scholarly journals Inducible epithelial resistance against acute Sendai virus infection prevents chronic asthma‐like lung disease in mice

2020 ◽  
Vol 177 (10) ◽  
pp. 2256-2273 ◽  
Author(s):  
David L. Goldblatt ◽  
Jose R. Flores ◽  
Gabriella Valverde Ha ◽  
Ana M. Jaramillo ◽  
Sofya Tkachman ◽  
...  
Keyword(s):  
Virus Infection ◽  
Lung Disease ◽  
Sendai Virus ◽  
Chronic Asthma ◽  
Epithelial Resistance

Aerosolized Toll-Like Receptor Agonists Suppress Acute Sendai Virus Burden and Chronic Asthma-Like Lung Disease in Mice

2019 ◽  
Author(s):  
D.L. Goldblatt ◽  
J.R. Flores Gonzalez ◽  
G. Valverde ◽  
A.M. Jaramillo ◽  
S. Tkachman ◽  
...  
Keyword(s):  
Lung Disease ◽  
Sendai Virus ◽  
Chronic Asthma ◽  
Toll Like Receptor ◽  
Receptor Agonists

scholarly journals Distinctive Kinetics of the Antibody-Forming Cell Response to Sendai Virus Infection of Mice in Different Anatomical Compartments

Virology ◽  
1995 ◽  
Vol 207 (1) ◽  
pp. 287-291 ◽  
Author(s):  
Mark Sangster ◽  
Lisa Hyland ◽  
Robert Sealy ◽  
Christopher Coleclough
Keyword(s):  
Virus Infection ◽  
Cell Response ◽  
Sendai Virus ◽  
Kinetics Of

Inhibitory effect of pulmonary surfactant on Sendai virus infection in rat lungs

1996 ◽  
Vol 141 (8) ◽  
pp. 1571-1577 ◽  
Author(s):  
M. Tashiro ◽  
Y. Beppu ◽  
K. Sakai ◽  
H. Kido
Keyword(s):  
Virus Infection ◽  
Pulmonary Surfactant ◽  
Sendai Virus ◽  
Inhibitory Effect ◽  
Rat Lungs

scholarly journals Comparative lung pathology of inbred strains of mice resistant and susceptible to Sendai virus infection.

1991 ◽  
Vol 53 (2) ◽  
pp. 275-279 ◽  
Author(s):  
Toshio ITOH ◽  
Hiroshi IWAI ◽  
Katsumoto UEDA
Keyword(s):  
Virus Infection ◽  
Sendai Virus ◽  
Inbred Strains ◽  
Lung Pathology ◽  
Inbred Strains Of Mice

Protection of mice against virulent virus infection by a temperature-sensitive mutant derived from an HVJ (Sendai virus) carrier culture

1979 ◽  
Vol 61 (4) ◽  
pp. 297-304 ◽  
Author(s):  
Y. Kimura ◽  
H. Aoki ◽  
K. Shimokata ◽  
Y. Ito ◽  
Michiko Takano ◽  
...  
Keyword(s):  
Virus Infection ◽  
Sendai Virus ◽  
Temperature Sensitive ◽  
Sensitive Mutant ◽  
Temperature Sensitive Mutant ◽  
Virulent Virus ◽  
Virus Carrier

Sendai Virus Infection in the Brains of Mice: Distribution of Viral Antigens Studied with Monoclonal Antibodies

1983 ◽  
Vol 147 (2) ◽  
pp. 297-301 ◽  
Author(s):  
K. Kristensson ◽  
C. Orvell ◽  
J. Leestma ◽  
E. Norrby
Keyword(s):  
Monoclonal Antibodies ◽  
Virus Infection ◽  
Sendai Virus ◽  
Viral Antigens

scholarly journals Novel Mode of ISG15-Mediated Protection against Influenza A Virus and Sendai Virus in Mice

2014 ◽  
Vol 89 (1) ◽  
pp. 337-349 ◽  
Author(s):  
David J. Morales ◽  
Kristen Monte ◽  
Lulu Sun ◽  
Jessica J. Struckhoff ◽  
Eugene Agapov ◽  
...  
Keyword(s):  
Tissue Culture ◽  
Virus Infection ◽  
Influenza A Virus ◽  
Virus Replication ◽  
Influenza A ◽  
Type I Interferon ◽  
Sendai Virus ◽  
Type I ◽  
Induced Genes

ABSTRACTISG15 is a diubiquitin-like modifier and one of the most rapidly induced genes upon type I interferon stimulation. Hundreds of host proteins and a number of viral proteins have been shown to be ISGylated, and understanding how these modifications affect the interferon response and virus replication has been of considerable interest. ISG15−/−mice exhibit increased susceptibility to viral infection, and in the case of influenza B virus and vaccinia virus, ISG15 conjugation has been shown to restrict virus replicationin vivo. A number of studies have also found that ISG15 is capable of antagonizing replication of some viruses in tissue culture. However, recent findings have demonstrated that ISG15 can protect mice from Chikungunya virus infection without affecting the virus burden. In order to better understand the function of ISG15in vivo, we characterized the pathogenesis of influenza A virus and Sendai virus in ISG15−/−mice. We found that ISG15 protects mice from virus induced lethality by a conjugation-dependent mechanism in both of these models. However, surprisingly, we found that ISG15 had minimal effect on virus replication and did not have an obvious role in the modulation of the acute immune response to infection. Instead, we observed an increase in the number of diseased small airways in mice lacking ISG15. This ability of ISG15 to protect mice in a conjugation-dependent, but nonantiviral, manner from respiratory virus infection represents a previously undescribed role for ISG15 and demonstrates the importance of further characterization of ISG15in vivo.IMPORTANCEIt has previously been demonstrated that ISG15−/−mice are more susceptible to a number of viral infections. Since ISG15 is one of the most strongly induced genes after type I interferon stimulation, analysis of ISG15 function has largely focused on its role as an antiviral molecule during acute infection. Although a number of studies have shown that ISG15 does have a small effect on virus replication in tissue culture, few studies have confirmed this mechanism of protectionin vivo. In these studies we have found that while ISG15−/−mice are more susceptible to influenza A virus and Sendai virus infections, ISGylation does not appear to mediate this protection through the direct inhibition of virus replication or the modulation of the acute immune response. Thus, in addition to showing a novel mode of ISG15 mediated protection from virus infection, this study demonstrates the importance of studying the role of ISG15in vivo.

scholarly journals TREM-2 promotes macrophage survival and lung disease after respiratory viral infection

2015 ◽  
Vol 212 (5) ◽  
pp. 681-697 ◽  
Author(s):  
Kangyun Wu ◽  
Derek E. Byers ◽  
Xiaohua Jin ◽  
Eugene Agapov ◽  
Jennifer Alexander-Brett ◽  
...  
Keyword(s):  
Lung Disease ◽  
Viral Infections ◽  
Sendai Virus ◽  
Acute Infection ◽  
Chronic Respiratory Disease ◽  
Chronic Inflammatory Disease ◽  
Soluble Form ◽  
Lung Macrophages ◽  
Lung Macrophage ◽  
Macrophage Apoptosis

Viral infections and type 2 immune responses are thought to be critical for the development of chronic respiratory disease, but the link between these events needs to be better defined. Here, we study a mouse model in which infection with a mouse parainfluenza virus known as Sendai virus (SeV) leads to long-term activation of innate immune cells that drive IL-13–dependent lung disease. We find that chronic postviral disease (signified by formation of excess airway mucus and accumulation of M2-differentiating lung macrophages) requires macrophage expression of triggering receptor expressed on myeloid cells-2 (TREM-2). Analysis of mechanism shows that viral replication increases lung macrophage levels of intracellular and cell surface TREM-2, and this action prevents macrophage apoptosis that would otherwise occur during the acute illness (5–12 d after inoculation). However, the largest increases in TREM-2 levels are found as the soluble form (sTREM-2) long after clearance of infection (49 d after inoculation). At this time, IL-13 and the adapter protein DAP12 promote TREM-2 cleavage to sTREM-2 that is unexpectedly active in preventing macrophage apoptosis. The results thereby define an unprecedented mechanism for a feed-forward expansion of lung macrophages (with IL-13 production and consequent M2 differentiation) that further explains how acute infection leads to chronic inflammatory disease.

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