IL-6-deficient mice.

Abstract：

:Interleukin 6 (IL-6) and related gp130-signalling cytokines rapidly activate latent cytoplasmic Stat transcription factors and these are believed to play pivotal roles in the expression of downstream cytokine-responsive genes. We have previously shown in IL-6-deficient (-/-) mice that IL-6 is absolutely required for the transcriptional induction of acute phase response (APR) genes in the liver following localized tissue damage caused by subcutaneous injection of turpentine oil, but is not required when the inflammatory stimulus is administered systemically by intraperitoneal injection of bacterial lipopolysaccharide (LPS). In this paper we show that Stat3 is the only Stat factor induced in liver tissue upon localized inflammatory stimuli, and that its activation is virtually absent in IL-6 deficient mice. During LPS-induced inflammation both Stat1 and Stat3 are activated, and only minor kinetic alterations are detected in IL-6-/- mice. These defects are not due to altered intracellular signal transduction, since they could be complemented by injection of recombinant cytokines. These results establish a direct causal relationship in vivo between Stat activation and acute phase gene expression and define unique functions of IL-6 in Stat3 activation upon localized inflammation.

journal_name

Cytokine

journal_title

Cytokine

authors

Alonzi T,Fattori E,Cappelletti M,Ciliberto G,Poli V

doi

10.1006/cyto.1997.0250

subject

Has Abstract

pub_date

1998-01-01 00:00:00

pages

13-8

issue

1

eissn

1043-4666

issn

1096-0023

pii

S1043-4666(97)90250-7

journal_volume

10

pub_type

杂志文章

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