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PLoS One. 2014 Mar 7;9(3):e90720. doi: 10.1371/journal.pone.0090720. eCollection 2014.

Depletion of alveolar macrophages ameliorates virus-induced disease following a pulmonary coronavirus infection.

Author information

1
Department of Microbiology, University of Iowa, Iowa City, Iowa, United States of America.
2
Department of Microbiology, University of Iowa, Iowa City, Iowa, United States of America; Interdisciplinary Graduate Program in Immunology, University of Iowa, Iowa City, Iowa, United States of America; Department of Pathology, University of Iowa, Iowa City, Iowa, United States of America.

Abstract

Coronaviruses cause respiratory disease in humans that can range from mild to severe. However, the pathogenesis of pulmonary coronavirus infections is poorly understood. Mouse hepatitis virus type 1 (MHV-1) is a group 2 coronavirus capable of causing severe morbidity and mortality in highly susceptible C3H/HeJ mice. We have previously shown that both CD4 and CD8 T cells play a critical role in mediating MHV-1-induced disease. Here we evaluated the role of alveolar macrophages (AM) in modulating the adaptive immune response and subsequent disease. Depletion of AM using clodronate liposomes administered prior to MHV-1 infection was associated with a significant amelioration of MHV-1-induced morbidity and mortality. AM depletion resulted in a decreased number of virus-specific CD4 T cells in the lung airways. In addition, a significant increase in the frequency and total number of Tregs in the lung tissue and lung airways was observed following MHV-1 infection in mice depleted of AM. Our results indicate that AM play a critical role in modulating MHV-1-induced morbidity and mortality.

PMID:
24608125
PMCID:
PMC3946553
DOI:
10.1371/journal.pone.0090720
[Indexed for MEDLINE]
Free PMC Article
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