INTRODUCTION
Bacteria colonize the gastrointestinal tract as early as a few hours after birth. This relationship that develops at an early stage between humans and bacteria is shared with other mammals. Gastrointestinal epithelial cells play a crucial role in maintaining a quiescent environment while being bathed with normal flora, and yet at the same time they must possess functions that allow them to participate in immune surveillance. In addition to screening for and responding to the presence of pathogens in the intestinal lumen, gastrointestinal epithelial cells provide barrier function and transport of ions and solutes.
Enteric pathogens, as opposed to normal flora, cause disease by exploiting the host cytoskeleton or signaling pathways, which ultimately alters the physiologic functions of the intestinal epithelium. For example, pathogens can induce or suppress inflammatory responses, alter the transport of fluid, solutes, and ions, perturb the tight-junction barrier, and activate programmed cell death (apoptosis). This chapter summarizes the cross-talk between bacterial pathogens and host cells that leads to gastrointestinal symptoms.
ENTERIC PATHOGENS AND INTESTINAL EPITHELIAL CELL RECEPTORS
The interaction that occurs between pathogenic or non-pathogenic bacteria and intestinal epithelial cells begins with the adherence of bacteria to the cellular surface. This is a common mechanism by which bacteria cause disease, not only in the gastrointestinal tract but also in other systems where epithelial cells face the external environment, such as the genitourinary and respiratory systems. Adherence of bacteria to the cellular surface is essential to reduce the washout effect caused by intestinal secretion and peristalsis.