Intestinal permeability – a new target for disease prevention and therapy

BMC Gastroenterology

Table 3 Pathogen interactions with epithelial tight junctions

Bacteria	Bacterial factors	Mechanism of TJ disruption	Host targets	References
H. pylori	CagA	Cdx2-mediated increase in claudin 2 expression	PAR1	[64]-[66]
	Urease	Phosphorylation of myosin light chain kinase and occludin internalization	MLCK, ROCK	[67]
	Unknown	Rho kinase (ROCK)-dependent loss of TJ claudin-4	IL-1R1, ROCK	[68]
EPEC	Map	Cdc42-dependent filopodia and pedestal formation	Cdc42	[69]
	EspM	Activation of RhoA and TJ disruption	RhoA	[70]-[72]
	NleA	Inhibition of host cell protein trafficking through COPII-dependent pathways	COPII	[73]
V. parahemo- lyticus	T3SS effectors	Alteration of actomycin ring and TJ disruption	Rho GTPase	[74],[75]
Salmonella enterica serovar typhimur.	T3SS effectors SipA, SopB, SopE, SopE2	Filopodia formation and alteration of actomycin ring	Rho GTPase	[76]
Clostridium difficile	enterotoxin A and B	Inactivation of Rho family proteins causing degradation of filamentous actin	Rho and Cdc	[77]
Bacteroides fragilis	Enterotoxin or fragilysin	Toxin degradation of E- cadherin and alteration of actomycin ring	E-cadherin	[78]
Vibrio cholera	HA protease	HA induced cleavage of occludin, alteration of ZO-1 and rearrangement of actin	Occludin	[79]

Abbreviations: TJ tight junctions, PAR1 phytochrome rapidly regulated 1 gene, MLCK myosin light chain kinase, ROCK Rho-associated, coiled-coil containing protein kinase 1, IL-1R1 interleukin 1 receptor, type I, Cdc42 cell division cycle 42, RhoA ras homolog family member A, COPII Rho GTPase, EPEC enteropathogenic Escherichia coli. Other explanations see text.

ISSN: 1471-230X