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Background    Shigella , an enteroinvasive bacteria induces a major inflammatory response responsible for acute rectocolitis in humans. However, early effect of  Shigella flexneri (S. flexneri)  infection upon the human mucosa and its microenvironement, in particular the enteric nervous system, remains currently unknown. Therefore, in this study, we sought to characterize  ex vivo  the early events of shigellosis in a model of human colonic explants. In particular, we aimed at identifying factors produced by  S. flexneri  and responsible for the lesions of the barrier. We also aimed at determining the putative lesions of the enteric nervous system induced by  S. flexneri .    Methodology/Principal Findings  We first showed that, following 3 h of infection, the invasive but not the non-invasive strain of  S. flexneri  induced significant desquamation of the intestinal epithelial barrier and a reduction of epithelial height. These changes were significantly reduced following infection with SepA deficient  S. flexneri  strains. Secondly,  S. flexneri  induced rapid neuronal morphological alterations suggestive of cell death in enteric submucosal neurones. These alterations were associated with a significant increase in the proportion of vasoactive intestinal peptide (VIP) immunoreactive (IR) neurons but not in total VIP levels. The NMDA receptor antagonist MK-801 blocked neuronal morphological changes induced by  S. flexneri , but not the increase in the proportion of VIP-IR.    Conclusions/Significance  This human explant model can be used to gain better insight into the early pathogenic events following  S. flexneri  infection and the mechanisms involved.

Characterisation of Early Mucosal and Neuronal Lesions Following Shigella flexneri Infection in Human Colon