Effects of traditional oriental medicine on influenza virus infection—Role of the component crude drugs of Mao-bushi-saishin-to (MBST: Ma-huang-fu-zi-xi-xin-tang) in the primary immune response of mice-

2004 ◽  
Vol 1263 ◽  
pp. 536-541
Author(s):  
N Higashi ◽  
Y Takagi ◽  
A Maeda ◽  
N Ueba
PLoS ONE ◽  
2010 ◽  
Vol 5 (10) ◽  
pp. e13099 ◽  
Author(s):  
Vidya A. Arankalle ◽  
Kavita S. Lole ◽  
Ravi P. Arya ◽  
Anuradha S. Tripathy ◽  
Ashwini Y. Ramdasi ◽  
...  

1998 ◽  
Vol 72 (6) ◽  
pp. 4825-4831 ◽  
Author(s):  
Juanita M. Monteiro ◽  
Catherine Harvey ◽  
Giorgio Trinchieri

ABSTRACT The effect of endogenous interleukin-12 (IL-12) on the influenza virus immune response in BALB/c mice was evaluated. Following primary influenza virus infection, IL-12 mRNA and protein are detected in the lung, with live virus being required for cytokine induction. Endogenous IL-12 contributes to early NK cell-dependent gamma interferon (IFN-γ) production (days 3 and 5) but not late T-cell-dependent IFN-γ secretion (day 7). IL-12 contributes to the inhibition of early virus replication but is not required for virus clearance. IL-12 also modestly contributes to the activation of cytotoxic T lymphocytes. Thus, in this model of experimental influenza virus infection, endogenous IL-12 contributes primarily to the early development and activation of the innate immune response.


Viruses ◽  
2020 ◽  
Vol 12 (4) ◽  
pp. 379 ◽  
Author(s):  
Norbert J. Roberts

Human monocytes/macrophages play a central role in the immune response and defense of the host from influenza virus infection. They classically act as antigen-presenting cells for lymphocytes in the context of an immune cell cluster. In that setting, however, monocytes/macrophages exhibit additional, unexpected, roles. They are required for influenza virus infection of the lymphocytes in the cluster, and they are responsible for lymphocyte apoptosis via their synthesis and expression of the viral neuraminidase. Surprisingly, human alveolar macrophages, expected to be among the first cells to encounter the virus, are not susceptible to direct infection by a human influenza virus but can be infected when the virus is complexed with an antibody. Such monocyte/macrophage responses to influenza virus challenge should be considered part of a very complex but quite effective defense, since the common outcome is recovery of the host with development of immunity to the challenging strain of virus.


1998 ◽  
Vol 274 (1) ◽  
pp. L134-L142 ◽  
Author(s):  
Katharine Knobil ◽  
Augustine M. K. Choi ◽  
Gordon W. Weigand ◽  
David B. Jacoby

Influenza virus-induced epithelial damage may be mediated, in part, by reactive oxygen intermediates (ROIs). In this study, we investigated the role of ROIs in the influenza virus-induced gene expression of antioxidant enzymes and in the activation of nuclear factor-κB (NF-κB), an oxidant-sensitive transcriptional factor. Influenza virus infection increased production of intracellular ROIs in A549 pulmonary epithelial cells. Induction of manganese superoxide dismutase (MnSOD) mRNA correlated with increased MnSOD protein and enzyme activity. Influenza virus infection also activated NF-κB binding as determined by an electrophoretic mobility shift assay. Pretreatment of A549 cells with N-acetyl-l-cysteine attenuated virus-induced NF-κB activation and interleukin (IL)-8 mRNA induction but did not block induction of MnSOD mRNA. In contrast, pyrrolidine dithiocarbamate blocked activation of NF-κB and induction of MnSOD and IL-8 mRNAs. Treatment with pyrrolidine dithiocarbamate also markedly decreased virus-induced cell death. Thus oxidants are involved in influenza virus-induced activation of NF-κB, in the expression of IL-8 and MnSOD, and in virus-induced cell death.


Author(s):  
Yuan Jiang ◽  
Xiaowen Cai ◽  
Jiwen Yao ◽  
Huanhuan Guo ◽  
Liangjun Yin ◽  
...  

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