Inhibitory Effects of an Antisense Oligonucleotide in an Experimentally Infected Mouse Model of Influenza A Virus

2000 ◽  
Vol 279 (1) ◽  
pp. 158-161 ◽  
Author(s):  
Tadashi Mizuta ◽  
Masatoshi Fujiwara ◽  
Takayuki Abe ◽  
Naoko Miyano-Kurosaki ◽  
Tomoyuki Yokota ◽  
...  
2013 ◽  
Vol 55 (3) ◽  
pp. 203-211 ◽  
Author(s):  
Prashant Kumar ◽  
Binod Kumar ◽  
Roopali Rajput ◽  
Latika Saxena ◽  
Akhil C. Banerjea ◽  
...  

mBio ◽  
2016 ◽  
Vol 7 (6) ◽  
Author(s):  
Adeline Barthelemy ◽  
Stoyan Ivanov ◽  
Maya Hassane ◽  
Josette Fontaine ◽  
Béatrice Heurtault ◽  
...  

ABSTRACT Influenza A virus infection can predispose to potentially devastating secondary bacterial infections. Invariant natural killer T (iNKT) cells are unconventional, lipid-reactive T lymphocytes that exert potent immunostimulatory functions. Using a mouse model of postinfluenza invasive secondary pneumococcal infection, we sought to establish whether α-galactosylceramide (α-GalCer [a potent iNKT cell agonist that is currently in clinical development]) could limit bacterial superinfection. Our results highlighted the presence of a critical time window during which α-GalCer treatment can trigger iNKT cell activation and influence resistance to postinfluenza secondary pneumococcal infection. Intranasal treatment with α-GalCer during the acute phase (on day 7) of influenza virus H3N2 and H1N1 infection failed to activate (gamma interferon [IFN-γ] and interleukin-17A [IL-17A]) iNKT cells; this effect was associated with a strongly reduced number of conventional CD103 + dendritic cells in the respiratory tract. In contrast, α-GalCer treatment during the early phase (on day 4) or during the resolution phase (day 14) of influenza was associated with lower pneumococcal outgrowth and dissemination. Less intense viral-bacterial pneumonia and a lower morbidity rate were observed in superinfected mice treated with both α-GalCer (day 14) and the corticosteroid dexamethasone. Our results open the way to alternative (nonantiviral/nonantibiotic) iNKT-cell-based approaches for limiting postinfluenza secondary bacterial infections. IMPORTANCE Despite the application of vaccination programs and antiviral drugs, influenza A virus (IAV) infection is responsible for widespread morbidity and mortality (500,000 deaths/year). Influenza infections can also result in sporadic pandemics that can be devastating: the 1918 pandemic led to the death of 50 million people. Severe bacterial infections are commonly associated with influenza and are significant contributors to the excess morbidity and mortality of influenza. Today’s treatments of secondary bacterial (pneumococcal) infections are still not effective enough, and antibiotic resistance is a major issue. Hence, there is an urgent need for novel therapies. In the present study, we set out to evaluate the efficacy of α-galactosylceramide (α-GalCer)—a potent agonist of invariant NKT cells that is currently in clinical development—in a mouse model of postinfluenza, highly invasive pneumococcal pneumonia. Our data indicate that treatment with α-GalCer reduces susceptibility to superinfections and, when combined with the corticosteroid dexamethasone, reduces viral-bacterial pneumonia.


2020 ◽  
Vol 18 (1) ◽  
pp. 303-310
Author(s):  
Kaveh Sadeghi ◽  
Vahid Salimi ◽  
Farhad Rezaei ◽  
Farid azizi Jalilian ◽  
Nastaran Ghavami ◽  
...  

1952 ◽  
Vol 95 (2) ◽  
pp. 135-145 ◽  
Author(s):  
Harold S. Ginsberg ◽  
Frank L. Horsfall

Influenza A virus, PR8 strain, increases in amount in the infected mouse lung at a relatively constant rate. When more than 25 M.S.50 doses of virus is inoculated, the rate of multiplication appears to be independent of the amount of virus introduced; has a value of 1,100-fold increase per day. The rate of increase in the pulmonary lesions induced by infection of the mouse lung with PR8 also appears to be relatively constant and independent of the amount of virus inoculated; has a value of 8.5-fold increase per day. The essential variables in the PR8-mouse lung system appear to be equated satisfactorily by functions which were derived previously (4) during a similar quantitative investigation on pneumonia virus of mice (PVM). Evidence in support of the hypothesis that the processes of multiplication of PR8 and PVM are different in the mouse lung is presented.


PLoS ONE ◽  
2017 ◽  
Vol 12 (2) ◽  
pp. e0173008 ◽  
Author(s):  
Akira Kawaguchi ◽  
Tadaki Suzuki ◽  
Yuki Ohara ◽  
Kenta Takahashi ◽  
Yuko Sato ◽  
...  

1982 ◽  
Vol 145 (3) ◽  
pp. 320-330 ◽  
Author(s):  
D. Armerding ◽  
H. Rossiter ◽  
I. Ghazzouli ◽  
E. Liehl

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