English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

Shigella , the causative agent of bacillary dysentery invades intestinal epithelial cells using a type III secretion system (T3SS). Through the injection of type III effectors,  Shigella  manipulates the actin cytoskeleton to induce its internalization in epithelial cells. At early invasion stages,  Shigella  induces atypical Ca 2+  responses confined at entry sites allowing local cytoskeletal remodeling for bacteria engulfment. Global Ca 2+  increase in the cell triggers the opening of connexin hemichannels at the plasma membrane that releases ATP in the extracellular milieu, favoring  Shigella  invasion and spreading through purinergic receptor signaling. During intracellular replication,  Shigella  regulates inflammatory and death pathways to disseminate within the epithelium. At later stages of infection,  Shigella  downregulates hemichannel opening and the release of extracellular ATP to dampen inflammatory signals. To avoid premature cell death,  Shigella  activates cell survival by upregulating the PI3K/Akt pathway and downregulating the levels of p53. Furthermore,  Shigella  interferes with pro-apoptotic caspases, and orients infected cells toward a slow necrotic cell death linked to mitochondrial Ca 2+  overload. In this review, we will focus on the role of Ca 2+  responses and their regulation by  Shigella  during the different stages of bacterial infection.

How Shigella Utilizes Ca2+ Jagged Edge Signals during Invasion of Epithelial Cells