tailieunhanh - Chapter 114. Molecular Mechanisms of Microbial Pathogenesis (Part 6)

Encounters with Epithelial Cells Over the past decade, many bacterial pathogens have been shown to enter epithelial cells (Fig. 114-2); the bacteria often use specialized surface structures that bind to receptors, with consequent internalization. However, the exact role and the importance of this process in infection and disease are not well defined for most of these pathogens. Bacterial entry into host epithelial cells is seen as a means for dissemination to adjacent or deeper tissues or as a route to sanctuary to avoid ingestion and killing by professional phagocytes. Epithelial cell entry appears, for instance, to be a critical aspect. | Chapter 114. Molecular Mechanisms of Microbial Pathogenesis Part 6 Encounters with Epithelial Cells Over the past decade many bacterial pathogens have been shown to enter epithelial cells Fig. 114-2 the bacteria often use specialized surface structures that bind to receptors with consequent internalization. However the exact role and the importance of this process in infection and disease are not well defined for most of these pathogens. Bacterial entry into host epithelial cells is seen as a means for dissemination to adjacent or deeper tissues or as a route to sanctuary to avoid ingestion and killing by professional phagocytes. Epithelial cell entry appears for instance to be a critical aspect of dysentery induction by Shigella. ÛJGO- 3 UD ip LUÍ í p-3n J ft J Ell J H -3U í ufrduJỬ3 IIIH-MtJÊPM l- ĩ ỊMÔHrtdO 3WÂR dịỊL EUopipj Lp I Jor Wff eưj ýưj jfữ stfc îum If t tsfil rlf ustUJUTf 10 oSusi TS iMntH 3 Plt unt 1Q ndlta SU oritj I xr eî c-fl I gjiiSjj Entry of bacteria into epithelial cells. A. Internalization of P. aeruginosa by cultured human airway epithelial cells expressing wild-type cystic fibrosis transmembrane conductance regulator CFTR the cell receptor for bacterial ingestion. B. Entry of P. aeruginosa into murine tracheal epithelial cells after infection by the intranasal route. Curiously the less virulent strains of many bacterial pathogens are more adept at entering epithelial cells than are more virulent strains examples include pathogens that lack the surface polysaccharide capsule needed to cause serious disease. Thus for Haemophilus influenzae Streptococcus pneumoniae Streptococcus agalactiae group B Streptococcus and Streptococcus pyogenes isogenic mutants or variants lacking capsules enter epithelial cells better than the wild-type encapsulated parental forms that cause disseminated disease. These observations have led to the proposal that epithelial cell entry may be primarily a manifestation of host defense resulting in bacterial clearance by

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