REJUVENATION RESEARCH Volume 11, Number 2, 2008 © Mary Ann Liebert, Inc. DOI: 10.1089/rej.2008.0666 TLR2 and Age-Related Diseases: Potential Effects of Arg753Gln and Arg677Trp Polymorphisms in Acute Myocardial Infarction Carmela Rita Balistreri, 1 Guiseppina Candore, 1 Monica Mirabile, 1 Domenico Lio, 1 Gregorio Caimi, 2 Egle Incalcaterra, 1,2 Marco Caruso, 2 Enrico Hoffmann, 2 and Calogero Caruso 1 ABSTRACT Inflammation is a key component of immune system. It is involved in both defense and patho- physiological events maintaining the dynamic homeostasis of host organism. Its function is controlled by innate immunity genes. Both their polymorphisms and environmental condi- tions give rise to different phenotypes in human population. Proinflammatory genotype may be beneficial in early life but not in old people. With advancing age, indeed, it increases the vulnerability and the intensity to inflammatory reactions responsible for the chronic inflam- matory diseases, such as atherosclerosis and myocardial infarction (MI). Several studies have looked for detecting a genetic risk profile that might allow a pharmacogenomic approach to prevent and treat age-related diseases such as MI. We have evaluated the possible associa- tion between two polymorphisms of TLR2 gene—Arg677Trp and Arg753Gln—and MI. How- ever, we found no association between TLR2 polymorphisms and MI. 293 INTRODUCTION E MERGING PATHOLOGICAL EVIDENCE suggests that aging-related diseases, such as athero- sclerosis and cardiovascular diseases (CVD), dementia, arthritis, osteoporosis, and cancer, are inflammation related. 1 Inflammation is a crucial process—evolutionary conserved, de- signed for survival, and aimed to counteract and neutralize pathogenic agents. Recently, it has also been examined as a possible under- lying basis for the molecular alterations that link aging and age-related pathological pro- cesses. 1,2 Accordingly, it has been strongly sug- gested that lifelong antigenic burden influences the immune system, determining persistent activation of macrophages and related cells, production of several inflammatory mediators peculiar of senescence, and ultimately tissue damage and organ dysfunction responsible for the onset of age-related diseases and death. 3 In the different phases of human life, the in- flammatory response seems to have “opposite” effects. In fact, inflammation is designed to guarantee optimal survival until the time of reproduction, being involved in the host de- fense. In old age, not foreseen by evolution, the chronic inflammatory response, essentially in- 1 Gruppo di studio sull’Immunosenescenza, Dipartimento di Biopatologia e Metodologie Biomediche, Università degli Studi di Palermo, Italy. 2 Dipartimento di Medicina Interna, Malattie Cardiovascolari e Nefrourologiche, Università di Palermo, Palermo, Italy.