Role of toll-like receptor 4 in alcohol-induced neuroinflammation and behavioral dysfunctions

Abstract

Until quite recently, the central nervous system (CNS) has been considered an autonomous unit nourished by blood and shielded not only from circulating immune cells but also from pathogens and toxins originating from circulation. However, it is now well established that immune surveillance occurs in the normal CNS and that inflammatory responses can take place in the neural plasticity and disease context. The CNS presents a well-organized series of innate immune reactions in response to systematic bacterial and viral infections and to cerebral injury [1, 2]. Activation of the innate immune system is an important component of inflammatory response.