Bifidobacterium bifidum BF-1 suppresses Helicobacter pylori-induced genes in human epithelial cells.
Helicobacter pylori infection alters gene expression in host cells. Specifically, inflammatory chemokines such as IL-8 are upregulated in the gastric mucosa during H. pylori infection. Although the mechanism by which H. pylori causes inflammation of the gastric mucosa is not yet understood, many studies have suggested that nuclear factor kappa B (NF-κB) plays a key regulatory role in host cells. We have shown that preincubation with Bifidobacterium bifidum strain BF-1, a probiotic strain known to improve H. pylori-associated gastritis, suppresses induction of IL-8 by the pathogen. To investigate how how BF-1 affects gene expression in H. pylori-infected cells, we performed microarray analysis to assess gene expression in epithelial cells, which had been preincubated with BF-1 and infected with H. pylori. We found that preincubation with BF-1 suppresses the expression of H. pylori-induced genes in human cells and that most of the affected genes are related to the NF-κB signaling pathways. These results suggest that BF-1 can affect the regulatory mechanism of the NF-κB signaling pathways.
Shirasawa
Y
Y
Yakult Central Institute for Microbiological Research, Kunitachi, Tokyo, 186-8650, Japan. yukio-shirasawa@yakult.co.jp
Shibahara-Sone
H
H
Iino
T
T
Ishikawa
F
F
D001644:Bifidobacterium / Q000145:classification / Q000378:metabolism*; D018929:Cell Culture Techniques; D002460:Cell Line; D004847:Epithelial Cells / Q000382:microbiology*; D005753:Gastric Mucosa / Q000382:microbiology*; D005786:Gene Expression Regulation; D016480:Helicobacter pylori / Q000502:physiology*; D006801:Humans; D016209:Interleukin-8 / Q000378:metabolism; D016328:NF-kappa B / Q000502:physiology; D019936:Probiotics; D015398:Signal Transduction
D016209:Interleukin-8; D016328:NF-kappa B