Journal
CELLULAR IMMUNOLOGY
Volume 273, Issue 1, Pages 41-51Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.cellimm.2011.11.008
Keywords
Type I interferon; Listeria monocytogenes; Neutrophils; Monocytes; Chemokines; Cellular recruitment; Type I interferon signaling; Bacterial infection; Inflammatory infiltrate; Neutrophil recruitment
Categories
Funding
- US Public Health Service [R01AI057770, K08 GM083154]
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Type I IFN is key to the immune response to viral pathogens, however its role in bacterial infections is less well understood. Mice lacking the type I IFN receptor (IFNAR-/-) demonstrate enhanced resistance to infection with Listeria monocytogenes. We have now determined that following infection with Listeria, the composition of innate cells recruited to the peritoneal cavity of IFNAR-/- mice reflects an increase in the frequency of neutrophils and a decrease in monocyte frequency compared to WT controls. These differences in inflammatory infiltrates could not be attributed to distinct bone marrow composition prior to infection or to level of apoptosis. We also observed no differences in neutrophil oxidative burst. However, blocking CXCR2 prevented enhanced neutrophil influx and hampered bacterial clearance. Taken together, these studies highlight a novel mechanism by which type I interferon signaling regulates the immune response to Listeria, through negative regulation of chemokines driving neutrophil recruitment. (C) 2011 Elsevier Inc. All rights reserved.
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