Depletion of alveolar macrophages prolongs survival in response to acute pneumovirus infection

Peter Rigaux, Kristin E. Killoran, Zhijun Qiu, Helene F. Rosenberg

Producción científica: Articlerevisión exhaustiva

20 Citas (Scopus)

Resumen

Alveolar macrophages are immunoregulatory effector cells that interact directly with respiratory virus pathogens in vivo. We examined the role of alveolar macrophages in acute infection with pneumonia virus of mice (PVM), a rodent pneumovirus that replicates the clinical sequelae of severe human respiratory syncytial virus disease. We show that PVM replicates in primary mouse macrophage culture, releasing infectious virions and proinflammatory cytokines. Alveolar macrophages isolated from PVM-infected mice express activation markers Clec43 and CD86, cytokines TNFα, IL-1, IL-6, and numerous CC and CXC chemokines. Alveolar macrophage depletion prior to PVM infection results in small but statistically significant increases in virus recovery but paradoxically prolonged survival. In parallel, macrophage depleted PVM-infected mice exhibit enhanced NK cell recruitment and increased production of IFNγ by NK, CD4 + and CD8 + T cells. These results suggest a protective, immunomodulatory role for IFNγ, as overproduction secondary to macrophage depletion may promote survival despite increased virus recovery.

Idioma originalEnglish (US)
Páginas (desde-hasta)338-345
Número de páginas8
PublicaciónVirology
Volumen422
N.º2
DOI
EstadoPublished - ene 20 2012
Publicado de forma externa

ASJC Scopus subject areas

  • Virology

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