The Struggle Within: Microbial Influences on Colorectal Cancer

被引:96
作者
Arthur, Janelle C.
Jobin, Christian [1 ]
机构
[1] Univ N Carolina, Div Gastroenterol & Hepatol, Dept Med, Chapel Hill, NC 27599 USA
基金
美国国家卫生研究院;
关键词
colorectal cancer; inflammatory bowel disease; intestinal microbiota; CYTOLETHAL DISTENDING TOXIN; PROMOTES COLON TUMORIGENESIS; MUCIN-DEPLETED FOCI; STREPTOCOCCUS-ANGINOSUS INFECTION; MULTIPLE INTESTINAL NEOPLASIA; PASTEURELLA-MULTOCIDA TOXIN; TUMOR-SUPPRESSOR GENE; CORE GUT MICROBIOME; TOLL-LIKE RECEPTORS; N-NITROSO COMPOUNDS;
D O I
10.1002/ibd.21354
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
Recently, an unprecedented effort has been directed at understanding the interplay between chronic inflammation and development of cancer, with the case of inflammatory bowel disease (IBD)-associated colorectal cancer at the forefront of this research endeavor. The last decade has been particularly fertile, with the discovery of numerous innovative paradigms linking various inflammatory, proliferative, and innate and adaptive immune signaling pathways to the development of colorectal cancer. Because of the preponderant role of the intestinal microbiota in the initiation and progression of IBD, recent efforts have been directed at understanding the relationship between bacteria and colorectal cancer. The microbiota and its collective genome, the microbiome, form a diverse and complex ecological community that profoundly impacts intestinal homeostasis and disease states. This review will discuss the differential influence of the microbiota on the development of IBD-associated colorectal cancer and highlight the role of innate immune sensor-dependent as well as -independent mechanisms in this pathology.
引用
收藏
页码:396 / 409
页数:14
相关论文
共 243 条
[1]   Stimulation of TLR2 and TLR4 differentially skews the balance of T cells in a mouse model of arthritis [J].
Abdollahi-Roodsaz, Shahla ;
Joosten, Leo A. B. ;
Koenders, Marije I. ;
Devesa, Isabel ;
Roelofs, Mieke F. ;
Radstake, Timothy R. D. J. ;
Heuvelmans-Jacobs, Marleen ;
Akira, Shizuo ;
Nicklin, Martin J. H. ;
Ribeiro-Dias, Fatima ;
Van den Berg, Wim B. .
JOURNAL OF CLINICAL INVESTIGATION, 2008, 118 (01) :205-216
[2]   InterIeukin-23/Th17 Pathways and Inflammatory Bowel Disease [J].
Abraham, Clara ;
Cho, Judy .
INFLAMMATORY BOWEL DISEASES, 2009, 15 (07) :1090-1100
[3]   TLR signaling in the gut in health and disease [J].
Abreu, MT ;
Fukata, M ;
Arditi, M .
JOURNAL OF IMMUNOLOGY, 2005, 174 (08) :4453-4460
[4]  
ACANI PD, 2009, CURR PHARM DESIGN, V15, P1546
[5]  
*ACS, 2010, WHAT AR RISK FACT EC
[6]   The NLRP3 inflammasome functions as a negative regulator of tumorigenesis during colitis-associated cancer [J].
Allen, Irving C. ;
TeKippe, Erin McElvania ;
Woodford, Rita-Marie T. ;
Uronis, Joshua M. ;
Holl, Eda K. ;
Rogers, Arlin B. ;
Herfarth, Hans H. ;
Jobin, Christian ;
Ting, Jenny P. -Y. .
JOURNAL OF EXPERIMENTAL MEDICINE, 2010, 207 (05) :1045-1056
[7]  
ARCHER MC, 1989, CANCER SURV, V8, P241
[8]   Helicobacter pylori CagA induces a transition from polarized to invasive phenotypes in MDCK cells [J].
Bagnoli, F ;
Buti, L ;
Tompkins, L ;
Covacci, A ;
Amieva, MR .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2005, 102 (45) :16339-16344
[9]   Enterococcus faecalis induces inflammatory bowel disease in interleukin-10 knockout mice [J].
Balish, E ;
Warner, T .
AMERICAN JOURNAL OF PATHOLOGY, 2002, 160 (06) :2253-2257
[10]  
BARTHOLD SW, 1977, CANCER RES, V37, P4352