Inflamm-aging model is attractive because it derives from the knowledge that aged humans develop low-grade inflammatory state. It is conjectured that the state of low-grade inflammation is a consequence of multiple protective immune responses that develop in order to combat pathogenic infections throughout life. Whereas the notion that chronic inflammatory state could result from multiple immune responses is credible it remains to be demonstrated experimentally. Once this is demonstrated experimentally it will be of interest to demonstrate that experimentally induced immune responses over a period of time correlate with accelerated aging of the whole organism. Long term goals of the experiments proposed in this report aim to establish the role of multiple immune responses in generating a chronic inflamed state, which in turn contributes to accelerated aging in mice. In the short term we will determine if macrophages from young and old mice respond to a common inducer, lipopolysaccharide (LPS), respond differently by measuring waves of gene expression patterns. These studies will set the stage for assaying effects of induced inflamed state in the inflamm-aging model on innate immunity.
|Sharma, Archna; Chen, Qinghua; Nguyen, Trang et al. (2012) T cell factor-1 and ?-catenin control the development of memory-like CD8 thymocytes. J Immunol 188:3859-68|