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Published in: Inflammation 3/2012

01-06-2012

Fractalkine Upregulates Inflammation through CX3CR1 and the Jak–Stat Pathway in Severe Acute Pancreatitis Rat Model

Authors: Li-ya Huang, Ping Chen, Ling-xiao Xu, Yu-fen Zhou, Yong-ping Zhang, Yao-zong Yuan

Published in: Inflammation | Issue 3/2012

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Abstract

Based on the function of chemokine fractalkine (FKN), acting as both adhesion and chemoattractant, FKN plays a role in acute inflammatory response. In this study, we investigated the mechanism of FKN mediated upregulation inflammation in severe acute pancreatitis (SAP) rat models. Western blot, reverse transcriptase-polymerase chain reaction, and immunofluorescence demonstrated that FKN and its receptor CX3CR1 were overexpressed in cerulein-stimulated AR42J cells. AG490 and FKN-siRNA inhibited activation of Janus kinase/signal transducers and activators of transcription (Jak/Stat) in cerulein-stimulated AR42J cells. Following exposure AG490 and FKN-siRNA inhibited tumor necrosis factor-alpha expression by enzyme-linked immunosorbent assay and immunohistochemistry in vivo the SAP rat models. These results showed FKN and CX3CR1 were involved inflammatory response in cerulein-stimulated AR42J cells. FKN upregulates inflammation through CX3CR1 and the Jak/Stat pathway in SAP rat models.
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Metadata
Title
Fractalkine Upregulates Inflammation through CX3CR1 and the Jak–Stat Pathway in Severe Acute Pancreatitis Rat Model
Authors
Li-ya Huang
Ping Chen
Ling-xiao Xu
Yu-fen Zhou
Yong-ping Zhang
Yao-zong Yuan
Publication date
01-06-2012
Publisher
Springer US
Published in
Inflammation / Issue 3/2012
Print ISSN: 0360-3997
Electronic ISSN: 1573-2576
DOI
https://doi.org/10.1007/s10753-011-9406-5

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