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97 Foodborne Infection: Salmonella Enterica Streptococcus Pneumonia Haemophilus Influenzae

The document discusses how various bacteria, including Salmonella, Campylobacter, and Clostridium, disrupt epithelial tight junctions to increase paracellular permeability, facilitating bacterial translocation across the epithelium. It highlights the mechanisms employed by these bacteria, such as the activation of specific signaling pathways and the mislocalization of tight junction proteins. Additionally, it emphasizes the importance of iron acquisition for bacterial survival and growth.
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0% found this document useful (0 votes)
13 views1 page

97 Foodborne Infection: Salmonella Enterica Streptococcus Pneumonia Haemophilus Influenzae

The document discusses how various bacteria, including Salmonella, Campylobacter, and Clostridium, disrupt epithelial tight junctions to increase paracellular permeability, facilitating bacterial translocation across the epithelium. It highlights the mechanisms employed by these bacteria, such as the activation of specific signaling pathways and the mislocalization of tight junction proteins. Additionally, it emphasizes the importance of iron acquisition for bacterial survival and growth.
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© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
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Download as PDF, TXT or read online on Scribd

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

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