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Dissecting Innate Immune Signaling in Viral Evasion of Cytokine Production
08:32

Dissecting Innate Immune Signaling in Viral Evasion of Cytokine Production

Published on: March 2, 2014

MAPK signaling contributes to rotaviral-induced cholangiocyte injury and viral replication

Mubeen Jafri1, Bryan Donnelly, Monica McNeal

  • 1Department of Pediatric and Thoracic Surgery, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio, USA.

Surgery
|August 11, 2007
PubMed
Abstract

Insights

Rhesus rotavirus (RRV) infection activates Mitogen Associated Protein Kinase (MAPK) signaling in bile duct cells. Inhibiting p38 and ERK 1/2 pathways reduced viral replication and cell damage, offering insights into biliary atresia.

Area of Science:

  • Hepatology and Virology
  • Cellular Signaling Pathways

Background:

  • Biliary atresia is a neonatal disease causing bile duct obliteration.
  • Rhesus rotavirus (RRV) infection in mice models human biliary atresia.
  • Mitogen Associated Protein Kinase (MAPK) pathways are activated by viral infections.

Purpose of the Study:

  • To investigate the role of MAPK signaling in RRV-induced cholangiopathy.
  • To determine if RRV infection activates MAPK signaling in cholangiocytes.

Main Methods:

  • Analyzed MAPK phosphorylation (p38, ERK 1/2, JNK 1/2) in RRV-infected mice and cholangiocytes via Western blots.
  • Utilized MAPK inhibitors to assess pathway activity.
  • Evaluated viral replication and cytolysis post-MAPK inhibition.

Main Results:

  • RRV infection significantly increased MAPK phosphorylation in both mice and cholangiocytes.
  • Inhibition of p38 and ERK 1/2 pathways reduced viral replication.
  • ERK 1/2 inhibition decreased cholangiocyte cytolysis without impacting viral entry.

Conclusions:

  • RRV infection activates MAPK signaling in cholangiocytes.
  • Targeting p38 and ERK 1/2 pathways impacts rotavirus replication.
  • Findings elucidate signaling pathways in RRV-induced biliary injury.

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