Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology · 2013
Cholera toxin suppresses expression of ubiquitin editing enzyme A20 and enhances transcytosis.
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Li Ming-Yang, Zhu Min, Zhu Bing, Wang Zhi-Qiang
Аннотация
BACKGROUND: The ubiquitin editing enzyme A20 plays an important role in maintaining the homeostasis in the body Microbe-derived adjuvants are commonly used in animal models of intestinal allergy.
OBJECTIVE: This study aims to investigate the role of cholera toxin-induced A20 suppression in compromising intestinal barrier function.
METHODS: Human intestinal epithelial cells were cultured into monolayers as an in vitro epithelial barrier model. Ovalbumin (OVA) was used as a specific allergen to test the degrading capability of intestinal epithelial cells for the endocytic allergens. The fusion of endosomes and lysosomes in epithelial cells was observed by immunocytochemistry. The antigenicity of OVA was tested by T cell proliferation assay.
RESULTS: A20 was detectable in the intestinal cell lines and mouse intestinal epithelialum. A20 was required in the degradation of endocytic allergens in HT-29 cells. The allergen, OVA, could pass through A20-deficient HT-29 monolayer barrier. Exposure to microbial adjuvant, cholera toxin, suppressed the expression of A20 in HT-29 cells, which compromised the epithelial barrier function.
CONCLUSION: The microbial product, cholera toxin, interferes with the expression of A20 in intestinal epithelial cells, which compromises the intestinal epithelial barrier function.
OBJECTIVE: This study aims to investigate the role of cholera toxin-induced A20 suppression in compromising intestinal barrier function.
METHODS: Human intestinal epithelial cells were cultured into monolayers as an in vitro epithelial barrier model. Ovalbumin (OVA) was used as a specific allergen to test the degrading capability of intestinal epithelial cells for the endocytic allergens. The fusion of endosomes and lysosomes in epithelial cells was observed by immunocytochemistry. The antigenicity of OVA was tested by T cell proliferation assay.
RESULTS: A20 was detectable in the intestinal cell lines and mouse intestinal epithelialum. A20 was required in the degradation of endocytic allergens in HT-29 cells. The allergen, OVA, could pass through A20-deficient HT-29 monolayer barrier. Exposure to microbial adjuvant, cholera toxin, suppressed the expression of A20 in HT-29 cells, which compromised the epithelial barrier function.
CONCLUSION: The microbial product, cholera toxin, interferes with the expression of A20 in intestinal epithelial cells, which compromises the intestinal epithelial barrier function.
Предметные рубрики MeSH
AnimalsCaco-2 CellsCell LineCholera ToxinDNA-Binding ProteinsEndosomesGene ExpressionHT29 CellsHumansImmunohistochemistryIntracellular Signaling Peptides and ProteinsLysosomesMaleMiceMice, Inbred BALB CMice, TransgenicNuclear ProteinsOvalbuminRNA InterferenceRNA, Small InterferingTranscytosisTumor Necrosis Factor alpha-Induced Protein 3