Woappi Yvon, Singh Om V
Division of Biological and Health Sciences, University of Pittsburgh, Bradford, PA-16701, USA.
Br Microbiol Res J. 2016;15(3). doi: 10.9734/BMRJ/2016/26690. Epub 2016 Jun 10.
Major shifts in intestinal commensal bacteria often result in changes in CD4 T lymphocyte populations, leading to an influx of Th17 cells, chronic inflammation, and eventually cancer. Consequently, the inappropriate propagation of certain commensal species in the gut has been associated with mucosal inflammatory diseases and cancer development. Recent experiments investigating the relationships between food-borne pathogens, enteric bacteria, and cancer have exposed the ability of certain bacterial species to significantly reduce tumor size and tumor progression in mice. In similar studies, pro-inflammatory Th17 and Th1 cells were at times found present along with anti-inflammatory Treg populations in the intestinal mucosa. This antitumor response was mediated by a balanced production of pro- and anti-inflammatory cytokines, resulting in a controlled threshold of mucosal immunity largely moderated by CD4 T lymphocyte populations, through a dendritic cell-dependent pathway. These findings provide new evidence that certain species of bacteria can help manage subcutaneous tumor development by calibrating mucosal and, in some instances, systemic thresholds of innate and adaptive immunity.
肠道共生菌的重大变化通常会导致CD4 T淋巴细胞群体的改变，从而导致Th17细胞的涌入、慢性炎症，最终引发癌症。因此，肠道中某些共生菌的不适当繁殖与黏膜炎症性疾病和癌症发展有关。最近关于食源性病原体、肠道细菌与癌症之间关系的实验表明，某些细菌物种能够显著减小小鼠的肿瘤大小并减缓肿瘤进展。在类似的研究中，有时会在肠道黏膜中发现促炎性Th17和Th1细胞与抗炎性Treg群体同时存在。这种抗肿瘤反应是由促炎和抗炎细胞因子的平衡产生介导的，通过树突状细胞依赖的途径，在很大程度上由CD4 T淋巴细胞群体调节黏膜免疫的可控阈值。这些发现提供了新的证据，表明某些细菌物种可以通过校准固有免疫和适应性免疫的黏膜阈值，在某些情况下还可以校准全身阈值，来帮助控制皮下肿瘤的发展。
