Open AccessFusobacterium nucleatum-Induced Impairment of Autophagic Flux Enhances the Expression of Proinflammatory Cytokines via ROS in Caco-2 Cells
Author(s) -
Bin Tang,
Kun Wang,
Yin-ping Jia,
Pan Zhu,
Fang Yao,
Zhu-jun Zhang,
Xuhu Mao,
Qian Li,
DaWu Zeng
Publication year - 2016
Publication title -
plos one
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.99
H-Index - 332
ISSN - 1932-6203
DOI - 10.1371/journal.pone.0165701
Subject(s) - proinflammatory cytokine , fusobacterium nucleatum , autophagy , ccl20 , atg5 , inflammation , reactive oxygen species , biology , chemistry , immunology , microbiology and biotechnology , chemokine , porphyromonas gingivalis , biochemistry , apoptosis , genetics , chemokine receptor , bacteria
Fusobacterium nucleatum ( F . nucleatum ) plays a critical role in gastrointestinal inflammation. However, the exact mechanism by which F . nucleatum contributes to inflammation is unclear. In the present study, it was revealed that F . nucleatum could induce the production of proinflammatory cytokines (IL-8, IL-1β and TNF-α) and reactive oxygen species (ROS) in Caco-2 colorectal) adenocarcinoma cells. Furthermore, ROS scavengers (NAC or Tiron) could decrease the production of proinflammatory cytokines during F . nucleatum infection. In addition, we observed that autophagy is impaired in Caco-2 cells after F . nucleatum infection. The production of proinflammatory cytokines and ROS induced by F . nucleatum was enhanced with either autophagy pharmacologic inhibitors (3-methyladenine, bafilomycin A1) or RNA interference in essential autophagy genes (ATG5 or ATG12) in Caco-2 cells. Taken together, these results indicate that F . nucleatum -induced impairment of autophagic flux enhances the expression of proinflammatory cytokines via ROS in Caco-2 Cells.