Fas activity mediates airway inflammation during mouse adenovirus type 1 respiratory infection

Virology. 2018 Aug:521:129-137. doi: 10.1016/j.virol.2018.06.002. Epub 2018 Jun 13.

Abstract

CD8 T cells play a key role in clearance of mouse adenovirus type 1 (MAV-1) from the lung and contribute to virus-induced airway inflammation. We tested the hypothesis that interactions between Fas ligand (FasL) and Fas mediate the antiviral and proinflammatory effects of CD8 T cells. FasL and Fas expression were increased in the lungs of C57BL/6 (B6) mice during MAV-1 respiratory infection. Viral replication and weight loss were similar in B6 and Fas-deficient (lpr) mice. Histological evidence of pulmonary inflammation was similar in B6 and lpr mice, but lung mRNA levels and airway proinflammatory cytokine concentrations were lower in MAV-1-infected lpr mice compared to infected B6 mice. Virus-induced apoptosis in lungs was not affected by Fas deficiency. Our results suggest that the proinflammatory effects of CD8 T cells during MAV-1 infection are mediated in part by Fas activation and are distinct from CD8 T cell antiviral functions.

Keywords: Adenovirus; CD8 T cells; Fas; Respiratory infection.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adenoviridae Infections / physiopathology*
  • Animals
  • CD8-Positive T-Lymphocytes / immunology*
  • Cytokines / biosynthesis
  • Disease Models, Animal
  • Fas Ligand Protein / metabolism
  • Gene Expression Profiling
  • Histocytochemistry
  • Immunohistochemistry
  • Inflammation / physiopathology*
  • Lung / pathology
  • Mice
  • Mice, Inbred C57BL
  • RNA, Messenger / analysis
  • Real-Time Polymerase Chain Reaction
  • Respiratory Tract Infections / physiopathology*
  • Viral Load
  • fas Receptor / deficiency
  • fas Receptor / metabolism*

Substances

  • Cytokines
  • Fas Ligand Protein
  • Fas protein, mouse
  • Fasl protein, mouse
  • RNA, Messenger
  • fas Receptor