Foodborne Infection 97
Fig. 4.6 Schematic showing bacteria or bacterial components mediated epithelial tight junction disruption and enteric
bacterial paracellular translocation
paracellular permeability by generating cell- by activating NF-κB and MLCK to facilitate bac-
signaling events that counteract the normal func- terial paracellular translocation across the epithe-
tion of protein kinase C (PKC). Salmonella lium. Streptococcus pneumonia and Haemophilus
enterica serovar Typhimurium induces increased influenzae exploit toll-like receptor (TLR)-
paracellular permeability associated with the mediated downregulation of TJ protein to facili-
mislocalization of occludin and ZO-1. tate translocation across the epithelium.
Campylobacter jejuni also increases paracellular
permeability by activating phosphoinositide
3-kinase (PI3-K). Clostridium difficile toxin B Iron Acquisition
increases PKC-dependent RhoA glycosylation
and actin depolymerization to increase paracel- Iron (Fe3+) is essential for metabolic process, sur-
lular permeability. Shigella flexneri also increases vival, and growth in all living organisms. It is
paracellular permeability by regulating tight required for electron transport, metalloenzyme
junction-associated proteins. In Listeria monocy- activity (oxidoreductases, cytochromes, and non-
togenes, LAP disrupts intestinal barrier functions heme oxidases), and oxygen transport (higher