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

作者：Rigaux Peter; Killoran Kristin E; Qiu Zhijun; Rosenberg Helene F^*

来源：Virology, 2012, 422(2): 338-345.

DOI：10.1016/j.virol.2011.10.031

• Inflammation
• Cytokines
• Respiratory virus
• Infection

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 TNF alpha, 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 IFN gamma by NM, CD4(+) and CD8(+) T cells. These results suggest a protective, immunomodulatory role for IFN gamma, as overproduction secondary to macrophage depletion may promote survival despite increased virus recovery. Published by Elsevier Inc.

• 出版日期2012-1-20