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Proinflammatory effects of pancreatic elastase are mediated through TLR4 and NF-kappaB.

Abstract：

:Pancreatic elastase has been implicated in the pathophysiology of severe acute pancreatitis, characterized by systemic inflammatory response, distant organ failure, and high mortality. Here we show that pancreatic elastase activates transcription factors NF-kappaB, AP-1, and NFAT in human myeloid cells (U-937 and THP-1) in culture. Pancreatic elastase also induces TNF-alpha secretion and increased expression of CD11b in THP-1 cells which can be inhibited by neutralizing anti-Toll-like receptor 4 (TLR4) antibodies. NF-kappaB blocking agents (MG-132, PGA1) prevented elastase-induced TNF-alpha secretion from THP-1 cells. Our results suggest that pancreatic elastase-induced proinflammatory effects are mediated by TLR4 and NF-kappaB in human myeloid cells.

journal_name

Biochem Biophys Res Commun

journal_title

Biochemical and biophysical research communications

authors

Hietaranta A,Mustonen H,Puolakkainen P,Haapiainen R,Kemppainen E

doi

10.1016/j.bbrc.2004.08.077

subject

Has Abstract

pub_date

2004-10-08 00:00:00

pages

192-6

issue

1

eissn

0006-291X

issn

1090-2104

pii

S0006-291X(04)01827-3

journal_volume

323

pub_type

杂志文章

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