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Figure 1

Figure 1. The distal portion of the signal transduction pathway leading to S. typhimurium and S. flexneri-induced HXA3 release is conserved. From: The Role of Neutrophils in the Event of Intestinal Inflammation.

S. typhimurium interacts with intestinal epithelial cells from the apical surface and the effector protein, SipA, activates a novel signal transduction cascade that leads to the activation of PKC. We postulate that this PKC-dependent signal transduction cascade leads to the activation of iPLA2, which liberates archidonic acid (AA) from membranes for subsequent metabolism by the 12/15-LOX pathway culminating in the synthesis of HXA3 (pathway shown in blue). S. flexneri gains access to and interacts with the intestinal epithelium from the basolateral surface. Once inside the host cell, S. flexneri secretes the effector proteins OspF and OspC1 that leads to the phosphorylation of ERK1/2. ERK1/2 activation is a prominent trigger, which leads to the activation of cPLA2. This enzyme releases arachidonic acid (AA) from membranes where ii becomes an available substrate for the 12/15-LOX pathway and leads to the eventual production of HXA3 (pathway shown in red).

Karen L. Mumy, et al. Curr Opin Pharmacol. ;9(6):697-701.

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