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. 2010 Jan-Feb;1(1):4–21. doi: 10.4161/gmic.1.1.11036

Figure 4.

Figure 4

Invasion and inflammation caused by Shigella. Shigella species cross the epithelial barrier through M-cells where they encounter and eliminate macrophages. Binding of lipoprotein to TLR2 results in the production of the chemoattractant IL-1β. After translocation through M-cells LPS can bind to basolateral TLR4 which causes the production of IL-6 and IL-8. This effect is somewhat diminished due to the acetylation of LPS in Shigella. IL-8 is a potent chemoattractant for PMNs and is also produced due to activation of intracellular Nod1 by peptidoglycan. PMNs are the primary destructive force in Shigella infection. PMNs cause Cl secretion through generation of a precursor to the secretagogue adenosine and can also cause ulceration of the epithelium, which results in a decrease in the absorptive surface but also maximizes permeability and allows easy access of gut flora to the basolateral surface of cells further driving inflammation.