Abstract
The host-pathogen interface is a crucial battleground during bacterial infection in which host defenses are met with an array of bacterial counter-mechanisms whereby the invader aims to make the host environment more favorable to survival and dissemination. Interestingly, the eukaryotic Wnt signaling pathway has emerged as a key player in the host and pathogen tug-of-war. Although studied for decades as a regulator of embryogenesis, stem cell maintenance, bone formation, and organogenesis, Wnt signaling has recently been shown to control processes related to bacterial infection in the human host. Wnt signaling pathways contribute to cell cycle control, cytoskeleton reorganization during phagocytosis and cell migration, autophagy, apoptosis, and a number of inflammation-related events. Unsurprisingly, bacterial pathogens have evolved strategies to manipulate these Wnt-associated processes in order to enhance infection and survival within the human host. In this review, we examine the different ways human bacterial pathogens with distinct host cell tropisms and lifestyles exploit Wnt signaling for infection and address the potential of harnessing Wnt-related mechanisms to combat infectious disease.
Highlights
The innate immune response is the first, and in many successful cases, the primary barrier between bacterial invader and human host
C. trachomatis infection in the fallopian tube has been shown to disrupt adherens junctions and cause redistribution of β-catenin from the plasma membrane to the chlamydial inclusion [25] (Figure 3B). It is unclear if disruption of these junctions amplifies β-catenin nuclear localization and target gene expression, but infected epithelium does demonstrate increased Wnt pathway activity evidenced by phosphorylationdependent inactivation of glycogen synthase kinase 3β (GSK3β) and redistribution of adenomatous polyposis coli (APC) which indicates inactivation of the β-catenin destruction complex [25]
The former two pathogens appear to stimulate canonical Wnt signaling to prolong host cell survival by inducing either proliferation or differentiation of the host cell
Summary
The innate immune response is the first, and in many successful cases, the primary barrier between bacterial invader and human host. It is unclear if disruption of these junctions amplifies β-catenin nuclear localization and target gene expression, but infected epithelium does demonstrate increased Wnt pathway activity evidenced by phosphorylationdependent inactivation of GSK3β and redistribution of APC which indicates inactivation of the β-catenin destruction complex [25].
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