Home Acta Virologica 2009 Acta Virologica Vol.53, No.4, p.225-231, 2009

Journal info


Quarterly, 72-88 pp. per issue
Founded: 1957
ISSN 0001-723X
E-ISSN 1336-2305

Published in English

Aims and Scope
Editorial Info

Abstracted and Indexed
Submission Guidelines

Select Journal







Webshop Cart

Your Cart is currently empty.

Info: Your browser does not accept cookies. To put products into your cart and purchase them you need to enable cookies.

Acta Virologica Vol.53, No.4, p.225-231, 2009

Title: Role of macrophage migration inhibitory factor in influenza H5N1 virus pneumonia
Author: X. Q. Hou, Y. W. Gao, S. T. Yang, C. Y. Wang, Z. Y. Ma, X. Z. Xia

Abstract: The severe and often fatal disease in humans and birds caused by H5N1 influenza viruses has been attributed to aberrant pulmonary inflammatory responses. We investigated the role of macrophage migration inhibitory factor (MIF), a proinflammatory cytokine and a pivotal regulator of innate immunity, in H5N1 influenza virus pneumonia in murine model. We found increased MIF mRNA levels in the lungs and MIF protein levels in the serum of infected mice. Although the inhibition of MIF action by isoxazolone-1 (ISO-1) did not render mice more resistant to the lethality of infection, it caused a significant reduction in pulmonary inflammatory cytokines interleukin-1 beta (IL-1β), IL-6 and tumor necrosis factor alpha (TNF-αlfa) and chemokine interferon-inducible protein-10 (IP-10). These results indicate the involvement of MIF in inflammatory responses to H5N1 influenza virus infections by induction of pulmonary inflammatory cytokines and chemokines, and suggest that pharmacotherapeutic approaches targeting MIF may hold promise for the treatment of H5N1 influenza virus pneumonia.

Keywords: MIF; H5N1 influenza virus; mice; pneumonia; isoxazolone-1
Year: 2009, Volume: 53, Issue: 4 Page From: 225, Page To: 231
doi:10.4149/av_2009_04_225


download file



© AEPress s.r.o
Copyright notice: For any permission to reproduce, archive or otherwise use the documents in the ELiS, please contact AEP.