scholarly journals Productive infection of isolated human alveolar macrophages by respiratory syncytial virus.

1990 ◽  
Vol 86 (1) ◽  
pp. 113-119 ◽  
Author(s):  
J R Panuska ◽  
N M Cirino ◽  
F Midulla ◽  
J E Despot ◽  
E R McFadden ◽  
...  
Keyword(s):  
Respiratory Syncytial Virus ◽  
Alveolar Macrophages ◽  
Productive Infection ◽  
Human Alveolar Macrophages ◽  
Syncytial Virus

scholarly journals Restricted replication of respiratory syncytial virus in human alveolar macrophages

1993 ◽  
Vol 74 (8) ◽  
pp. 1527-1537 ◽  
Author(s):  
N. M. Cirino ◽  
J. R. Panuska ◽  
A. Villani ◽  
H. Taraf ◽  
N. A. Rebert ◽  
...  
Keyword(s):  
Respiratory Syncytial Virus ◽  
Alveolar Macrophages ◽  
Human Alveolar Macrophages ◽  
Syncytial Virus

RESPIRATORY SYNCYTIAL VIRUS LUNG INFECTION IN INFANTS: IMMUNOREGULATORY ROLE OF INFECTED ALVEOLAR MACROPHAGES

PEDIATRICS ◽  
1995 ◽  
Vol 96 (2) ◽  
pp. 391-391
Author(s):  
Leon S. Greos
Keyword(s):  
Immune Response ◽  
Respiratory Syncytial Virus ◽  
Lung Injury ◽  
Alveolar Macrophages ◽  
Lung Infection ◽  
Local Immune Response ◽  
Rsv Infection ◽  
Syncytial Virus

Alveolar macrophages are infected by RSV in vivo and coexpress potent immunomodulatory molecules that potentially regulate local immune response or lung injury caused by RSV infection.

scholarly journals Priming of the Respiratory Tract with ImmunobioticLactobacillus plantarumLimits Infection of Alveolar Macrophages with Recombinant Pneumonia Virus of Mice (rK2-PVM)

2015 ◽  
Vol 90 (2) ◽  
pp. 979-991 ◽  
Author(s):  
Kimberly D. Dyer ◽  
Rebecca A. Drummond ◽  
Tyler A. Rice ◽  
Caroline M. Percopo ◽  
Todd A. Brenner ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
Respiratory Syncytial Virus ◽  
Respiratory Tract ◽  
Alveolar Macrophages ◽  
Human Respiratory Syncytial Virus ◽  
Content Type ◽  
Cellular Basis ◽  
Syncytial Virus ◽  
Insight Into

ABSTRACTPneumonia virus of mice (PVM) is a natural rodent pathogen that replicates in bronchial epithelial cells and reproduces many clinical and pathological features of the more severe forms of disease associated with human respiratory syncytial virus. In order to track virus-target cell interactions during acute infectionin vivo, we developed rK2-PVM, bacterial artificial chromosome-based recombinant PVM strain J3666 that incorporates the fluorescent tag monomeric Katushka 2 (mKATE2). The rK2-PVM pathogen promotes lethal infection in BALB/c mice and elicits characteristic cytokine production and leukocyte recruitment to the lung parenchyma. Using recombinant virus, we demonstrate for the first time PVM infection of both dendritic cells (DCs; CD11c+major histocompatibility complex class II+) and alveolar macrophages (AMs; CD11c+sialic acid-binding immunoglobulin-like lectin F+)in vivoand likewise detect mKATE2+DCs in mediastinal lymph nodes from infected mice. AMs support both active virus replication and production of infectious virions. Furthermore, we report that priming of the respiratory tract with immunobioticLactobacillus plantarum, a regimen that results in protection against the lethal inflammatory sequelae of acute respiratory virus infection, resulted in differential recruitment of neutrophils, DCs, and lymphocytes to the lungs in response to rK2-PVM and a reduction from ∼40% to <10% mKATE2+AMs in association with a 2-log drop in the release of infectious virions. In contrast, AMs fromL. plantarum-primed mice challenged with virusex vivoexhibited no differential susceptibility to rK2-PVM. Although the mechanisms underlyingLactobacillus-mediated viral suppression remain to be fully elucidated, this study provides insight into the cellular basis of this response.IMPORTANCEPneumonia virus of mice (PVM) is a natural mouse pathogen that serves as a model for severe human respiratory syncytial virus disease. We have developed a fully functional recombinant PVM strain with a fluorescent reporter protein (rK2-PVM) that permits us to track infection of target cellsin vivo. With rK2-PVM, we demonstrate infection of leukocytes in the lung, notably, dendritic cells and alveolar macrophages. Alveolar macrophages undergo productive infection and release infectious virions. We have shown previously that administration of immunobioticLactobacillusdirectly to the respiratory mucosa protects mice from the lethal sequelae of PVM infection in association with profound suppression of the virus-induced inflammatory response. We show here thatLactobacillusadministration also limits infection of leukocytesin vivoand results in diminished release of infectious virions from alveolar macrophages. This is the first study to provide insight into the cellular basis of the antiviral impact of immunobioticL. plantarum.

Interaction of alveolar macrophages and respiratory syncytial virus

1994 ◽  
Vol 174 (1-2) ◽  
pp. 173-184 ◽  
Author(s):  
G. Franke ◽  
J. Freihorst ◽  
C. Steinmüller ◽  
W. Verhagen ◽  
S. Hockertz ◽  
...  
Keyword(s):  
Respiratory Syncytial Virus ◽  
Alveolar Macrophages ◽  
Syncytial Virus

scholarly journals Respiratory Syncytial Virus–Induced Activation of Nuclear Factor–κB in the Lung Involves Alveolar Macrophages and Toll‐Like Receptor 4–Dependent Pathways

2002 ◽  
Vol 186 (9) ◽  
pp. 1199-1206 ◽  
Author(s):  
Helene A. Haeberle ◽  
Ryuta Takizawa ◽  
Antonella Casola ◽  
Allan R. Brasier ◽  
Hans‐Juergen Dieterich ◽  
...  
Keyword(s):  
Respiratory Syncytial Virus ◽  
Alveolar Macrophages ◽  
Nuclear Factor Κb ◽  
Nuclear Factor ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4 ◽  
Syncytial Virus

scholarly journals Alveolar Macrophages Can Control Respiratory Syncytial Virus Infection in the Absence of Type I Interferons

2016 ◽  
Vol 8 (5) ◽  
pp. 452-463 ◽  
Author(s):  
Spyridon Makris ◽  
Monika Bajorek ◽  
Fiona J. Culley ◽  
Michelle Goritzka ◽  
Cecilia Johansson
Keyword(s):  
Respiratory Syncytial Virus ◽  
Viral Replication ◽  
Alveolar Macrophages ◽  
Ex Vivo ◽  
Type I Interferons ◽  
Type I ◽  
Proinflammatory Mediators ◽  
Rsv Infection ◽  
Syncytial Virus ◽  
Tract Infections

Respiratory syncytial virus (RSV) is a common cause of lower respiratory tract infections. Immunity to RSV is initiated upon detection of the virus by pattern recognition receptors, such as RIG-I-like receptors. RIG-I-like receptors signal via MAVS to induce the synthesis of proinflammatory mediators, including type I interferons (IFNs), which trigger and shape antiviral responses and protect cells from infection. Alveolar macrophages (AMs) are amongst the first cells to encounter invading viruses and the ones producing type I IFNs. However, it is unclear whether IFNs act to prevent AMs from serving as vehicles for viral replication. In this study, primary AMs from MAVS (Mavs-/-)- or type I IFN receptor (Ifnar1-/-)-deficient mice were exposed to RSV ex vivo. Wild-type (wt) AMs but not Mavs-/- and Ifnar1-/- AMs produced inflammatory mediators in response to RSV. Furthermore, Mavs-/- and Ifnar1-/- AMs accumulated more RSV proteins than wt AMs, but the infection was abortive. Thus, RIG-I-like receptor-MAVS and IFNAR signalling are important for the induction of proinflammatory mediators from AMs upon RSV infection, but this signalling is not central for controlling viral replication. The ability to restrict viral replication makes AMs ideal sensors of RSV infection and important initiators of immune responses in the lung.

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