The role of type I interferon in Shigella flexneri pathogenesis

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The type I interferon (IFN) response is part of the first line of defense against pathogens. Type I IFNs were first found to protect against viral infection, but, more recently, studies have shown that their involvement in bacterial infections can be either protective or exacerbative for the host. This study delves into the effects of type I IFN signaling on the various stages of Shigella flexneri pathogenesis. Shigella spp. are the cause of bacterial dysentery. This bacterial pathogen is spread via the fecal-oral route and invades the colonic epithelium. Following invasion, it replicates in the host cell cytosol and spreads to adjacent cells. This provokes an intense inflammatory response that is characteristic of shigellosis. Here, we show that type I IFN signaling inhibits invasion by S. flexneri; however, during later stages of S. flexneri pathogenesis, type I IFN signaling appears to promote cell-to-cell spread and host cell lysis. Type I IFN, IFNβ in particular, increased the size of plaques formed in cell culture monolayers by S. flexneri. Upon further investigation, we found that larger plaque sizes could be attributed to a combination of increasing the rate of cell-to-cell spread and the rate of host cell lysis by IFNβ signaling. We also found that IFNβ signaling produces larger plaque sizes in Listeria monocytogenes infections, suggesting that ISGs induced by IFNβ may have a generalizable effect on other invasive bacterial pathogens.


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