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研究新发现: 剖腹产儿童更易发生变态反应

来源:生物探索作者:热度:Loading...日期:2013-08-15, 11:44 AM
 导读:中国的剖腹产率异常偏高,越来越多的女性生孩子选择剖腹产。但多项研究表明,剖腹产明显影响后代的健康。剖腹产生下的孩子,由于肠道菌群建设与发育明显滞后,相比顺产生下的孩子更容易发生机体变态反应。剖腹产只应该用于有手术指征的情况下实施。对于剖腹产婴儿,更要注重其肠道菌群建设。

    现在,越来越多的女性生孩子选择剖腹产。但多项研究表明,相比顺产生下的孩子,剖腹产明显影响后代的机体健康。近日,刊登在国际杂志Gut上一篇研究报告中,来自瑞典和苏格兰的研究者通过研究发现,通过剖腹产出生的儿童更容易经常发生机体变态反应,这或许是因为这些儿童肠道中的微生物菌群多样性较低而导致的。

机体变态反应是指已免疫的机体在再次接触同一种抗原物质时所发生的一种异常反应,也叫超敏反应。常见变态反应性疾病有全身性的,如过敏性休克、血清过敏等;有局部性的,如发生在呼吸道的支气管哮喘、喉头水肿、过敏性鼻炎;发生在皮肤的荨麻疹、湿疹;发生在消化道的呕吐、腹痛、腹泻等。

这项研究中,研究者对年龄段从0-2岁的24名儿童的肠道菌群的发育进行研究,其中9名儿童通过剖腹产出生,而其它15名顺产出生;研究者使用DNA测序及计算机分析方法,对这些儿童肠道中存在的多样性细菌进行了全面的分析。结果发现,那些通过剖腹产出生的儿童在其出生两年的时间里,其肠道中微生物菌群的多样性较低,尤其是拟杆菌类细菌比较低,而且这些儿童发生变态反应的风险较高。

研究者Maria Jenmalm表示,有时候进行剖腹产手术非常有必要,但是这明显会影响到出生后代的机体健康。肠道细菌菌群或许被认为是人体最大的器官,在成年人的大肠和小肠中的细菌数量至少是机体其它部位的十倍以上。肠道菌群对人体的健康程度有着非常重要的影响。

肠道菌群与健康的关系

说到肠道菌群,我们很容易将它与消化、营养作用联系在一起,但实际上,肠道菌群不只在消化过程中发挥作用,它和我们的健康有着极为密切的联系。

首先,肠道菌群能通过自身屏蔽和影响机体免疫系统,阻止病原菌入侵人体。肠道菌群附着在肠道内壁表面的粘膜层之上,构成了一层由细菌构成的屏障,抑制致病菌的生长,同时阻止致病菌透过这层屏障进入人体。同时,肠道菌群可以使免疫系统处于一种适度的活跃状态,以此对入侵体内的病原菌保持有效的免疫作用。而肠道菌群的失调,则可造成免疫系统的过度活跃,从而产生自体免疫疾病。

其次,肠道菌群对肠道自身具有调节和营养作用。肠道菌群的存在,尤其是其产生的短链脂肪酸的营养作用,可以使得肠道上皮细胞的生长更为活跃。相比于无菌肠道,具有正常肠道菌群的肠粘膜绒毛下侧会产生更多的可分泌粘液和酶的组织——隐窝,同时肠粘膜细胞更替更为迅速。此外,肠道菌群还可调控肠粘膜上皮细胞的分化。这意味着,具有正常的肠道菌群可以使得肠粘膜更快的修复其破损。

再次,肠道菌群和人体的代谢疾病具有重要关系。肠道菌群失衡可能是造成肥胖、糖尿病等多种多种代谢异常的重要原因之一。造成代谢异常的主要原因,是失衡的肠道菌群产生的脂多糖等内毒素进入人体,被免疫细胞识别后产生多种炎症因子,使得机体进入低度炎症状态,从而产生代谢异常。此外,低度炎症还能促使机体对胰岛素相应程度下降,造成胰岛素抵抗,进而发展为糖尿病。

最后,肠道菌群与健康还有其他更多元的关系。比如,肠道菌群产生的类胡萝卜素类物质可一定程度上降低动脉粥样硬化和中风的风险。正常肠道菌群可通过对淋巴细胞的影响,调节机体对过敏原的反应,从而影响过敏疾病的产生。更令人惊奇的是,还有证据显示,肠道菌群的结构变化甚至可以影响机体的行为模式。

从以上各方面可以看出,肠道菌群的功能更像是一个影响到机体各个方面的“器官”,这个器官的正常与否,对人体的健康程度有着重要影响,而我们对它的了解只是刚刚起步而已。

为什么剖腹产儿童肠道菌群“有问题”?

上海交通大学医学院附属新华医院临床营养中心张红波等专家做了分娩方式对母乳喂养婴儿肠道菌群和粪便性状的影响研究(临床儿科杂志 2010年03期),研究结果显示:剖腹产出生的婴儿组肠道乳酸杆菌和长双歧杆菌数量低于自然分娩组。

这是什么原因呢?原来肠道菌群并非是生来就有的,它们实际上是身体的“外来户”。在母体子宫内,胎儿所处的是一个几乎无菌的环境,因此新生儿刚出生时肠道内是无菌的。当胎儿出生之后的几天内,细菌通过分娩时阴道物质摄入、哺乳时的口腔摄入以及空气吸入等途径进入新生儿体内,并在肠道内定植,形成新生儿最初的肠道菌群。随着婴儿的成长,肠道菌群的种类结构逐渐趋于稳定,最终形成成熟的肠道菌群。这些微小的生物的群体就这样不知不觉的定居到人体之内,悄无声息的与主人相随一生。

经研究分析,自然分娩的婴儿最初的肠道菌群主要来源于母亲的产道和外周的细菌,对于剖腹产婴儿而言,没有接触到母体消化道和产道内的微生物,并且暴露于特定的医院无菌环境,因此较自然分娩的婴儿,其肠道菌群建设与发育明显滞后。有研究显示,消化道早期定植的肠道菌群在婴儿免疫系统的发育成熟过程中扮演着重要角色。自然分娩可促进新生儿免疫系统细胞因子的产生,而剖腹产可以改变或延迟新生儿肠道菌群早期定植并增加特异性疾病的发生率。慕尼黑Ludwigh-Maximilians大学的研究者们也发现,肠道菌群是免疫系统发育成熟的重要因素。

因此,剖腹产不但有可能影响婴儿免疫系统成熟、降低抗病能力,还可能是剖腹产儿童易患感染性疾病或过敏性疾病风险升高的主要原因——即前文所述的更易导致机体变态反应。

目前中国的剖腹产率异常偏高,有数据显示,中国平均剖腹产率达到50%,远超过WHO推荐的15%的上限,这里面原因很多,一方面剖腹产需要住院时间长,手术费用也高,医院可以从中获利;另一方面现在的年轻女性普遍怕疼,想找个方便的方式解脱,还有一些其它的原因,多半是一些陋习,比如有人希望选择一个“吉利”的日子或者赶在9月1日入学分界线之前把孩子生下来。

剖腹产儿童怎么“补救”?

已经经过剖腹产手术生下的婴儿,怎样“补救”增加其免疫力呢?答案是尽量选择母乳喂养。母乳是婴儿成长唯一最自然、最安全、最完整的天然食物。它含有婴儿成长所需的所有营养和抗体,保证婴儿的正常、健康发育。研究人员通过DNA测序发现,母乳含有超过700种细菌,其中包括益生菌,这些对婴儿肠道益生菌的尽早定植有明显的优势,能尽早建立婴儿肠道正常菌群,调节婴儿的免疫功能,促进肠道的成熟,完善婴儿正常免疫功能,使孩子对食物逐渐产生耐受的状态,对今后能够接受更多、更丰富的食物奠定基础。

完全母乳喂养的婴儿,其肠道菌群中80% ~ 90% 是双歧杆菌和乳酸杆菌,而且以双歧杆菌占绝对的优势。而配方奶粉喂养的婴儿,虽然他们的肠道菌群中同样有双歧杆菌和乳酸杆菌,但是比例仅占到40% ~ 50%。为什么会有这么大的差异?研究人员发现,原来母乳中有一种叫做低聚糖的物质。它是一种溶解性的食物纤维,属于糖类。就是在它的帮助下,双歧杆菌才得以大量繁殖。但是,母乳中的低聚糖很难模拟,因此,母乳的优势也很难模拟。

另外,母乳喂养给婴儿带来的也绝不仅仅是营养方面的好处。当婴儿躺在妈妈温暖的怀抱里,吸吮着乳汁的时候,小家伙与妈妈之间皮肤的接触、眼神的交流,或者听着妈妈对自己温柔地说着话,这些对于婴儿的心理发育、早期安全感的建立、培养良好的亲子关系,以及促进婴儿的大脑发育都起着非常重要的作用。这些都可以对剖腹产的缺陷起到一定弥补作用。

 

不同分娩方式对母乳喂养婴儿肠道菌群的影响

不同分娩方式对母乳喂养婴儿肠道菌群的影响

目的
新生儿出生后其肠道立即被来自母体和周围环境中的微生物定植,许多研究表明,消化道早期定植的肠道菌群在婴儿免疫系统的发育过程中起重要的作用。该研究探讨了分娩方式对母乳喂养婴儿肠道菌群和粪便性状的影响。
方法
以60例40~47日龄的健康足月母乳喂养婴儿为观察对象,按分娩方式分为自然分娩组和剖宫产组(n=30)。在6、8、10、12周龄采集婴儿粪便标本,并同时记录婴儿体质量、头围及粪便性状。应用实时荧光定量PCR技术对婴儿肠道乳酸杆菌属、双歧杆菌属及双歧杆菌亚种(长双歧杆菌和短双歧杆菌)进行定量检测。
结果
剖宫产娩出的婴儿肠道乳酸杆菌和长双歧杆菌数量低于自然分娩组(P0.05);自然分娩的婴儿粪便pH值低于剖宫产组(6.2对6.9,P﹤0.05);分娩方式对粪便性状和婴儿的生长发育无影响。
结论
剖宫产降低母乳喂养婴儿肠道乳酸杆菌和双歧杆菌的水平。
 

 

The Inhibitory Receptor PD-1 Regulates IgA Selection and Bacterial Composition in the Gut

The Inhibitory Receptor PD-1 Regulates IgA Selection and Bacterial Composition in the Gut

Immunoglobulin A (IgA) is essential to maintain the symbiotic balance between gut bacterial communities and the host immune system. Here we provide evidence that the inhibitory co-receptor programmed cell death–1 (PD-1) regulates the gut microbiota through appropriate selection of IgA plasma cell repertoires. PD-1 deficiency generates an excess number of T follicular helper (TFH) cells with altered phenotypes, which results in dysregulated selection of IgA precursor cells in the germinal center of Peyer’s patches. Consequently, the IgAs produced in PD-1–deficient mice have reduced bacteria-binding capacity, which causes alterations of microbial communities in the gut. Thus, PD-1 plays a critical role in regulation of antibody diversification required for the maintenance of intact mucosal barrier.
 

Symptomatic atherosclerosis is associated with an altered gut metagenome

文献检索:doi:10.1038/ncomms2266
Recent findings have implicated the gut microbiota as a contributor of metabolic diseases through the modulation of host metabolism and inflammation. Atherosclerosis is associated with lipid accumulation and inflammation in the arterial wall, and bacteria have been suggested as a causative agent of this disease. Here we use shotgun sequencing of the gut metagenome to demonstrate that the genus Collinsella was enriched in patients with symptomatic atherosclerosis, defined as stenotic atherosclerotic plaques in the carotid artery leading to cerebrovascular events, whereas Roseburia and Eubacterium were enriched in healthy controls. Further characterization of the functional capacity of the metagenomes revealed that patient gut metagenomes were enriched in genes encoding peptidoglycan synthesis and depleted in phytoene dehydrogenase; patients also had reduced serum levels of β-carotene. Our findings suggest that the gut metagenome is associated with the inflammatory status of the host and patients with symptomatic atherosclerosis harbor characteristic changes in the gut metagenome.
 

An opportunistic pathogen isolated from the gut of an obese human causes obesity in germfree mice

Lipopolysaccharide endotoxin is the only known bacterial product which, when subcutaneously infused into mice in its purified form, can induce obesity and insulin resistance via an inflammation-mediated pathway. Here we show that one endotoxin-producing bacterium isolated from a morbidly obese human's gut induced obesity and insulin resistance in germfree mice. The endotoxin-producing Enterobacter decreased in relative abundance from 35% of the volunteer's gut bacteria to non-detectable, during which time the volunteer lost 51.4 kg of 174.8 kg initial weight and recovered from hyperglycemia and hypertension after 23 weeks on a diet of whole grains, traditional Chinese medicinal foods and prebiotics. A decreased abundance of endotoxin biosynthetic genes in the gut of the volunteer was correlated with a decreased circulating endotoxin load and alleviated inflammation. Mono-association of germfree C57BL/6J mice with strain Enterobacter cloacae B29 isolated from the volunteer's gut induced fully developed obesity and insulin resistance on a high-fat diet but not on normal chow diet, whereas the germfree control mice on a high-fat diet did not exhibit the same disease phenotypes. The Enterobacter-induced obese mice showed increased serum endotoxin load and aggravated inflammatory conditions. The obesity-inducing capacity of this human-derived endotoxin producer in gnotobiotic mice suggests that it may causatively contribute to the development of obesity in its human host.
 
 

 

Sex differences in the gut microbiome drive hormone-dependent regulation of autoimmunity

Sex differences in the gut microbiome drive hormone-dependent regulation of autoimmunity

Microbial exposures and sex hormones exert potent effects on autoimmune diseases, many of which are more prevalent in women. We demonstrate that early-life microbial exposures determine sex hormone levels and modify progression to autoimmunity in the nonobese diabetic (NOD) mouse model of type 1 diabetes (T1D). Colonization by commensal microbes elevated serum testosterone and protected NOD males from T1D. Transfer of gut microbiota from adult males to immature females altered the recipient's microbiota, resulting in elevated testosterone and metabolomic changes, reduced islet inflammation and autoantibody production, and robust T1D protection. These effects were dependent on androgen receptor activity. Thus, the commensal microbial community alters sex hormone levels and regulates autoimmune disease fate in individuals with high genetic risk.
 
 

 

Onecut1 Is Essential for Horizontal Cell Genesis and Retinal Integrity

Onecut1 Is Essential for Horizontal Cell Genesis and Retinal Integrity

Horizontal cells are interneurons that synapse with photoreceptors in the outer retina. Their genesis during development is subject to regulation by transcription factors in a hierarchical manner. Previously, we showed that Onecut 1 (Oc1), an atypical homeodomain transcription factor, is expressed in developing horizontal cells (HCs) and retinal ganglion cells (RGCs) in the mouse retina. Herein, by knocking out Oc1 specifically in the developing retina, we show that the majority (∼80%) of HCs fail to form during early retinal development, implying that Oc1 is essential for HC genesis. However, no other retinal cell types, including RGCs, were affected in the Oc1 knock-out. Analysis of the genetic relationship between Oc1 and other transcription factor genes required for HC development revealed that Oc1 functions downstream of FoxN4, in parallel with Ptf1a, but upstream of Lim1 and Prox1. By in utero electroporation, we found that Oc1 and Ptf1a together are not only essential, but also sufficient for determination of HC fate. In addition, the synaptic connections in the outer plexiform layer are defective in Oc1-null mice, and photoreceptors undergo age-dependent degeneration, indicating that HCs are not only an integral part of the retinal circuitry, but also are essential for the survival of photoreceptors. In sum, these results demonstrate that Oc1 is a critical determinant of HC fate, and reveal that HCs are essential for photoreceptor viability, retinal integrity, and normal visual function.

本文引自:http://www.biodiscover.com/news/research/105425.html

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