Table 1. Modulation of TJ structures by human intestinal pathogens.
| Pathogen | Effector molecules | Effects on TJs and epithelial barrier |
|---|---|---|
| EPEC | T3SS, EspF, EspG, Map20, 176, 177 | Altered localization of claudin, ZO-1 and occludin; loss of TER and increased flux of small molecules |
| EHEC | Altered TJ protein expression.178 TNF-α produced by infection increases expression of claudin-2 20 | |
| Salmonella typhimurium | T3SS, SPI1 effectors; SopB, SopE SopE2 and SipA have been implicated179, 180 | Decreased ZO-1 expression, and decreased phosphorylation of occludin180 |
| Helicobacter pylori | T4SS, CagA | Mislocalization of ZO-1 in the cytoplasm181, 182 |
| Shigella flexneri | Disruption of TJ structures, decreased expression of claudin-1 and TER after 90 min | |
| Clostridium perfringens | Enterotoxin binding to claudin proteins | The C-terminal region of C. perfringens enterotoxin can bind to specific claudin proteins, resulting in the disintegration of TJs and an increase in paracellular permeability183 |
| Vibrio cholerae | ZOT26 | Altered flux and ZO-1 density in the TJs |
| Reovirus | Protein σ1 | Binding of σ1 to TJ protein N-terminal part of JAM-A promotes internalization184 |
| Rotaviruses | VP8, NSP4 | VP8 is released from the protein core by trypsin leading to disruption of barrier integrity; toxin NSP4 blocks TJ formation185, 186 |
Abbreviations: EHEC, enterohemorrhagic E. coli; EPEC, enteropathogenic E. coli; JAM, junctional adhesion molecule; NSP4, nonstructural protein 4; TER, transepithelial electrical resistance; TJ, tight junction; TNF-α, tumor necrosis factor-α ZO-1, zonulin-1; ZOT, zonula occludens toxin.