Clostridium difficile toxin B intoxicated mouse colonic epithelial CT26 cells stimulate the activation of dendritic cells.
Clostridium difficile causes antibiotic-associated diarrhea and pseudomembranous colitis mainly through two exotoxins TcdA and TcdB that target intestinal epithelial cells. Dendritic cells (DCs) play an important role in regulating intestinal inflammatory responses. In the current study, we explored the interaction of TcdB-intoxicated epithelial cells with mouse bone marrow-derived DCs. TcdB induced cell death and heat shock protein translocation in mouse intestinal epithelial CT26 cells. The intoxicated epithelial cells promoted the phagocytosis and the TNF-α secretion by DCs. Incubation with TcdB-intoxicated CT26 cells stimulated DC maturation. Moreover, TcdB-treated CT26 cells induced DC immigration when they were injected into mice subcutaneously. Taken together, these data demonstrate that TcdB-intoxicated intestinal epithelial cells are able to stimulate DC activation in vitro and attract DCs in vivo, indicating that epithelial cells may be able to regulate DC activation under the exposure of TcdB during C. difficile infection.
School of Bioscience and Bioengineering, South China University of Technology (SCUT), Guangzhou 51006, China Department of Microbial Pathogenesis, University of Maryland Dental School, Baltimore, MD 21021, USA.
Tuxiong
T
Huang
Department of Microbial Pathogenesis, University of Maryland Dental School, Baltimore, MD 21021, USA.
Gregorio
G
Perez-Cordon
Department of Microbial Pathogenesis, University of Maryland Dental School, Baltimore, MD 21021, USA.
Lianfa
L
Shi
School of Bioscience and Bioengineering, South China University of Technology (SCUT), Guangzhou 51006, China.
Guangchao
G
Li
Department of Infectious Disease and Global Health, Tufts Cummings School of Veterinary Medicine, North Grafton, MA 01536, USA.
Xingmin
X
Sun
Institute of Life Science, General Hospital of the People's Liberation Army, Beijing 100853, China.
Xiaoning
X
Wang
School of Bioscience and Bioengineering, South China University of Technology (SCUT), Guangzhou 51006, China.
Jufang
J
Wang
Department of Microbial Pathogenesis, University of Maryland Dental School, Baltimore, MD 21021, USA hfeng@umaryland.edu.
Hanping
H
Feng
D000818:Animals; D001426:Bacterial Proteins / Q000633:toxicity*; D001427:Bacterial Toxins / Q000633:toxicity*; D002450:Cell Communication; D016923:Cell Death / Q000187:drug effects; D002454:Cell Differentiation; D002465:Cell Movement; D003713:Dendritic Cells / Q000276:immunology* / Q000502:physiology; D004847:Epithelial Cells / Q000187:drug effects* / Q000276:immunology* / Q000502:physiology; D006360:Heat-Shock Proteins / Q000378:metabolism; D008297:Male; D008807:Mice, Inbred BALB C; D010587:Phagocytosis; D021381:Protein Transport; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
D001426:Bacterial Proteins; D001427:Bacterial Toxins; D006360:Heat-Shock Proteins; D014409:Tumor Necrosis Factor-alpha; C031815:toxB protein, Clostridium difficile
Clostridium difficile; TcdB; dendritic cells; epithelial cells; inflammation