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

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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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Correspondence to Yao-zong Yuan.

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Huang, Ly., Chen, P., Xu, Lx. et al. Fractalkine Upregulates Inflammation through CX3CR1 and the Jak–Stat Pathway in Severe Acute Pancreatitis Rat Model. Inflammation 35, 1023–1030 (2012). https://doi.org/10.1007/s10753-011-9406-5

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