消化道疾病患者胃微生态环境的改变

本文对５９例具有消化不良症状的患者做了内镜检查。取胃粘膜组织进行细菌的分离培养,镜检,测定胃液中的ｓＩｇＡ的含量及ｐＨ。结果表明,不同消化道疾病,胃的微生态环境会发生不同的改变。其中胃癌患者改变最明显,胃内微生物检出率高,ｐＨ均大于４,ｓＩｇＡ含量１４０．５７±３７．４５μｇ／ｍｌ,幽门螺杆菌（ＨＰ）的检出率为６６．７％;溃疡组,ＨＰ的检出率为７９．２％,其它微生物检出率较胃癌组低,ｓＩｇＡ含量１３３．８０±６５．８４μｇ／ｍｌ;胃炎组,微生物的检出率较低,ｓＩｇＡ含量７１．００±６０．３８μｇ／ｍｌ,ｐＨ大部分在２一４。     

消化道微生态标准化样本库共识

生物样本库主要是指标准化收集、处理、储存和应用健康和疾病生物体的器官、组织、细胞、血液、体液、分泌物、排泄物及生物大分子衍生物等各种生物样本,以及与这些样本相关的临床、检验、病理、影像、治疗、随访、患者知情同意等信息,包括质量控制、信息管理与应用系统。人类消化道生存着众多微生物,包括细菌、古生菌、真菌、病毒和原虫等[1]。肠道微生物与宿主长期共同进化,构成肠道微生态,影响着宿主的健康。随着测序等高通量技术和生物信息学发展,以消化道微生态（主要是细菌和真菌）样本为基础的研究使得我们对消化道微生态的认知和应用向前推进了一大步[2],成为国内外重要的研究热点。然而,消化道微生态样本的采集、制备、储存等是后续研究的第一步,对检测和分析结果有着重要的影响[3]。统一标准、高质量的生物样本是研究数据真实性、可重复性、一致性及整合数据和应用等的根本基础,也是进行基础和临床大数据研究的重要保障。消化道微生态样本可用于基因组、转录组、蛋白质组、代谢组、培养组、营养组、微生态移植、转化医学等多方面研究。目前尚缺乏消化道微生态样本库构建的标准及规范,制定共识意见非常迫切和必要。     

微生态肠内营养在消化道瘘治疗中作用

目的探讨微生态肠内营养在消化道瘘治疗中的临床效果。方法将23例消化道瘘患者随机分为微生态制剂肠内营养组(MEN组)和普通肠内营养组(EN组),MEN组12例,EN组11例,检测患者鼻空肠饲养前后血清总蛋白、血清白蛋白、外周血白细胞、中性粒细胞比率、淋巴细胞计数及消化道症状。结果 MEN组与EN组血清总蛋白、血清白蛋白、外周血白细胞、中性粒细胞比率、淋巴细胞计数比较差异无统计学意义(P>0.05),但MEN组与EN组在消化道症状方面差异有统计学意义(P<0.05)。结论早期肠内微生态营养可以明显减轻消化道瘘患者的胃肠道症状,有利于肠道功能的恢复。     

肠道微生态与非消化系统疾病的研究进展

人体肠道微生态系统是人体微生态系统中最大最复杂的一部分,参与机体代谢、免疫等各方面的生理作用。由于内外源性的病理因素导致肠道微生态的破坏可能会引起人体疾病。随着肠道微生态与消化道疾病研究的不断深入,越来越多的学者开始关注肠道微生态与非消化道疾病的相关性。近年来大量研究表明,肠道微生态与肥胖、神经精神病、皮肤病、心脑血管疾病、消化道外肿瘤、感染性疾病和自身免疫病等非消化系统疾病具有相关性。微生态制剂和粪菌移植可以通过调节肠道微生态平衡参与这类疾病的预防和治疗。肠道微生态系统与消化系统疾病的相关性已被广泛研究和阐述,本文侧重对肠道微生态与非消化系统疾病的研究进展进行综述。     

消化道选择性脱污染和微生态制剂的应用评价

消化道选择性脱污染和微生态制剂的应用评价云南省玉溪地区卫生防疫站玉溪６５３１００王树坤健康成人肠内细菌约有１,０００克,占肠内容物的７５％,为人体总微生物量的７８．６７％,每克肠内容物含１０１４个属于４００多个种群可培养的厌氧、兼性厌氧、需氧菌〔１,...     

消化道微生态与胆石症关系研究进展

胆石症（gallstone disease,GSD）是消化外科领域常见的疾病,严重影响机体健康。既往研究发现GSD形成机制可能与饮食习惯、肥胖、遗传因素及基因调控水平、胆汁胆固醇过饱和、胆囊运动障碍和胆汁排出受阻、黏蛋白异常积累和胆汁酸代谢障碍等有关。近年来随着宏基因组鸟枪测序及16S rRNA基因测序等分子生物学技术的广泛应用,大量研究发现消化道微生态（包括口腔微生态、胆道微生态和肠道微生态等）与胆道结石的形成密切相关。本文对消化道微生态与GSD关系的相关研究进行梳理与综述,旨在为GSD的预防、治疗和改善预后提供新的策略。

     

消化道微生态学（续）

消化道优势菌群的作用由众多不同的细菌所组成的消化道菌群具有大量的不同的酶活潜势,因此可以认为存在于消化道中的这些酶群可显著地影响动物宿主的主要新陈代谢活动。以下(消化道菌群的作用)列举了至今所见到的由菌群所引起的动物宿主的某些改变。 1、消化道内容物质量的修饰:物理(pH;氧化还原电位);生化学(细菌代谢物)。 2、消化道解剖学的修饰:不同腔窒的体积:消化道壁的结构;消化道粘膜可吸收面积。 3、消化道生理学的修饰:肠蠕动;消化道上皮细胞的再生;脂、糖、氮、水、无机物等物质的吸     

人体微生态与健康和疾病

人体微生态是人体内的微生物生态群落,是存在于人体组织和体液中的共生和病原微生物的总和,也是近年来发现的\"新器官\",它在维持人体健康过程中扮演着重要角色。微生态与宿主间有着全面广泛的相互作用机制,微生态失衡与疾病的发生发展密切相关。本文概述了人体微生态与健康和疾病研究的重要意义,并对国内外研究进展作总结评述。     

从消化道微生态学说起

从消化道微生态学说起日本国立富山医科药科大学药学部,小桥恭一同校药学部博士课程研究生杨凌（译）近代宏观生态学是以保护地球环境之运动而盛兴,注目的焦点诸如二氧化碳气体排放使植物同化、地球生温,氟里昂的排放使臭氧层崩溃等等问题。１９９４年,在德国则见诸行...     

胰腺疾病的肠道微生物群研究进展

肠道微生物群是指存在于人体消化道内的微生物组成的复杂群落。随着16S rRNA基因测序和宏基因组测序等高通量测序技术的发展,肠道微生物群已被证明与多种疾病息息相关。三大胰腺疾病与肠道微生物群密切相关,急性胰腺炎（acute pancreatitis,AP）、慢性胰腺炎（chronic pancreatitis,CP）和胰腺癌患者肠道微生物群的构成和丰度均与健康人群不同。反之,肠道微生物群的改变会减慢或加速胰腺疾病的发生发展。益生菌和抗菌药物的使用及粪菌移植等可减轻胰腺炎症反应,缓解胃肠道症状,影响胰腺癌化疗和免疫治疗的效果,因此可为胰腺疾病的诊疗提供新策略。本文总结了AP、CP和胰腺癌的肠道微生物群研究,阐述了疾病发生时肠道微生物群的变化、与胰腺相互作用的机制以及目前的主要研究技术,探讨了肠道微生物群在胰腺疾病诊疗中的研究进展。

     

急性胰腺炎患者肠道菌群的研究进展

急性胰腺炎（acute pancreatitis,AP）是临床常见的急腹症之一,肠道黏膜损伤和肠道菌群紊乱是AP常见的并发症,影响AP的进展和预后。近年来,肠道菌群在疾病中的作用逐渐引起人们的重视,各种肠道轴的发现为临床疑难疾病的诊治打开了一扇新的大门,其中肠道菌群代谢产物发挥着极其重要的作用。本文对AP患者肠道菌群的变化、肠道菌群紊乱对AP病情进展的影响、肠道菌群代谢产物对肠道黏膜的保护作用及其在AP发生发展中的作用、肠道菌群相关治疗方法在AP治疗中的应用等方面进行综述,以期为AP的临床诊疗提供新的思路。     

急性胰腺炎大鼠腺泡细胞凋亡及X连锁凋亡抑制蛋白XIP的表达

目的:研究急性胰腺炎(AP)大鼠腺泡细胞凋亡,X连锁凋亡抑制蛋白(XIAP)的表达及其与疾病严重程度的关系。方法:通过胰胆管逆行注射不同浓度的牛黄胆酸钠,制备急性水肿型胰腺炎(AEP)和急性坏死性胰腺炎(ANP)大鼠模型,同时设假手术(SO)组为对照。收集各模型组3,6和12h标本,对胰腺组织进行病理学评分,并测定血清淀粉酶和腹水量;用TUNEL染色检测胰腺腺泡细胞的凋亡,分别RT-PCR和Western Blotting法测定大鼠胰腺组织XIAP mRNA及蛋白的表达。结果:成功建立了大鼠AP模型。同SO组相比,ANP和AEP组胰腺组织在各时间点均有不同程度的病理损害,血清淀粉酶也显著增高(P均<0.01)。且ANP组显著高于AEP组(P均<0.01)。造模成功3h后,各组大鼠胰腺腺泡细胞均出现少量凋亡,但ANP和AEP组凋亡显著多于SO组(P<0.05),ANP和AEP组间没有差别(P>0.05)。同SO组相比,ANP和AEP组在6h和12h时凋亡均增多(P<0.01),且AEP组显著高于ANP组(P<0.01)。造模成功3h后,各模型组XIAP mRNA表达没有差异(P>0.05);6h和12h时AEP组XIAP mRNA表达明显下降,而ANP组明显升高,两组间差异有显著性(P<0.01)。XIAP蛋白表达水平与mRNA表达水平相一致。结论:急性胰腺炎大鼠胰腺组织XIAP表达与腺泡细胞凋亡情况相反,且与疾病严重程度平行。XIAP可能负性调控AP大鼠胰腺腺泡细胞的凋亡。     

Ascitic fluid and serum from rats with acute pancreatitis injure rat pancreatic tissues and alter the expression of heat shock protein 60

Acute pancreatitis (AP) is an inflammatory process in which cytokines and chemokines are involved. After onset, extrapancreatic stimuli can induce the expression of cytokines in pancreatic acinar cells, thereby amplifying this inflammatory loop. To further determine the role and mechanism of irritating agents in the pathogenesis of AP, rat pancreatic tissues were stimulated with ascitic fluid (APa) and serum (APs) from rats with AP or with lipopolysaccharide (LPS). In addition, the alteration of heat shock protein 60 (HSP60) expression was evaluated. Rat pancreas was removed and meticulously snipped to fragments. The snips were cultured for up to 48 h. During this period, the tissue viability as well as amylase and TNF-α levels in the supernatant and the HSP60 expression in the pancreatic tissue before and after stimulation by APa, APs, and LPS were assayed time-dependently. At different time-points during the culture, the viability and the amylase activity in the pancreatic tissue remained largely stable. After stimulation with APa, APs, or LPS for 1 h, the pancreatic tissues showed some damage, and this was followed by a sharp decrease in the viability accompanied by increased levels of amylase and TNF-α in the culture medium 2 or 4 h after stimulation (p < 0.05). In contrast, both the HSP60 mRNA and protein levels had a relatively high expression in the freshly prepared tissue fragments (0 h). As the culturing period was extended, the expression of HSP60 mRNA decreased only slightly; at the same time, the HSP60 protein levels decreased over a prolonged culture time, significantly so from 12 through 48 h (p < 0.05). After stimulation with APs, APa, or LPS, both the expression of HSP60 mRNA and protein in the tissue fragments increased slightly at 1 h and decreased significantly thereafter at 2 and 4 h (p < 0.05). APa, APs, or LPS induce injuries on isolated pancreatic tissues, accompanied by an altered HSP60 expression pattern in a time-dependent manner.     

Supplementation of pancreatic digestive enzymes alters the composition of intestinal microbiota in mice

Although pancreatic enzyme replacement therapy (PERT) is effective in the alleviation of pancreatic exocrine insufficiency (PEI)-related symptoms in patients with chronic pancreatitis, its mechanism of action is poorly understood. Recent studies suggest that the intestinal microbiota is associated with the pathogenesis of chronic pancreatitis. Therefore, we hypothesized that PERT exerts its effect by modifying the intestinal microbiota in addition to its presumed role in promoting fat and protein absorption. To explore the mechanism of action of PERT, we analyzed the intestinal microbiotas of two groups of mice treated with either pancrelipase or tap water by using 16S rRNA amplicon sequencing. The results revealed that the bacterial compositions of the pancrelipase-treated mice were significantly different from those of the control samples. Akkermansia muciniphila, a key beneficial bacterium in the intestinal tract, showed a higher relative abundance in the pancrelipase-treated samples than in the control samples. Lactobacillus reuteri, a widely used probiotic bacterium known to relieve intestinal inflammation, also showed a higher relative abundance in the pancrelipase-treated samples. These results suggested that PERT induces the colonization of beneficial bacteria, thereby contributing to the attenuation of PEI-associated symptoms in addition to improvement of the nutritional state.     

Alteration of Cpn60 expression in pancreatic tissue of rats with acute pancreatitis

The expression of heat-shock protein 60 (also known as chaperonin 60, Cpn60) in experimental acute pancreatitis (AP) is considered to play an active role in the prevention of abnormal enzyme accumulation and activation in pancreatic acinar cells. However, there are controversial results in the literature regarding the relationship between the abnormality of Cpn60 expression and AP onset and development. The purpose of this study was to investigate the alternations of Cpn60 expression and the relationship between the abnormal expression of Cpn60 and AP progression in rat severe acute pancreatitis (SAP) models. In this report, we induced SAP in Sprague–Dawley (SD) rats by reverse injection of sodium deoxycholate into the pancreatic duct, and examined the dynamic changes of Cpn60 expression in pancreatic tissues from different time points and at different levels with techniques of real-time PCR, western blotting, and immunohistochemistry. At 1 h after SAP induction, the expression of Cpn60 mRNA in the AP pancreatic tissues was higher than those in the sham-operation group and normal control group, but decreased sharply as the time period was extended, and there was a significant difference between 1 h and 10 h after SAP induction (p < 0.05). In the AP process, Cpn60 protein expression showed transient elevation as well, and the increased protein expression occurred predominantly in affected, but not totally destroyed, pancreatic acinar cells. As AP progressed, the pancreatic tissues were seriously damaged, leading to a decreased overall Cpn60 protein expression. Our results show a complex pattern of Cpn60 expression in pancreatic tissues of SAP rats, and the causality between the damage of pancreatic tissues and the decrease of Cpn60 level needs to be investigated further. Xue-Li Li and Kun Li contributed equally to this work.     

Chronic pancreatitis, pancreatic adenocarcinoma and the black box in-between

Pancreatic cancer is a challenging disease for patients, doctors and researchers who for decades have searched for a cure for this deadly malignancy. Although existing mouse models of pancreatic cancer have shed light on the mechanistic basis of the neoplastic conversion of the pancreas, their impact in terms of offering new diagnostics and therapeutic modalities remains limited. Chronic pancreatitis is an inflammatory disease of the pancreas that is associated with a gradual damage of the organ and an increased risk of developing neoplastic lesions. In this review, we propose that detailed studies of chronic inflammatory processes in the pancreas will provide insights into the evolution of pancreatic cancer. This information may prove useful in the design of effective therapeutic strategies to battle the disease.