Fusobacterium nucleatum-Induced Impairment of Autophagic Flux Enhances the Expression of Proinflammatory Cytokines via ROS in Caco-2 Cells
Fusobacterium nucleatum
Proinflammatory cytokine
CCL20
DOI:
10.1371/journal.pone.0165701
Publication Date:
2016-11-09T18:49:10Z
AUTHORS (9)
ABSTRACT
Fusobacterium nucleatum (F. nucleatum) plays a critical role in gastrointestinal inflammation. However, the exact mechanism by which F. contributes to inflammation is unclear. In present study, it was revealed that could induce production of proinflammatory cytokines (IL-8, IL-1β and TNF-α) reactive oxygen species (ROS) Caco-2 colorectal) adenocarcinoma cells. Furthermore, ROS scavengers (NAC or Tiron) decrease during infection. addition, we observed autophagy impaired cells after The induced enhanced with either pharmacologic inhibitors (3-methyladenine, bafilomycin A1) RNA interference essential genes (ATG5 ATG12) Taken together, these results indicate nucleatum-induced impairment autophagic flux enhances expression via Cells.
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