香菇多糖对微生态失调小鼠肠道菌群及免疫功能的调节作用

目的 探讨香菇多糖对微生态失调小鼠肠道菌群及免疫功能的调节作用.方法 经盐酸林可霉素灌胃建立肠道微生态失调小鼠模型,香菇多糖灌胃治疗,同时设正常对照组、自然恢复组和丽珠肠乐组.7d后处死各组小鼠,进行肠道菌群定量、免疫器官体重及其淋巴细胞转化率检测.结果 用香菇多糖对肠道微生态失调小鼠进行治疗后,小鼠肠道双歧杆菌、乳酸杆菌数量显著增加,而肠杆菌和肠球菌的数量显著降低;脾脏指数明显增加,对胸腺指数无影响;显著增强了淋巴细胞转化率.结论 盐酸林克霉素灌胃能诱导微生态失调小鼠模型的有效建立.香菇多糖能调整小鼠肠道菌群及免疫功能.     

马齿苋多糖对肠道微生态失调小鼠的调整作用研究

目的研究应用马齿苋多糖对肠道微生态失调小鼠进行调整治疗,达到从微生态学角度防治感染的目的。方法应用林可霉素灌胃建立肠道微生态失调小鼠模型,然后用马齿苋多糖进行治疗,同时设正常对照组、阳性对照组和阴性对照组,于给药7 d后处死小鼠,进行肠道菌群定量、肠内容物挥发性脂肪酸检测及肠黏膜电镜观察。结果林可霉素灌胃3 d后,小鼠肠道菌群失调,肠内容物挥发性脂肪酸含量明显下降,肠黏膜损伤严重。持续7 d治疗后,治疗组小鼠肠道双歧杆菌和乳酸杆菌数量明显上升,肠内容物挥发性脂肪酸含量明显上升,损伤的肠黏膜基本修复。结论应用林可霉素可以成功建立肠道微生态失调动物模型;马齿苋多糖具有扶植肠道正常菌群生长,调整菌群失调,防治感染的作用,是理想的中药微生态调节剂。     

低聚木糖对模拟失重大鼠肠道微生态的影响

目的 研究低聚木糖对模拟失重大鼠肠道微生态的影响。方法 采用大鼠尾部悬吊法模拟失重。32只雄性SD大鼠随机分为4组,每组8只：FC组（地面对照组,饲喂基础饲料）,FS组（地面处理组,饲喂添加低聚木糖的饲料）,SC组（尾吊对照组,饲喂基础饲料）。SS组（尾吊处理组,饲喂添加低聚木糖的饲料）,实验21d,SC和SS组解除尾吊继续观察。实验21d。采用选择性培养基对大鼠粪便肠杆菌、肠球菌、类杆菌、双歧杆菌以及乳杆菌进行定量测定。结果 SC组与FC组相比,双歧杆菌数量减少,肠杆菌和肠球菌数量增加;FS组比FC组双歧杆菌数量增加显著,肠杆菌和肠球菌有不同程度的减少,SS组比SC组双歧杆菌数量增加显著,肠杆菌和肠球菌也有不同程度的减少。类杆菌和乳杆菌变化不明显。尾吊解除期,SS组双歧杆菌数量比SC组更快恢复到正常水平。结论 低聚木糖可促进尾吊大鼠肠道益生菌主要是双歧杆菌的增殖,一定程度上促进由于模拟失重造成肠道微生态失调的平衡,并对条件致病菌具有一定的抑制作用。     

肠道微生态失调与脆弱类杆菌感染的实验研究

应用对四环素具有高度耐药性的厌氧脆弱类杆菌,经口灌注于肠道微生态矢调的小白鼠胃内,以观察肠道微生态失调和脆弱类杆菌感染关系。实验证明：耐药脆弱类杆菌在菌群失调的小白鼠（实验组）体内大量增殖并侵袭入血和肠系膜淋巴结,最后在皮下形成脓肿,而对照组虽也于粪便、血、淋巴结中发现供试菌,但随时间推移迅速减少至消失,两组间有非常显著性差异（Ｐ＜０．０１）。据此可以认为肠道微主态平衡可有效预防脆弱类杆菌感染,即使侵入人体也可使之消灭。本试验为脆弱类杆菌感染与肠道微生态关系,提供了有价值的数据。     

施普瑞螺旋藻对尾吊模拟失重大鼠肠道微生态失调的调整作用研究

目的：研究模拟失重条件下,施普瑞螺旋藻对大鼠肠道微生态失调的调整作用。方法：将基础饲料中加入5%的螺旋藻作为处理组饲喂大鼠,用选择性培养基分别对肠球菌、肠杆菌、类杆菌、乳杆菌以及双歧杆菌定量测定,扫描电镜观察大鼠盲肠上皮细胞的组织变化,结果：螺旋藻处理组过路菌群中肠杆菌和肠球菌数量变化并不明显;原籍菌群中双歧杆菌较对照组显著增多,类杆菌和乳杆菌的数量差异没有显著性,模拟失重条件下SD大鼠盲肠上皮有肿胀细胞出现,并且肠道上皮绒毛排列紊乱、稀疏、而螺旋藻处理组中只发现有少量的肿胀细胞,上皮绒毛致密,排列较整齐。结论：旋普瑞螺旋藻具有纠正在模拟失重条件下大鼠肠道微生态平衡失调的作用。     

八珍制剂对60Co辐射小鼠微生态失调的促恢复作用

目的观察中药八珍制剂对60Co辐射小鼠微生态失调的调整作用.方法 60Co辐射昆明种小鼠制成微生态失调模型,用中药八珍制剂对其进行调整,检测肠道膜菌群与腔菌群中双歧杆菌、乳酸杆菌、肠杆菌、肠球菌及肝脏细菌易位数量,血浆内毒素水平,小肠黏膜中二胺氧化酶的活性和丙二醛的含量等指标,观测中药对辐射性微生态失调的调整作用.结果:中药八珍制剂具有调整小鼠肠道菌群失调,降低肠道菌易位和血浆内毒素水平,减少丙二醛含量,升高肠黏膜中二胺氧化酶的活性.中药治疗组各项指标与自然恢复组相比,差异均有显著性( P<0.001或P<0.01或P<0.05).结论八珍制剂对60Co辐射小鼠微生态失调有促恢复作用.     

应用丽珠肠乐治疗小儿肠道菌丛失调症的疗效观察

应用丽珠肠乐治疗小儿肠道菌丛失调症的疗效观察河南医科大学第三附属医院小儿内科郑州市４５００５２王宏,王玉梅,朱绍先,张素珍丽珠肠乐（回春生）胶囊为活的双歧杆菌制剂,通过恢复肠道微生态平衡,达到治疗肠道菌丛失调的目的。我们自１９９３．２～９３．９应用丽...     

微生态调整疗法防治急性坏死性胰腺炎肠道细菌易位的初步观察

目的：观察双歧杆菌合剂对急性坏死性胰腺炎（ＡＮＰ）时肠道细菌易位的影响。方法：杂种犬２３只,分３组：对照组（ｎ＝７）仅作剖腹探查,另１６只复制ＡＮＰ模型后,分为微生态调理组（ｎ＝８）和ＡＮＰ组（ｎ＝８）。测定血中胰淀粉酶、内毒素,作脏器细菌培养、病理检查和肠粘膜菌群分析。结果：ＡＮＰ组胰、肠病理损害严重,血淀粉酶（ＡＭＹ）和内毒素（ＬＰＳ）持续升高。肠粘膜大肠杆菌及类杆菌数量增加,双歧杆菌和乳杆菌减少,脏器细菌培养阳性率１００％。与ＡＮＰ组比较,微生态组胰、肠病理损害减轻,肠粘膜类杆菌、大肠杆菌数量减少,双歧杆菌和乳杆菌增加,肠道微生态趋于平衡,脏器中细菌移位率由１００％降为６２．５％,数量减少１０－４０倍,血淀粉酶及内毒素水平下降２～３倍。结论：双歧杆菌合剂可减轻ＡＮＰ后肠粘膜的损害,调整菌群失调,保护肠屏障功能,对防治ＡＮＰ后肠道细菌易位和肠源性感染具有重要作用。     

八珍制剂对~(60)Co辐射小鼠微生态失调的促恢复作用

目的　观察中药八珍制剂对60 Co辐射小鼠微生态失调的调整作用。方法　60 Co辐射昆明种小鼠制成微生态失调模型 ,用中药八珍制剂对其进行调整 ,检测肠道膜菌群与腔菌群中双歧杆菌、乳酸杆菌、肠杆菌、肠球菌及肝脏细菌易位数量 ,血浆内毒素水平 ,小肠黏膜中二胺氧化酶的活性和丙二醛的含量等指标 ,观测中药对辐射性微生态失调的调整作用。结果 :中药八珍制剂具有调整小鼠肠道菌群失调 ,降低肠道菌易位和血浆内毒素水平 ,减少丙二醛含量 ,升高肠黏膜中二胺氧化酶的活性。中药治疗组各项指标与自然恢复组相比 ,差异均有显著性(P <0 .0 0 1或P <0 .0 1或P <0 .0 5 )。结论　八珍制剂对60 Co辐射小鼠微生态失调有促恢复作用     

马齿苋多糖对衰老小鼠肠道微生态调节作用的研究

目的探讨中药马齿苋多糖对衰老小鼠微生态调节作用。方法皮下注射D-半乳糖建立衰老小鼠模型,用马齿苋多糖进行治疗,同时设正常对照组、阳性对照组和阴性对照组,用药30d后处死小鼠,进行肠道微生态指标检测。结果用D-半乳糖造模以后,小鼠肠道双歧杆菌及乳酸杆菌数量降低（P〈0．05）,而肠杆菌及肠球菌数量增加说明模型建立,血内毒素含量也升高（P〈0．05）。用马齿苋治疗后,益生菌数量升高而肠杆菌和肠球菌数量减少,血内毒素含量也降低（P〈0．05）。结论马齿苋多糖对衰老小鼠的肠道菌群和血内毒素具有调节作用。     

High‐fat diet‐induced dysbiosis mediates MCP‐1/CCR2 axis‐dependent M2 macrophage polarization and promotes intestinal adenoma‐adenocarcinoma sequence

High‐fat diet (HFD) is a well‐known risk factor for gut microbiota dysbiosis and colorectal cancer (CRC). However, evidence relating HFD, gut microbiota and carcinogenesis is limited. Our study aimed to demonstrate that HFD‐induced gut dysbiosis promoted intestinal adenoma‐adenocarcinoma sequence. In clinical study, we found that HFD increased the incidence of advanced colorectal neoplasia (AN). The expression of monocyte chemoattractant protein 1 (MCP‐1), CC chemokine receptor 2 (CCR2) and CD163 in CRC patients with HFD was significantly higher than that in CRC patients with normal diet. When it comes to the Apc^min/+ mice, HFD consumption could induce gut dysbiosis and promote intestinal carcinogenesis, accompanying with activation of MCP‐1/CCR2 axis that recruited and polarized M2 tumour‐associated macrophages. Interestingly, transfer of faecal microbiota from HFD‐fed mice to another batch of Apc^min/+ mice in the absence of HFD could also enhance carcinogenesis without significant body weight gain and induced MCP‐1/CCR2 axis activation. HFD‐induced dysbiosis could also be transmitted. Meanwhile, antibiotics cocktail treatment was sufficient to inhibit HFD‐induced carcinogenesis, indicating the vital role of dysbiosis in cancer development. Conclusively, these data indicated that HFD‐induced dysbiosis accelerated intestinal adenoma‐adenocarcinoma sequence through activation of MCP‐1/CCR2 axis, which would provide new insight into better understanding of the mechanisms and prevention for HFD‐related CRC.     

Interrelationship between the 5-lipoxygenase pathway and microbial dysbiosis in the progression of Alzheimer's disease

Alzheimer's disease (AD) is an age-related neurodegenerative disorder involving neurofibrillary tangles and amyloid plaques. The tau phosphorylation responsible for neurofibrillary tangles and amyloid deposition which causes plaques are both accelerated through the activity of 5-lipoxygenase (5-LO). In addition to these pathological pathways, 5-LO has also been linked to the neuro-inflammation associated with disease progression as well as to dysbiosis in the gut. Interestingly, gut dysbiosis itself has been correlated to AD development. Not only do gut metabolites have direct effects on the brain, but pro-inflammatory mediators such as LPS, BMAA and bacterial amyloids produced in the gut due to dysbiosis reach the brain causing increased neuro-inflammation. While microbial dysbiosis and 5-LO exert detrimental effects in the brain, the cause/effect relationship between these factors remain unknown. These issues may be addressed using mouse models of AD in the context of different knockout mice in the 5-LO pathway in specific pathogen-free, germ-free as well as gnotobiotic conditions.     

Decreased Enterobacteriaceae translocation due to gut microbiota remodeling mediates the alleviation of premature aging by a high-fat diet

Aging-associated microbial dysbiosis exacerbates various disorders and dysfunctions, and is a major contributor to morbidity and mortality in the elderly, but the underlying cause of this aging-related syndrome is confusing. SIRT6 knockout (SIRT6 KO) mice undergo premature aging and succumb to death by 4 weeks, and are therefore useful as a premature aging research model. Here, fecal microbiota transplantation from SIRT6 KO mice into wild-type (WT) mice phenocopies the gut dysbiosis and premature aging observed in SIRT6 KO mice. Conversely, an expanded lifespan was observed in SIRT6 KO mice when transplanted with microbiota from WT mice. Antibiotic cocktail treatment attenuated inflammation and cell senescence in KO mice, directly suggesting that gut dysbiosis contributes to the premature aging of SIRT6 KO mice. Increased Enterobacteriaceae translocation, driven by the overgrowth of Escherichia coli, is the likely mechanism for the premature aging effects of microbiome dysregulation, which could be reversed by a high-fat diet. Our results provide a mechanism for the causal link between gut dysbiosis and aging, and support a beneficial effect of a high-fat diet for correcting gut dysbiosis and alleviating premature aging. This study provides a rationale for the integration of microbiome-based high-fat diets into therapeutic interventions against aging-associated diseases.     

口炎清颗粒调整菌群失调有效组分的研究

目的 探讨口炎清组分玄参对于小鼠肠道菌群的调节作用.方法 应用抗生素头孢曲松钠灌胃的方法建立小鼠肠道菌群失衡模型.利用观察称量等方法观察小鼠临床表征的变化,以及盲肠指数和脾指数的变化.利用活菌计数法分析肠道优势菌群的变化趋势.结果 (1)菌群失衡组盲肠指数增高(P＜0.05);自然恢复组盲肠指数变化不明显;玄参流膏与大豆低聚糖回灌组盲肠指数均显著下降(P＜0.05),呈恢复趋势.(2)菌群失衡组脾脏指数有下降趋势,自然恢复组脾脏指数无明显变化;玄参流膏组与大豆低聚糖回灌组脾脏指数均有所上升,呈恢复趋势.(3)菌群失衡组厌氧菌被抑制,需氧球菌大量繁殖.自然恢复组菌群种类和数量变化不明显,玄参组厌氧菌重新出现,尤其是双歧杆菌、乳杆菌、韦荣球菌和类杆菌的出现预示着菌群正在逐渐恢复正常.结论 玄参流膏可以促进菌群失衡小鼠盲肠和脾脏大小的恢复,可以调节小鼠肠道菌群失衡,具有类似大豆低聚糖的益生元功效.     

An Alternative Explanation for Alzheimer’s Disease and Parkinson’s Disease Initiation from Specific Antibiotics,Gut Microbiota Dysbiosis and Neurotoxins

The late onset neuropathologies, including Alzheimer’s disease and Parkinson’s disease, have become increasingly prevalent. Their causation has been linked to genetics, gut microbiota dysbiosis (gut dysbiosis), autoimmune diseases, pathogens and exposures to neurotoxins. An alternative explanatory hypothesis is provided for their pathogenesis. Virtually everyone has pervasive daily exposures to neurotoxins, through inhalation, skin contact, direct blood transmission and through the gastrointestinal tract by ingestion. As a result, every individual has substantial and fluctuating neurotoxin blood levels. Two major barriers to neurotoxin entry into the central nervous system are the blood–brain barrier and the intestinal wall, in the absence of gut dysbiosis. Inflammation from gut dysbiosis, induced by antibiotic usage, can increase the intestinal wall permeability for neurotoxins to reach the bloodstream, and also increase the blood–brain barrier permeability to neurotoxins. Gut dysbiosis, including gut dysbiosis caused by antibiotic treatments, is an especially high risk for neurotoxin entry into the brain to cause late onset neuropathologies. Gut dysbiosis has far-reaching immune system and central nervous system effects, and even a transient gut dysbiosis can act in combination with neurotoxins, such as aluminum, mercury, lead, arsenic, cadmium, selenium, manganese, organophosphate pesticides and organochlorines, to reach neurotoxin blood levels that can initiate a late onset neuropathology, depending on an individual’s age and genetic vulnerability.

     

口炎清颗粒对小鼠肠道菌群失衡的调节作用

目的探讨口炎清颗粒对肠道菌群失衡的调节作用。方法小鼠随机分为6组：正常对照组、重度失调组、自然恢复组、口炎清低剂量组、口炎清高剂量组和大豆低聚糖对照组。正常对照组小鼠灌服蒸馏水,其他组以头孢曲松钠终浓度为8 g/（kg.d）的剂量,连续灌胃8 d,建立小鼠菌群失衡模型,自然恢复组在失衡模型建立后不使用任何药物,自然恢复7 d;口炎清低剂量组、高剂量组、大豆低聚糖对照组分别灌服相应剂量的药物7 d,观察各组小鼠盲肠指数和肠道内双歧杆菌、类杆菌、韦荣球菌、乳酸杆菌、消化球菌、优杆菌、葡萄球菌、肠球菌、大肠埃希菌、链球菌和酵母菌11种菌群变化。结果与菌群失衡组比较,口炎清组与大豆低聚糖组盲肠指数均显著下降（P〈0.05）,呈恢复趋势。自然恢复组肠道菌群种类和数量变化不明显,口炎清组厌氧菌重新出现,尤其是低剂量组双歧杆菌、优杆菌和类杆菌的出现预示着肠道菌群正在逐渐恢复正常。结论一定浓度的口炎清可以明显促进菌群失衡小鼠盲肠大小的恢复,对小鼠肠道菌群有调节作用,具有类似大豆低聚糖的益生元功效。     

阴道菌群移植治疗细菌性阴道炎的发展现状及展望

细菌性阴道炎 (Bacterial vaginosis,BV) 是由患者阴道内菌群失调导致的一类疾病。当前常规的抗生素疗法可进一步加剧阴道菌群失衡、破坏阴道酸性环境、导致耐药,因此其对BV治愈率低,复发率高。作为一种新兴的活菌疗法,阴道菌群移植 (Vaginal microbiota transplantation,VMT) 直接将健康妇女完整的阴道菌群“嫁接”给患者,可迅速恢复患者阴道菌群的平衡,改善患者的整体健康。文中对VMT的发展历程进行了回顾,讨论了VMT发展过程中面临的难题及发展方向,以期寻求新的治疗BV的策略,加速VMT的临床应用。     

Is Gut Dysbiosis an Epicenter of Parkinson’s Disease?

Once recognized as one of the most esoteric diseases of the central nervous system, Parkinson’s disease (PD) is now deemed to be a chronic illness contributed by the central, autonomic and enteric nervous systems. Most likely, an accumulation of α-synuclein in the central and enteric nervous systems is the key that supports this viewpoint. Constipation, one of the non-motor hallmarks in roughly two-third of PD patients, is regulated by the composition of gut bacteria, which is assumed to set off the enteric α-synuclein accrual. Vagus nerve is suggested to direct the signal for α-synuclein over-expression and accumulation to the brain. While trillions of microorganisms reside in the intestinal tract, only one third of the proportion inhabits evenly in all individuals. Existence of an impaired gut-microbe-brain axis consonant with dysbiosis could be an epicenter of this inexplicable disorder. Any alteration in the structure and function of the gastrointestinal tract owing to exposure of endogenous or exogenous chemicals or toxicants could lead to dysbiosis. However, inconsistency in the symptoms even after exposure to same chemical or toxicant in PD patients emphatically creates a conundrum. While the level of a few specific neurotransmitters and metabolites is influenced by microbes, implication of dysbiosis is still debatable. Nevertheless, the scientific literature is overflowing with the remarkable observations supporting the role of dysbiosis in PD. Lack of specificity to differentially diagnose PD with non-PD or PD-plus syndrome, to identify highly precise drug targets and to develop therapeutic stratagems to encounter the disease on the basis of this approach, causes us to be open-minded about the dysbiosis theory. The article reviews the facts supporting gut dysbiosis as the foremost trigger for PD onset along with disagreements.

     

The Vaginal Microbiota: What Have We Learned after a Decade of Molecular Characterization?

We conducted a systematic review of the Medline database (U.S. National Library of Medicine, National Institutes of Health, Bethesda, MD, U.S.A) to determine if consistent molecular vaginal microbiota (VMB) composition patterns can be discerned after a decade of molecular testing, and to evaluate demographic, behavioral and clinical determinants of VMB compositions. Studies were eligible when published between 1 January 2008 and 15 November 2013, and if at least one molecular technique (sequencing, PCR, DNA fingerprinting, or DNA hybridization) was used to characterize the VMB. Sixty three eligible studies were identified. These studies have now conclusively shown that lactobacilli-dominated VMB are associated with a healthy vaginal micro-environment and that bacterial vaginosis (BV) is best described as a polybacterial dysbiosis. The extent of dysbiosis correlates well with Nugent score and vaginal pH but not with the other Amsel criteria. Lactobacillus crispatus is more beneficial than L. iners. Longitudinal studies have shown that a L. crispatus-dominated VMB is more likely to shift to a L. iners-dominated or mixed lactobacilli VMB than to full dysbiosis. Data on VMB determinants are scarce and inconsistent, but dysbiosis is consistently associated with HIV, human papillomavirus (HPV), and Trichomonas vaginalis infection. In contrast, vaginal colonization with Candida spp. is more common in women with a lactobacilli-dominated VMB than in women with dysbiosis. Cervicovaginal mucosal immune responses to molecular VMB compositions have not yet been properly characterized. Molecular techniques have now become more affordable, and we make a case for incorporating them into larger epidemiological studies to address knowledge gaps in etiology and pathogenesis of dysbiosis, associations of different dysbiotic states with clinical outcomes, and to evaluate interventions aimed at restoring and maintaining a lactobacilli-dominated VMB.