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Abstract
Innate immunity against pathogenic bacteria is critical to protect host cells from invasion and infection as well as to develop an appropriate adaptive immune response. During bacterial infection, different signaling transduction pathways control the expression of a wide range of genes that orchestrate a number of molecular and cellular events to eliminate the invading microorganisms and regulate inflammation. The inflammatory response must be tightly regulated because uncontrolled inflammation may lead to tissue injury. Among the many signaling pathways activated, the canonical Wnt/β-catenin has been recently shown to play an important role in the expression of several inflammatory molecules during bacterial infections. Our main goal in this review is to discuss the mechanism used by several pathogenic bacteria to modulate the inflammatory response through the Wnt/β-catenin signaling pathway. We think that a deep insight into the role of Wnt/β-catenin signaling in the inflammation may open new venues for biotechnological approaches designed to control bacterial infectious diseases.
Highlights
Innate immunity against pathogenic bacteria is critical to protect host cells from invasion and infection as well as to develop an appropriate adaptive immune response
It was shown that corneal epithelial cells infected with P. aeruginosa express IL-6, IL-8, and TNF-α through a jun N-terminal kinases (JNKs)-dependent mechanism [26]. These results suggest that P. aeruginosa targets β-catenin degradation to induce proinflammatory cytokine expression by secreting acyl-homoserine lactone (AHL) and regulating the activity of JNKs
The evidence accumulated so far has pointed out that activation of the Wnt/β-catenin pathway reduces several molecular inflammatory processes that are triggered by bacterial pathogens
Summary
Models [7, 11,12,13] From these studies it is known that infection of colon epithelial cells (CEC) with Salmonella typhimurium causes an increase in GSK3β-dependent βcatenin phosphorylation, leading to an upregulation of IL6, IL-8, and Wnt, via TLR5/NF-κB activation [10, 14]. These results were confirmed in HCT116 and T84 cell lines by expressing constitutively active β-catenin mutants that, upon interaction with the NF-κB p50 subunit, decreased the NF-κB DNA binding and transcriptional activities [10]. This evidence indicates that Wnt and Wnt trigger a negative feedback mechanism that controls NF-κB activity through β-catenin activation
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