| Autor: |
Walker, John M., Proudfoot, Amanda E. I., Wells, Timothy N. C., Power, Christine A., Campbell, Emma M., Lukacs, Nicholas W. |
| Zdroj: |
Chemokine Protocols; 2000, p295-302, 8p |
| Abstrakt: |
The suitability of any animal model of allergic airway inflammation is assessed by its ability to mimic human asthma. Thus, the ideal model would exhibit early and late antigen-induced airway responses, reversible bronchial hyperresponsiveness, peribronchial eosinophilia, and chronic lung remodeling (1). In this regard, the guinea pig has traditionally been the species of choice for many investigators and has been especially invaluable in elucidating mechanisms governing changes in airway physiology (2). However, in recent years, murine models of allergic airway disease have been extensively employed since the mouse can also be sensitized to a number of different antigens, developing an associated lung inflammatory response. This increased use of the mouse has largely been due to the commercial availability of species-specific reagents, as well as the development of gene knockout mice. In addition, the murine immune system has been relatively well characterized and in practical terms, the mouse is cost effective for experimentation. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Supplemental Index |
| Externí odkaz: |
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