The Inflammatory Response during EnterohemorrhagicEscherichia coliInfection

Abstract

The mammalian host is equipped with two major types of immune response, innate and adaptive, that are essential for effective control and elimination of infectious agents. The innate immune system is the first line of host defense against invading microbial pathogens and is promptly activated by the recognition of pathogen-associated molecular patterns, such as lipopolysaccharide (LPS), flagellin, peptidoglycan, and CpG DNA ( 1 ). Pathogen-associated molecular patterns are recognized by specialized germline-encoded pattern recognition receptors (PRRs) expressed by immune cells. To date, a number of PRR families have been described, including the Toll-like receptors (TLRs), retinoic acid-inducible gene-I-like receptors, and nucleotide-binding oligomerization domain (NOD)-like receptors (NLRs) ( 2 , 3 ). The first and most significant consequence of PRR-mediated pathogen recognition in the host is the rapid production of proinflammatory cytokines that stimulates the innate immune response ( 2 , 3 ). In addition, the innate immune response directs the development of the more specific and long-term adaptive response to a particular pathogen, mediated by B and T cells.