Faecalibacterium prausnitzii Genomic DNA Enhances the Killing Activity of Peripheral Blood Mononuclear Cells against Human Colon Cancer LoVo Cells by Upregulating Th1 Immune Response
10.3969/j.issn.1008-7125.2015.08.002
- VernacularTitle:Faecalibacterium prausnitzii基因组 DNA 上调外周血单个核细胞 Th1型免疫应答增强对人结肠癌 LoVo 细胞的杀伤活性
- Author:
Tao ZHANG
;
Min ZHANG
;
Airong TANG
;
Ping CAO
;
Lijuan XIE
;
Chenggong YU
- Publication Type:Journal Article
- Keywords:
Faecalibacterium prausnitzii;
Interferon-gamma;
Interleukin-4;
Th1-Th2 Balance;
Colonic Neoplasms;
LoVo Cells
- From:
Chinese Journal of Gastroenterology
2015;(8):457-461
- CountryChina
- Language:Chinese
-
Abstract:
Background:Faecalibacterium prausnitzii(Fp)is a commensal intestinal bacterium that exhibits anti-inflammatory and immunomodulatory capacity in vivo and in vitro. It has been reported that Fp in intestinal lumen was reduced in patients with colorectal cancer,which might be a factor associated with cancer development. Aims:To investigate the effect and immunological mechanism of Fp and its genomic DNA(fDNA)on the killing activity of peripheral blood mononuclear cells (PBMCs)against human colon cancer LoVo cells. Methods:PBMCs derived from healthy adults were co-cultured in vitro with Fp,fDNA,or the digested fDNA(d-fDNA),respectively. Killing activity of PBMCs against LoVo cells was measured by MTT assay;concentrations of interferon-gamma(INF-γ),a Th1-type cytokine and interleukin-4(IL-4),a Th2-type cytokine in culture supernatant of PBMCs were determined by ELISA;and expressions of T-bet and GATA3,the transcription factors specific for Th1 and Th2 cells,were measured by real-time PCR. Results:Compared with the PBMCs not treated,fDNA could significantly enhance the killing activity of PBMCs against LoVo cells(P < 0. 05);meanwhile,it promoted IFN-γ secretion,up-regulated T-bet mRNA expression and inhibited IL-4 secretion and GATA3 mRNA expression in PBMCs(P < 0. 05). Similar effects were not observed in PBMCs treated with Fp and d-fDNA. Conclusions:fDNA enhances the killing activity of PBMCs against human colon cancer cells by up-regulating Th1 immune response.
