| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
1 Second Dept of Internal Medicine, Nagasaki University School of Medicine, and 2 Dept of Molecular Microbiology and Immunology, Nagasaki University Graduate School of Biomedical Science, Nagasaki, Japan
CORRESPONDENCE: K. Yanagihara, Second Dept of Internal Medicine, Nagasaki University School of Medicine, 1-7-1 Sakamoto, Nagasaki-shi, 852-8501, Japan. Fax: 81 958497285. E-mail: kyana-ngs@umin.ac.jp
Keywords: Cyclooxygenase-2, cytokine, influenza virus, mitogen-activated protein kinase, Streptococcus pneumoniae, Toll-like receptors
Received: November 11, 2003
Accepted February 17, 2004
Coinfections of bacteria and influenza are a major cause of excessive mortality during influenza epidemics. However, the mechanism of the synergy between influenza virus and bacteria are poorly understood.
In this study, mice were inoculated with influenza virus, followed 2 days later by inoculation with Streptococcus pneumoniae. The kinetics of viral titres, bacterial numbers and the immune response (cytokine and chemokine production) were also analysed.
Short-term survival correlated with pathological changes in the lungs of infected mice. Influenza virus or S. pneumoniae infection alone induced moderate pneumonia; however, severe bronchopneumonia with massive haemorrhage in coinfected mice, which caused death of these mice
These results suggest that immune mediators, including cytokines and chemokines, through Toll-like receptors/mitogen-activated protein kinase pathways, play important roles in the pathology of coinfection caused by influenza virus and Streptococcus pneumoniae.
2 days after inoculation with S. pneumoniae, was noted. Intrapulmonary levels of inflammatory cytokines/chemokines, type-1 T-helper cell cytokines and Toll-like receptors, and the related mitogen-activated protein kinase signalling molecules (phosphorylated extracellular signal-regulated kinase -1 and -2, p38 and c-Jun N-terminal kinase), were increased in coinfected mice.
This article has been cited by other articles:
|
|
 |
|
  H. Zhang Concerns of using sialidase fusion protein as an experimental drug to combat seasonal and pandemic influenza J. Antimicrob. Chemother., August 1, 2008; 62(2): 219 - 223. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. A. Wiley and A. G. Harmsen Pneumocystis Infection Enhances Antibody-Mediated Resistance to a Subsequent Influenza Infection J. Immunol., April 15, 2008; 180(8): 5613 - 5624. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 L. A. McNamee and A. G. Harmsen Both Influenza-Induced Neutrophil Dysfunction and Neutrophil-Independent Mechanisms Contribute to Increased Susceptibility to a Secondary Streptococcus pneumoniae Infection Infect. Immun., December 1, 2006; 74(12): 6707 - 6721. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 P. D. N'Guessan, S. Hippenstiel, M. O. Etouem, J. Zahlten, W. Beermann, D. Lindner, B. Opitz, M. Witzenrath, S. Rosseau, N. Suttorp, et al. Streptococcus pneumoniae induced p38 MAPK- and NF-{kappa}B-dependent COX-2 expression in human lung epithelium Am J Physiol Lung Cell Mol Physiol, June 1, 2006; 290(6): L1131 - L1138. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. C. Furze, T. Hussell, and M. E. Selkirk Amelioration of Influenza-Induced Pathology in Mice by Coinfection with Trichinella spiralis Infect. Immun., March 1, 2006; 74(3): 1924 - 1932. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
