Association of Helicobacter bilis Infection with the Development of Colorectal Cancer.

The role of Helicobacter_bilis (H.bilis) in the development of inflammatory bowel disease (IBD) and colitis-associated carcinogenesis (CAC) has seldom been investigated. We examined the abundance of H.bilis in 58 colorectal cancers (CRCs), 20 IBDs, 40 cases of normal colorectal mucosa (NCs), and 20...

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Detalles Bibliográficos
Publicado en:Nutrition & Cancer Vol. 73; no. 11/12; pp. 2785 - 2796
Autores principales: Peng, Wei, Li, Huan, Xu, Yun, Yan, Li, Tang, Zhenzhen, Hossein Mohseni, Amir, Taghinezhad-S, Sedigheh, Tang, Xiaowei, Fu, Xiangsheng
Formato: pictorial research tables/charts Journal Article
Publicado: Taylor & Francis Ltd 2021
Acceso en línea:Ver este registro en EBSCOhost
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Sumario:The role of Helicobacter_bilis (H.bilis) in the development of inflammatory bowel disease (IBD) and colitis-associated carcinogenesis (CAC) has seldom been investigated. We examined the abundance of H.bilis in 58 colorectal cancers (CRCs), 20 IBDs, 40 cases of normal colorectal mucosa (NCs), and 20 adenomas (ADs) by 16S rRNA fluorescence in situ hybridization (FISH). Number of CD4+CD45RB+T cell and expression of IFN-γ and TNF-α in these tissues was determined by immunofluorescence. The abundance of H.bilis was significantly higher in CRCs than that in IBDs (P = 0.006), ADs (P < 0.001) and NCs (P < 0.0001). The abundance of H.bilis in IBDs was significantly higher than that in ADs (P = 0.013). Moreover, the average number of CD4+CD45RB+T cell was significantly higher in CRCs than that in IBDs (P = 0.017) and NCs (P = 0.009). In addition, there was a positive correlation between the H.bilis abundance and density of CD4+CD45RB+T cells in 30 colorectal tissues (P < 0.0001). The frequency of co-staining for CD4+CD45RB+T cells and IFN-γ was significantly higher in H.bilis positive group than that in H.bilis negative group (P = 0.002). H.bilis may play a role in the initiation of IBD and CAC, possibly through promoting the transformation of T cells into CD4+CD45RB+T cells and increasing the expression of proinflammatory cytokines IFN-γ.