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Review
. 2012 Feb 1;590(3):433-40.
doi: 10.1113/jphysiol.2011.220822. Epub 2011 Nov 21.

Interspecies communication in the gut, from bacterial delivery to host-cell response

Kim Hodges  1 , Gail Hecht
Affiliations
Review

Interspecies communication in the gut, from bacterial delivery to host-cell response

Kim Hodges et al. J Physiol. .

Abstract

Intestinal pathogens have a wide variety of strategies for communicating with host epithelial cells. This review highlights a few key examples of those strategies. Enteropathogenic Escherichia coli (EPEC) use a type III secretion system (T3SS) to alter host ion transport through both transcriptional and post-translational mechanisms. Salmonella use a similar T3SS to invade host cells and modify an intracellular vacuole, which also impacts host vesicle trafficking. Helicobacter pylori use host cell integrins to provide a conformational change which drives the type IV secretion system into the host cell for delivery of CagA. The novel type VI section systems are phage-like apparati that deliver VgrG-1, which causes actin cross-linking and fluid accumulation in a suckling mouse model. An entirely different delivery mechanism is the outer membrane vesicle (OMV) which is composed of bacterial outer membrane wrapped around contents of the periplamsic space. Enterotoxigenic E. coli use OMVs to deliver bundles of heat labile enterotoxin to host cells. Finally we discuss the host responses to these varied methods of communication.

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Figures

Figure 1
Figure 1. Schematic of the type III, IV and VI secretion systems
The EPEC type III secretion system uses EscN, an ATPase, to drive secretion through a flagellum-like apparatus. H. pylori uses several NTPases, D4, B4 and B11 to power its pilus-like system. Finally, the phage-like type VI secretion system uses the ATPase ClpV to deliver effectors like VgrG.
Figure 2
Figure 2. Enteropathogenic E. coli (EPEC) use a type III secretion system to deliver effector proteins including Tir, EspF, Map and EspG1 and EspG2
Injected Tir binds to Intimin on the bacterial surface and promotes attaching and effacing lesion formation. EspF decreases both sodium–hydrogen exchanger 3 (NHE3) and sodium–glucose cotransport 1 (SGLT1) activity in addition to disruption of tight junctions. Map acts along with EspF to decrease SGLT1 activity and tight junction function. EspG1 and EspG2 decrease Cl−/OH− exchange by DRA and also impair tight junctions. The combined activities of these proteins on ion transport alter the osmotic gradient leading to subsequent movement of water into the intestinal lumen.
Figure 3
Figure 3. Salmonella containing vacuoles (SCVs) are located at the minus ends of microtubules due to trafficking via dynein, which is recruited to the SCV by the effector SseF
In contrast SifA through its interaction with SKIP inhibits the recruitment of kinesin, the plus end motor, preventing movement toward the cell periphery. Several effector proteins, SifA, SseF and SseG, also alter host cell trafficking toward the SCV.
Figure 4
Figure 4. H. pylori type IV secreted effector proteins Cag Y, L, I and A form an association with the type IV secretion system (T4SS) and bind to the β1 chain of integrins
Injection of Cag A via the T4SS requires a conformational change in the β1 chain in addition to integrin clustering. An antibody that locks the conformation of β1 integrin was able to prevent CagA delivery. It is concluded therefore that the physical change of the integrin upon binding is needed for insertion of the T4SS tip and subsequent injection of effector proteins.
Figure 5
Figure 5. Enterotoxigenic E. coli (ETEC) form outer membrane vesicles (OMVs) from lipid and proteins constituents of the bacterial outer membrane
These vesicles contain a periplasmic space which carries heat labile enterotoxin (LT) in addition to other proteins such as alkaline phosphatase. LT in OMVs can interact with its receptor GM1 and mediate delivery of OMVs into the host cell, thus enhancing toxin delivery.
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