Interaction of alveolar macrophages and respiratory syncytial virus

Franke, Gabi; Freihorst, Joachim; Steinmüller, Christiane; Verhagen, Willem; Hockertz, Stefan; Lohmann-Matthes, M.-L.

doi:10.1016/0022-1759(94)90020-5

Cited by 24 publications

(13 citation statements)

References 22 publications

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“…However, latter authors used a lower MOI (MOI = 1), a different incubation temperature (22 °C) and half the number of BAMs we used. Human or murine alveolar macrophages are reported to produce low amounts of infectious virus after exposure to HRSV [4,6,19], which agrees with our findings. Cirino et al [4] reported a progressive decrease in the proportion of human alveolar macrophages (HAM) that replicate virus, that is similar to our results (Table 1).…”

Section: Discussionsupporting

confidence: 95%

Bovine respiratory syncytial virus replicates minimally in bovine alveolar macrophages

Schrijver¹,

Kramps²,

Middel³

et al. 1995

Archives of Virology

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The interaction between two different bovine respiratory syncytial virus (BRSV) strains and bovine alveolar macrophages (BAMs) was studied in vitro. Bovine respiratory syncytial virus replicated minimally in BAMs and most of the virus produced remained cell-associated. Approximately 1 out of 1,000 BAMs produced infectious virus, a number that further declined during the 7 days of culture. In contrast, BAMs exposed to bovine parainfluenza 3 virus (PI3V) produced high amounts of infectious virus. The number of BAMs that contained BRSV antigen depended on the antigen load of the inoculum and not on the infectivity of the virus. Antibody mediated enhancement of infection was not detected. It is concluded that bovine alveolar macrophages exhibit a high intrinsic resistance to BRSV, but not to PI3V.

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Section: Discussionsupporting

confidence: 95%

Bovine respiratory syncytial virus replicates minimally in bovine alveolar macrophages

Schrijver¹,

Kramps²,

Middel³

et al. 1995

Archives of Virology

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“…1C]. Interestingly, little to no RSV replication was reported in primary mouse macrophage culture (Franke et al ., 1994; Franke-Ullmann et al . 1995; Stadnyck et al ., 1997), although Hegele and colleagues (1998) identified a minor population of high-density guinea pig alveolar macrophages that supported virion assembly.…”

Section: Resultsmentioning

confidence: 99%

“…Although virus antigens are detectable in alveolar macrophages isolated from RSV-infected human subjects (Midulla et al ., 1993) and virions are capable of inducing the synthesis and release of proinflammatory mediators by both human and mouse macrophages in culture (Tsutsumi et al ., 1996; Matsuda et al . 1996; Franke et al ., 1994; Franke-Ullmann, et al . 1995; Stadnyck et al ., 1997) the precise contributions of alveolar macrophages to the pathogenesis of RSV disease remains uncertain.…”

Section: Introductionmentioning

confidence: 99%

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

et al. 2012

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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.

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“…PG, prostaglandin; Tx, thromboxane; LT, leukotriene; HETE, hydroxyeicosatetraenoic acid; PDGF, platelet-derived growth factor. They also express high levels of scavenger receptors (e.g., MARCO, CD68, CD204, CD205/206, SR-A) and pattern recognition receptors (e.g., TLR4), as well as receptors for Fcg (CD64), hyaluronan (CD44), and SIRP-a (CD47), along with receptors for various cytokines, chemokines, and signaling molecules (Bilyk et al, 1988;Lehnert et al, 1990;Miller et al, 1992;Franke et al, 1994;Lohmann-Matthes et al, 1994;Kasper et al, 1995;Franke-Ullmann et al, 1996;Gjomarkaj et al, 1999;Gough et al, 1999;Van den Heuvel et al, 1999;Han et al, 2000;Taylor et al, 2000;Palecanda and Kobzik, 2001;Maus et al, 2002;Taylor et al, 2002;Trapnell and Whitsett, 2002;Arredouani et al, 2004;Grundy and Sentman, 2005;Pons et al, 2005;Garn et al, 2006;Singh Suri et al, 2006;Janssen et al, 2008;McComb et al, 2008;Thakur et al, 2008;Kovach and Standiford, 2011;Feng and Mao, 2012;Misharin et al, 2013;Zaynagetdinov et al, 2013) (Table 1). Bedoret et al, 2009;Misharin et al, 2013;Zaynagetdinov et al, 2013) (Table 2).…”

Section: Alveolar Macrophagesmentioning

confidence: 99%