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1.
近年来,肠道菌群在结直肠癌中的作用引起了广泛关注.越来越多的证据表明,肠道菌群与结直肠癌的发生、发展及治疗相关,潜在的致病菌和代谢标志物的发现将有助于结直肠癌的早期诊断和有效治疗.流行病学数据表明,不同地域人群结直肠癌发病率高低不一,西方化人群发病率普遍较高.西方化与非西方化人群有着不同的肠道菌群结构,因此考虑可能是饮...  相似文献   

2.
结直肠癌(colorectal cancer,CRC)目前发病率及死亡率均较高,严重威胁人们的健康.但其分期不同,预后差异较大,早发现早治疗能够明显改善预后.目前CRC主要筛查手段为肠镜检查,但部分患者不易接受.近期较多研究显示,肠道微生物群与CRC的发生有关,CRC的发生是一个多步骤的过程,在发生癌变前可能经过数十年...  相似文献   

3.
人体肠道菌群是一个复杂的系统,由大量的微生物构成.肠道菌群和人类健康与疾病密切相关,且始终保持着动态平衡.肠道菌群之间相互作用,同时与机体共同维持消化,吸收,代谢等功能.近年来,肠道菌群始终是研究的一大热点,有大量研究表明肠道菌群与结直肠癌的发生发展密切相关.本文就肠道菌群与结直肠癌的关系,发病机制及防治作用进行综述,为结直肠癌的研究提供一些新思路.  相似文献   

4.
正结直肠息肉虽是肠道良性肿瘤,但少数腺瘤性息肉可癌变,其中腺瘤-癌假说实验已被证实~([2])。据统计,在我国,结直肠癌是第5类最常见癌症,且近年来发病率呈迅速上升趋势~([3])。肠道菌群是人体内最复杂和最大的微生态系统,对维持机体健康有重要作用~([4])。研究发现肠道菌群与结直肠息肉密切相  相似文献   

5.
<正>越来越多的研究表明,肠道菌群可以影响结直肠癌(colorectal cancer ,CRC)的发生与发展。在正常情况下,肠道菌群可以作为肠道中其他病原体或感染的屏障,并通过影响宿主的免疫系统来调节炎症。肠道菌群与肿瘤相关的肠道炎症有关,还可以调节宿主对抗肿瘤药物的反应。本文讨论肠道菌群的作用,及其在抗癌治疗中的协同作用。背景CRC在所有癌症中发病率居第三,死亡率居第二。  相似文献   

6.
目的:观察大肠湿热型结直肠腺瘤患者肠道微生物菌群的变化规律。方法:通过结肠镜活检收集47例大肠湿热型结直肠腺瘤患者的腺瘤组织(观察组)以及20例大肠湿热型结直肠腺瘤的瘤旁黏膜组织(对照组),提取组织DNA,对细菌16S rDNA序列V3-V4高变区进行PCR扩增,定量检测PCR产物,纯化后的混合DNA产物在Illumina MiSeq平台上对2组样本的肠道菌群组成和丰度进行测定并分析组间的统计学差异。结果:在门水平上,2组样本的优势菌门均为变形菌门、厚壁菌门、拟杆菌门和放线菌门,差异无统计学意义(P>0.05)。其中排名前10种的菌门中,变形菌门的丰度比例观察组高于对照组,差异有统计学意义(P<0.05);酸杆菌门的丰度比例观察组低于对照组,差异有统计学意义(P<0.05)。在属水平上,2组样本的前20种优势菌种所共有的菌种中,埃希菌-志贺菌属的丰度比例观察组高于对照组,差异有统计学意义(P<0.05);假单胞菌属的丰度比例观察组低于对照组,差异有统计学意义(P<0.05)。结论:大肠湿热型结直肠腺瘤患者肠道菌群的多样性和构成与瘤旁黏膜存在明显差异,腺瘤患者黏膜菌群结构发生明显失衡,形成了易于肿瘤生长的肠道微生态环境。  相似文献   

7.
目的 分析维汉两民族之间早期结直肠癌(colorectal cancer,CRC)患者肠道菌群的分布情况.方法 选取2019年3月至2020年3月于新疆医科大学第一附属医院首次手术并经病理学证实为早期CRC的患者83例.根据不同民族分为汉族组(43例)和维吾尔族组(40例),收集两组患者术前5 d内的新鲜粪便标本,进行...  相似文献   

8.
结直肠癌是结肠癌和直肠癌的总称,目前其病因和发病机制尚未明确。现认为结直肠癌的发生可能与肠道微环境、宿主遗传易感性和高动物蛋白饮食等因素有关。近年来,随着微生态学的发展,肠道菌群与结直肠癌发病的关系日益受到关注。此文就结直肠癌发生过程中肠道菌群的变化、对结直肠癌的影响以及微生态制剂对结直肠癌的治疗作用等相关研究作一综述。  相似文献   

9.
杨静  朱元民  刘玉兰 《胃肠病学》2012,17(4):242-244
肠道菌群与人体健康有密切联系,炎症性肠病、结直肠癌等均与肠道菌群失调有关。摄入益生菌制剂是调节肠道菌群及其功能较为常用的方法。研究表明补充益生菌可能通过调节肠道黏膜免疫和炎症、抑制致病菌定植和繁殖、修复肠上皮屏障功能、抑制肿瘤细胞增殖、抑制致癌化学物活性以及抗氧化作用等.对结直肠肿瘤产生一定预防和治疗作用。本文就益生菌与结直肠癌发病的关系作一综述。  相似文献   

10.
胆汁酸是胆固醇分解代谢的终产物。肠道菌群指定植于人体肠道内的细菌。胆汁酸与肠道菌群可相互影响,生理浓度范围内的胆汁酸可参与维持肠道菌群的稳态,而肠道菌群参与了胆汁酸代谢,可影响胆汁酸的生物转化等。胆汁酸-肠道菌群轴的失调往往存在于肠道炎性反应和结直肠癌患者中。该文综述了胆汁酸-肠道菌群轴失调对肠道炎性反应和结直肠癌的影响。  相似文献   

11.
结直肠癌是全球最常见的恶性肿瘤之一,在西方国家尤其常见。饮食是结直肠癌的重要影响因素之一。大量的研究证据显示饮食可以通过改变肠道微生态从而影响结直肠癌的发生与发展。它既能通过病原菌产生一系列致癌活动,也能通过改变肠道微生态代谢从而影响肠道上皮细胞。近年来有数据表明,以丁酸盐为代表的短链脂肪酸具有抑制炎症及抗肿瘤作用;而以次级胆汁酸为代表的肠道菌群其他代谢产物,具有促进肿瘤发生发展的作用。在本文中,我们将围绕饮食对肠道微生态及其代谢产物的影响、肠道微生态与结直肠癌的相关作用以及结直肠癌的饮食预防进行介绍和讨论,呼吁未来需要更深入的研究探索饮食、肠道微生态与代谢组学、免疫学、基因宿主反应等的相互作用关系。  相似文献   

12.
Colorectal cancer(CRC) is one of the most commonly diagnosed cancers, and it is characterized by genetic and epigenetic alterations, as well as by inflammatory cell infiltration among malignant and stromal cells. However, this dynamic infiltration can be influenced by the microenvironment to promote tumor proliferation, survival and metastasis or cancer inhibition. In particular, the cancer microenvironment metabolites can regulate the inflammatory cells to induce a chronic inflammatory response that can be a predisposing condition for CRC retention. In addition, some nutritional components might contribute to a chronic inflammatory condition by regulating various immune and inflammatory pathways. Besides that, diet strongly modulates the gut microbiota composition,which has a key role in maintaining gut homeostasis and is associated with the modulation of host inflammatory and immune responses. Therefore, diet has a fundamental role in CRC initiation, progression and prevention. In particular,functional foods such as probiotics, prebiotics and symbiotics can have a potentially positive effect on health beyond basic nutrition and have antiinflammatory effects. In this review, we discuss the influence of diet on gut microbiota composition, focusing on its role on gut inflammation and immunity.Finally, we describe the potential benefits of using probiotics and prebiotics to modulate the host inflammatory response, as well as its application in CRC prevention and treatment.  相似文献   

13.
The gut microbiota acts as a real organ. The symbiotic interactions between resident micro-organisms and the digestive tract highly contribute to maintain the gut homeostasis. However, alterations to the microbiome caused by environmental changes(e.g., infection, diet and/or lifestyle) can disturb this symbiotic relationship and promote disease, such as inflammatory bowel diseases and cancer. Colorectal cancer is a complex association of tumoral cells, non-neoplastic cells and a large amount of micro-organisms, and the involvement of the microbiota in colorectal carcinogenesis is becoming increasingly clear. Indeed, many changes in the bacterial composition of the gut microbiota have been reported in colorectal cancer, suggesting a major role of dysbiosis in colorectal carcinogenesis. Some bacterial species have been identified and suspected to play a role in colorectal carcinogenesis, such as Streptococcus bovis, Helicobacter pylori, Bacteroides fragilis, Enterococcus faecalis, Clostridium septicum, Fusobacterium spp. and Escherichia coli. The potential pro-carcinogenic effects of these bacteria are now better understood. In this review, we discuss the possible links between the bacterial microbiota and colorectal carcinogenesis, focusing on dysbiosis and the potential pro-carcinogenic properties of bacteria, such as genotoxicity and other virulence factors, inflammation, host defenses modulation, bacterial derived metabolism, oxidative stress and anti-oxidative defenses modulation. We lastly describe how bacterial microbiota modifications could represent novel prognosis markers and/or targets for innovative therapeutic strategies.  相似文献   

14.
BACKGROUNDWe previously showed, using the Traditional Chinese Medicine System Pharmacology Database, that Gegen Qinlian decoction (GQD) had a direct antitumor effect, and was combined with programmed cell death protein (PD)-1 inhibitors to treat microsatellite stable (MSS) tumor-bearing mice. However, the effect of GQD on patients with colorectal cancer (CRC) is not clear.AIMTo determine the therapeutic mechanism of GQD in improving immune function, reducing inflammation and protecting intestinal barrier function.METHODSSeventy patients with CRC were included in this study: 37 in the control group and 33 in the treatment group. The proportions of CD4+ T, CD8+ T, natural killer (NK), NKT and T regulatory cells were measured by flow cytometry. Levels of the cytokines tumor necrosis factor (TNF)-α, interferon (IFN)-γ, interleukin (IL)-2, IL-6, IL-10 and serotonin (5-hydroxytryptamine; 5-HT) in serum were assessed by enzyme-linked immunosorbent assay (ELISA). The expression of zonula occludens (ZO)-1, occludin, nuclear factor (NF)-κB and TNF-α in tumor and normal tissues was measured by immunohistochemistry. The composition of gut microbiota from patients in the treatment group was assessed using 16S rDNA analysis. RESULTSThere were no adverse events in the treatment group. The proportion of CD4+ T cells and NKT cells in the post-treatment group was significantly higher than that in the pre-treatment and control groups (P < 0.05). The level of TNF-α in the post-treatment group was significantly lower than that in the pre-treatment and control groups (P < 0.05). The concentration of 5-HT in the post-treatment group was significantly lower than that in the pre-treatment group (P < 0.05). The expression of ZO-1 and occludin in tumor tissues in the treatment group was significantly higher than that in the control group (P < 0.05). The expression of ZO-1 in normal tissues of the treatment group was significantly higher than that in the control group (P = 0.010). Compared with the control group, expression of NF-κB and TNF-α in tumor tissues of the treatment group was significantly decreased (P < 0.05). Compared with the pre-treatment group, GQD decreased the relative abundance of Megamonas and Veillonella. In addition, GQD increased the relative abundance of Bacteroides, Akkermansia and Prevotella. CONCLUSIONGQD enhances immunity and protects intestinal barrier function in patients with CRC by regulating the composition of gut microbiota.  相似文献   

15.
16.
BACKGROUNDEmerging evidence links gut microbiota to various human diseases including colorectal cancer (CRC) initiation and development. However, gut microbiota profiles associated with CRC recurrence and patient prognosis are not completely understood yet, especially in a Chinese cohort.AIMTo investigate the relationship between gut mucosal microbiota profiles and CRC recurrence and patient prognosis.METHODSWe obtained the composition and structure of gut microbiota collected from 75 patients diagnosed with CRC and 26 healthy controls. The patients were followed up by regular examination to determine whether tumors recurred. Triplet-paired samples from on-tumor, adjacent-tumor and off-tumor sites of patients diagnosed with/without CRC recurrence were analyzed to assess spatial-specific patterns of gut mucosal microbiota by 16S ribosomal RNA sequencing. Next, we carried out bioinformatic analyses, Kaplan-Meier survival analyses and Cox regression analyses to determine the relationship between gut mucosal microbiota profiles and CRC recurrence and patient prognosis.RESULTSWe observed spatial-specific patterns of gut mucosal microbiota profiles linked to CRC recurrence and patient prognosis. A total of 17 bacterial genera/families were identified as potential biomarkers for CRC recurrence and patient prognosis, including Anaerotruncus, Bacteroidales, Coriobacteriaceae, Dialister, Eubacterium, Fusobacterium, Filifactor, Gemella, Haemophilus, Mogibacteriazeae, Pyramidobacter, Parvimonas, Porphyromonadaceae, Slackia, Schwartzia, TG5 and Treponema.CONCLUSIONOur work suggests that intestinal microbiota can serve as biomarkers to predict the risk of CRC recurrence and patient death.  相似文献   

17.
肠道菌群由数万亿个微生物组成,正常情况下它们与宿主保持着共生关系,在调节宿主新陈代谢中发挥着重要作用。近年来,肠道菌群在各系统疾病中的作用受到了大量科研工作者的关注,本文就肠道菌群与非消化系统疾病的关系作一概述,为相关疾病的诊治提供更多的理论支持。  相似文献   

18.
非酒精性脂肪肝是代谢综合征的肝脏表现,可发展为肝硬化和肝癌。非酒精性脂肪肝的病因尚未明确,近年来宿主肠道微生物在非酒精性脂肪肝的发生、发展及治疗中的作用越来越受到重视。目前认为人类肠道是一个内在重要的代谢及免疫器官,肠道微生物的组成可影响宿主代谢,改变肠道通透性,引起炎症及一系列免疫反应。本文就肠道微生物在非酒精性脂肪肝的病理生理过程中的作用机制进行综述。  相似文献   

19.
《Diabetes & metabolism》2014,40(4):246-257
The gut microbiota is now considered as a key factor in the regulation of numerous metabolic pathways. Growing evidence suggests that cross-talk between gut bacteria and host is achieved through specific metabolites (such as short-chain fatty acids) and molecular patterns of microbial membranes (lipopolysaccharides) that activate host cell receptors (such as toll-like receptors and G-protein-coupled receptors). The endocannabinoid (eCB) system is an important target in the context of obesity, type 2 diabetes (T2D) and inflammation. It has been demonstrated that eCB system activity is involved in the control of glucose and energy metabolism, and can be tuned up or down by specific gut microbes (for example, Akkermansia muciniphila). Numerous studies have also shown that the composition of the gut microbiota differs between obese and/or T2D individuals and those who are lean and non-diabetic. Although some shared taxa are often cited, there is still no clear consensus on the precise microbial composition that triggers metabolic disorders, and causality between specific microbes and the development of such diseases is yet to be proven in humans. Nevertheless, gastric bypass is most likely the most efficient procedure for reducing body weight and treating T2D. Interestingly, several reports have shown that the gut microbiota is profoundly affected by the procedure. It has been suggested that the consistent postoperative increase in certain bacterial groups such as Proteobacteria, Bacteroidetes and Verrucomicrobia (A. muciniphila) may explain its beneficial impact in gnotobiotic mice. Taken together, these data suggest that specific gut microbes modulate important host biological systems that contribute to the control of energy homoeostasis, glucose metabolism and inflammation in obesity and T2D.  相似文献   

20.
非酒精性脂肪性肝病(NAFLD)在世界范围内患病率逐渐升高,“二次打击学说”发病机制已经被认可,但是具体的病理生理学发病机制还不完全清楚。近期,已有大量研究的新观点来解释肠道菌群在 NAFLD 发病机制中的作用,包括调节肠粘膜通透性、低水平炎症反应和免疫平衡,调节饮食胆碱代谢,调节胆汁酸代谢和增加细菌产生的内源性乙醇等。这些因素在分子水平上解释了肠道菌群如何促发 NAFLD 的发生,并进一步诱导其向非酒精性脂肪性肝炎(NASH)进展。  相似文献   

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