Chinese Journal of Animal Nutrition >

2023 , Vol. 35 >Issue 4: 2063 - 2071

DOI: https://doi.org/10.12418/CJAN2023.193

REVIEW

Research Progress of Gastrointestinal Microbiota and Regulation of Oxidative Stress in Ruminants

  • FENG Xin , 1, 2 ,
  • LUAN Jiaming 1, 2 ,
  • ZHANG Min 1 ,
  • GENG Chunyin , 1, 2, *
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  • 1 College of Agriculture, Yanbian University, Yanji 133000, China
  • 2 Engineering Research Center of North-East Cold Region Beef Cattle Science and Technology Innovation, Ministry of Education, Yanji 133002, China
*associate professor, E-mail:

Received date: 2022-09-30

  Online published: 2023-04-12

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Abstract

The gastrointestinal tract of ruminants contains complex, diverse and dynamic microbiota that plays important roles in maintaining immune function, nutrient digestion and metabolic homeostasis. Oxidative stress is the result of excessive production of free radicals, insufficient antioxidant capacity, or both, which can endanger animal health and cause economic losses in severe cases. A growing number of studies have shown that there is a strong link between the gastrointestinal microbiota and oxidative stress, which can induce local and systemic inflammation and regulate oxidative stress through related metabolites. This paper reviewed the studies on the relationship between gastrointestinal microbiota and oxidative stress in ruminants, and discussed the regulation of oxidative stress by gastrointestinal microbiota metabolites and microbiome-gut-organ axes, aiming to provide a theoretical basis for further exploring the regulatory mechanism of gastrointestinal microflora on oxidative stress in ruminants.

Key words： ruminant; gastrointestinal tract; microbiota; oxidative stress; microbiome-gut-organ axes

Cite this article

FENG Xin , LUAN Jiaming , ZHANG Min , GENG Chunyin . Research Progress of Gastrointestinal Microbiota and Regulation of Oxidative Stress in Ruminants[J]. Chinese Journal of Animal Nutrition, 2023 , 35(4) : 2063 -2071 . DOI: 10.12418/CJAN2023.193

动物在生命周期的各个阶段需要面对生理变化带来的代谢需求,该过程会导致氧化代谢的显著上升,并伴随着器官和细胞中自由基的增加[1]。自由基为机体正常代谢活动的副产物,也是免疫系统针对入侵微生物的防御措施之一[2]。氧化应激是自由基产生过多、抗氧化能力不足或两者同步的结果。氧化应激下,大量的活性氧(reactive oxygen species,ROS)会引起细胞中生物大分子受损,从而进一步增加细胞衰老,损害细胞功能,威胁细胞生存[3]。胃肠道菌群与氧化应激之间存在联系,它们对维持免疫功能、营养物质消化和代谢动态平衡具有重要作用[4]。微生物及其代谢物抑制细胞内ROS的能力已在细胞模型中得到证实[5-6]。反刍动物拥有高度复杂的胃肠道微生物区系,明确其胃肠道菌群与宿主氧化应激反应之间的联系,对维护动物健康和畜牧业的发展尤为重要。本文通过对相关文献的梳理和回顾,综述了部分有关胃肠道菌群与氧化应激相互作用的报道,旨在为今后深入研究反刍动物胃肠道菌群调控氧化应激的机制提供理论依据。

1 反刍动物胃肠道菌群与氧化应激的关系

反刍动物的胃肠道包含四室胃(瘤胃、网胃、瓣胃和皱胃)、小肠(十二指肠、空肠和回肠)和大肠(盲肠、结肠和直肠),存在高度复杂的微生物区系,这些胃肠道菌群在维持宿主机体稳态方面发挥重要的作用。外界环境的剧烈变化(如断奶、运输、高温和高湿等)都可能引起反刍动物胃肠道微生物区系的改变,并伴随着微生物代谢和微生物酶活性的变化,导致营养代谢紊乱,自由基稳态失衡,对细胞和线粒体造成氧化损伤[1,7]。了解外界应激对胃肠道菌群的影响有助于制定相应的治疗策略,以有效地预防氧化应激(表1)[8⇓⇓⇓⇓⇓⇓⇓-16]。
表1 外界应激或处理对反刍动物胃肠道菌群的影响

Table 1 Effects of external stress or treatment on gastrointestinal microbiota of ruminants

应激或处理条件
Stress or treatment
conditions		 动物
Animal		 样品类型
Sample type		 菌群变化
Microbiota change		 参考文献
References
热应激
Heat stress		 奶牛 瘤胃液 Ruminobacter、Streptococcus、Treponema、
unclassified Bacteroidaceae、unclassified
Enterobacteriaceae ↑,Acetobacter ↓		 Zhao等[8]
水牛 瘤胃液 Lachnospiraceae_NK3A20_group ↑,
Lactococcus、Weissella ↓		 Wang等[9]
冷刺激
Cold stimulation		 绵羊 瘤胃液 Lachnospiraceae_XPB1014_group ↑,
Prevotellaceae_UCG_003 ↓		 Guo等[10]
运输
Transport		 肉牛 瘤胃液 Fibrobacter succinogenes、Prevotella albensis、
Ruminococcus flavefaciens、Ruminococcus
amylophilus ↑,Anaerovibrio lipolytica、Prevotella
ruminicola、Prevotella bryantii、
Succinivibrio dextrinosolvens ↓		 Deng等[11]
断奶
Weaning		 犊牛 瘤胃液 Fibrobacter、Rikenellaceae、Syntrophococcus、
Shuttleworthia ↑,Pyramidobacter ↓		 Hao等[12]
早期断奶
Early weaning		 羔羊 回肠食糜 Acetobacterium、Aeriscardovia、Bacteroides、
Bifidobacterium、Butyrivibrio、Escherichia、
Lactococcus、Methanobrevibacter、Prevotella、
Pseudoflavonifractor、Ruminococcus、Shigella、
Streptococcus、Succinivibrio、Succiniclasticum ↑,
Allobaculum、Anaerovibrio、Arthromitus、
Cellulosilyticum、Chlamydophila、Clostridium、
Lactobacillus、Pseudomonas、Sharpea、
Syntrophococcus、Turicibacter ↓		 Li等[13]
去角
Dehorning		 犊牛 粪便 轻体重Erysipelotrichaceae、Verrucomicrobiaceae ↑,
重体重Elusimicrobiaceae、Turicibacteraceae ↑		 Mir等[14]
去势
Castration		 犊牛 粪便 轻体重Anaeroplasmataceae、Bacteroidales_
UCG_001、Campylobacteraceae、Methanobacteriaceae、
Prevotellaceae、Pseudomonadaceae、Rhizobiaceae ↑,
重体重Aerococcaceae、Bacillaceae、
Fibrobacteraceae、Planococcaceae、Succinivibrionaceae ↑		 Mir等[14]
应激或处理条件
Stress or treatment
conditions		 动物
Animal		 样品类型
Sample type		 菌群变化
Microbiota change		 参考文献
References
高谷物饲粮
High-grain diet		 山羊 瘤胃上皮 Prevotella、unclassified Clostridiales ↑,
Fibrobacter、Shuttleworthia、unclassified
Neisseriaceae、unclassified Ruminococcaceae ↓		 Zhang等[15]
山羊 瘤胃液 Butyrivibrio、Prevotella、Ruminococcus、
Mogibacterium、Moryella ↑,BF311、CF231、
Clostridium、Coprococcus、Desulfovibrio、L7A_E11、
Pseudobutyrivibrio、YRC22、unclassified
Bacteroidales、unclassified BS11、unclassified
Christensenellaceae、unclassified Clostridiales、
unclassified LD1-PB3、unclassified Mogibacteriaceae、
unclassified RF39、unclassified Ruminococcaceae、
unclassified WCHB1-25、unclassified WPS-2 ↓		 Zhang等[16]

Acetobacter:醋杆菌属;Acetobacterium:醋小杆菌属:Aeriscardovia:卡多维亚氏菌属;Aerococcaceae:气球菌科;Allobaculum:异杆菌属;Anaeroplasmataceae:厌氧原体科;Anaerovibrio:厌氧弧菌属;Anaerovibrio lipolytica:脂解厌氧弧菌;Arthromitus:昆虫肠道菌属;Bacillaceae:芽孢杆菌科;Bacteroidales:拟杆菌目;Bacteroidales_UCG_001:拟杆菌目_UCG_001;Bacteroides:拟杆菌属;Butyrivibrio:丁酸弧菌属;Bifidobacterium:双歧杆菌属;Campylobacteraceae:弯曲菌科;Cellulosilyticum:栖瘤胃解纤维素菌属;Chlamydophila:嗜衣原体属;Clostridium:梭菌属;Coprococcus:粪球菌属;Desulfovibrio:脱硫弧菌属;Elusimicrobiaceae:迷踪菌科;Erysipelotrichaceae:丹毒丝菌科;Escherichia:埃希氏菌属;Fibrobacter:纤维杆菌属;Fibrobacter succinogenes:产琥珀酸丝状杆菌;Fibrobacteraceae:纤维杆菌科;Lachnospiraceae_NK3A20_group:毛螺菌科_NK3A20群;Lachnospiraceae_XPB1014_group:毛螺菌科_XPB1014群;Lactobacillus:乳酸杆菌属;Lactococcus:乳酸球菌属;Methanobacteriaceae:甲烷杆菌科;Methanobrevibacter:甲烷短杆菌属;Mogibacterium:艰难杆菌属;Planococcaceae:动球菌科;Prevotella:普雷沃氏菌属;Prevotella albensis:阿尔伯普雷沃氏菌;Prevotella bryantii:布氏普雷沃氏菌;Prevotella ruminicola:栖瘤胃普雷沃氏菌;Prevotellaceae:普雷沃氏菌科;Prevotellaceae_UCG_003:普雷沃氏菌科_UCG_003;Pseudobutyrivibrio:假丁酸弧菌属;Pseudomonas:假单胞菌属;Pseudomonadaceae:假单胞菌科;Pyramidobacter:锥形杆菌属;Rhizobiaceae:根瘤菌料;Rikenellaceae:理研菌科;Ruminobacter:瘤胃杆菌属;Ruminococcus:瘤胃球菌属;Ruminococcus flavefaciens:生黄瘤胃球菌;Ruminococcus amylophilus:嗜淀粉瘤胃球菌;Sharpea:夏普氏菌属;Shigella:志贺氏菌属;Shuttleworthia:沙特尔沃思菌属;Streptococcus:链球菌属;Succinivibrio:琥珀酸弧菌属;Succinivibrio dextrinosolvens:溶糊精琥珀酸弧菌;Succinivibrionaceae:琥珀酸弧菌科;Succiniclasticum:解琥珀酸菌属;Syntrophococcus:互营球菌属;Treponema:密螺旋体属;Turicibacter:苏黎世杆菌属;Turicibacteraceae:苏黎世杆菌科;Verrucomicrobiaceae:疣微菌科;Weissella:魏斯氏菌属;unclassified Bacteroidaceae:未分类的拟杆菌科;unclassified Bacteroidales:未分类的拟杆菌目;unclassified Christensenellaceae:未分类的克里斯滕森菌科;unclassified Clostridiales:未分类的梭菌目;unclassified Enterobacteriaceae:未分类的肠杆菌科;unclassified Mogibacteriaceae:未分类的艰难杆菌科;unclassified Neisseriaceae:未分类的奈瑟氏菌科;unclassified Ruminococcaceae:未分类的瘤胃球菌科。

↑表示提高,↓表示降低。

↑ indicated increase and ↓ indicated decrease.

2 胃肠道菌群对机体氧化应激的调控

2.1 胃肠道菌群代谢物与机体氧化应激的调控

反刍动物胃肠道菌群与机体氧化应激之间的相互作用依赖于多种代谢物,这些代谢物主要包括脂多糖(lipopolysaccharide,LPS)、挥发性脂肪酸(volatile fatty acid,VFA)和组胺(histamine release,HR)等。胃肠道菌群代谢物可以通过激活或抑制宿主细胞中不同的信号通路调节氧化应激,涉及的信号通路主要有核因子-κB(nuclear factor-kappa B,NF-κB)信号通路、丝裂原活化蛋白激酶(mitogen-activated protein kinase,MAPK)信号通路、核因子E2相关因子2(nuclear factor-erythroid 2-related factor 2,Nrf2)信号通路以及G蛋白偶联受体(G protein-coupled receptor,GPCR)信号通路等。

2.1.1 LPS

反刍动物的LPS主要来自胃肠道革兰氏阴性菌,外界压力、高谷物饲粮和亚急性瘤胃酸中毒疾病等因素可造成胃肠道菌群失调及胃肠道的pH降低,并诱导革兰氏阴性菌释放大量LPS,扰乱胃肠道屏障的通透性,使LPS进入血液和肝脏[17⇓-19]。LPS可刺激Toll样受体(Toll-like receptor,TLR)4选择性地激活不同的信号通路引起机体氧化应激,NF-κB和MAPK是较典型的信号通路。其中,NF-κB是对LPS刺激作出反应的重要下游信号通路,通过调控促炎细胞因子的释放,如肿瘤坏死因子(tumor necrosis factor,TNF)-α、白细胞介素(interleukin,IL)-1β和IL-6等,参与机体氧化应激的调控[20-21]。MARK信号通路包含c-Jun氨基末端激酶(c-Jun N-terminal kinases,JNK)、细胞外信号调节激酶1/2(extracellular signal-regulated kinases1/2,ERK1/2)和p38 MAPK等,LPS可通过JNK、ERK1/2和p38 MAPK的激活调节氧化应激[22-23]。

2.1.2 VFA

VFA是反刍动物胃肠道菌群的主要发酵代谢产物,对于调节氧化应激、减少局部炎症、防止病原体入侵和维持肠道屏障完整性至关重要[24]。VFA对氧化应激的调控可能涉及多个途径。研究显示,反刍动物胃肠道VFA浓度的改变,可激活GPCR(GPCR41或GPCR43)信号通路,产生细胞因子和化学因子(如TNF-α、IL-2和IL-6等),从而调控胃肠道炎症[25-26]。氧化应激与炎症反应可相互作用,氧化应激可诱发炎症反应,炎症反应亦可加重氧化应激,这表明胃肠道菌群可能通过VFA激活GPCR调节机体的氧化应激[27]。此外,VFA可作为Nrf2的靶分子,激活和编码多种抗氧化分子和抗氧化酶的基因表达抵消过量的ROS,还可通过抑制组蛋白去乙酰基酶的活性,调节Nrf2的激活,应对氧化应激[24,28-29]。

2.1.3 HR

反刍动物胃肠道菌群中存在分泌HR的微生物,其中产HR亚利氏菌(Allisonella histaminiformans)是瘤胃中HR的主要生产者[30]。在正常生理条件下,微量的HR存在于所有组织中,但当HR含量超过机体代谢能力时,HR就会进入血液和组织,引起氧化应激和炎症反应[31]。反刍动物在亚急性瘤胃酸中毒期间,瘤胃中的pH降低,瘤胃菌群失调,产生HR的细菌增加,致使瘤胃中HR浓度增加,激活NF-κB信号通路和促炎细胞因子的产生,从而导致瘤胃上皮细胞的损伤,引发氧化应激和炎症反应[32-33]。

2.1.4 其他

除上述主要的胃肠道菌群代谢物之外,细菌肽聚糖、脂磷壁酸、鞭毛蛋白、毒素和甲酰化肽等,均可能与反刍动物氧化应激存在联系。肽聚糖是存在于所有细菌细胞壁中的大聚合物分子,可通过激活部分肽聚糖识别蛋白或NOD样受体调节氧化应激[20]。脂磷壁酸是革兰氏阳性菌表面的特异性聚合物,可与TLR2或TLR6结合,通过髓样分化因子88(MyD88)依赖性信号途径,激活NF-κB或MAPK,调控促炎或抗炎细胞因子的产生和释放[34]。鞭毛蛋白是一种细菌蛋白,存在于有鞭毛的细菌中[如沙门氏菌(Salmonella)]。研究显示,鞭毛蛋白可能通过诱导肠道上皮细胞保护性热休克蛋白25(Hsp25)的表达,在保护肠道免受氧化损伤和维持肠道内稳态中发挥重要作用[35]。艰难梭菌(Clostridium difficile)是反刍动物胃肠道中的条件致病菌,其产生的外毒素(T-cdB)可以促进核内体上还原型烟酰胺腺嘌呤二核苷酸磷酸(NADPH)氧化酶复合物的形成,增加ROS的产生[20,36]。艰难梭菌的主要毒力因子还可由宿主细胞通过MAPK和Pyrin炎症小体感知,增加促炎细胞因子TNF-α、IL-1β、IL-6和IL-8的分泌,调节氧化应激和炎症反应[37]。肠道内的细菌产生的甲酰化肽,可以被位于肠上皮的甲酰肽受体感知,激活NADPH氧化酶,产生高度定位的ROS,转导微生物信号,从而影响氧化状态,调节氧化应激[38]。目前,尽管已知胃肠道菌群可通过代谢物调控机体氧化应激,但相关具体机制尚未完全阐明,未来有待继续深入研究。

2.2 微生物-肠道-器官轴与机体氧化应激的调控

近年来,越来越多的研究表明,胃肠道菌群对动物的影响不仅限于胃肠道的范围,而是扩展到身体的各个区域[39]。胃肠道菌群的代谢物可向全身的不同器官发送信号,并形成一个可以发送信号的“轴”,它们通过不同的微生物-肠道-器官轴与身体的各个方面相互作用,从而影响宿主生理[40]。氧化应激与动物的神经系统、生殖系统和乳腺的疾病等存在联系,通过微生物-肠道-器官轴能够更全面和深入地认识胃肠道菌群对机体各器官氧化应激调控。

2.2.1 微生物-肠道-脑轴

微生物、肠道和大脑通过多种机制和途径相互调节,这种相互调节主要通过神经交流、内分泌和免疫调节等途径实现[41]。
微生物-肠道-脑轴的神经交流主要发生在肠神经系统,肠神经系统主要负责调节肠道功能,通过神经递质以及感觉和运动神经元与自主神经系统和中枢神经系统相互作用,将信号从肠道传递到大脑[42-43]。肠道中的共生厌氧菌可通过脱氮作用产生一氧化氮(NO),NO是非肾上腺素能非胆碱能肠神经系统主要的神经递质,过量的NO可能导致氧化还原反应形成活性氮,引起氧化应激,诱发神经退行性疾病[44]。肠神经系统还可以与迷走神经形成突触,利用迷走神经的传导作用,允许微生物和大脑之间进行交流[45-46],瘤胃发酵的代谢物如氨和D-乳酸等,可通过该途径影响大脑功能和宿主压力[47]。
微生物-肠道-脑轴的另一个信号传导途径是肠内分泌细胞构成的胃肠道内分泌系统。VFA被认为是通过肠内分泌细胞介导宿主微生物通信的主要信号分子,它们通过作用于GPCR,在肠内分泌细胞中表达,并介导厌食性胃肠道激素酪酪肽和胰高血糖素-1的释放,调节食物的摄入和胰岛素分泌,增强肠道对膳食分子的敏感性,对抗氧化应激[48-49]。VFA还被证明可调节中枢神经系统的神经可塑性,改善生物行为[50]。也有研究表明,胃肠道菌群可通过下丘脑-垂体-肾上腺轴和中枢神经系统的神经内分泌途径,调节神经递质的产生,并影响激素水平和细胞因子的分泌,调控氧化应激和炎症反应[51-52]。
胃肠道菌群还可以与免疫系统相互作用。胃肠道菌群不仅调节肠道内的免疫细胞,还调节脑内的免疫细胞。胃肠道菌群衍生的微生物相关分子模式可被各种类型的免疫细胞表面的TLR受体识别,导致免疫细胞激活,产生促炎细胞因子,如TNF-α、IL-1β、IL-17A和IL-6等,它们通过血脑屏障进入脑循环,调节氧化应激和炎症反应[53]。胃肠道黏膜是免疫系统重要的组成部分,氧化应激会导致胃肠道黏膜层损伤和病原体入侵,黏膜上层或黏液层上的共生菌可抵抗病原体的定植,共生菌在与肠道上皮细胞接触时会产生ROS等调节免疫信号传导的代谢物或成分,激活上皮细胞迁移和组织修复,并促进免疫稳态[54-55]。

2.2.2 微生物-肠道-乳腺轴

胃肠道菌群和乳腺菌群之间可能通过微生物-肠道-乳腺轴交流。对于繁殖母畜和奶用动物而言,乳腺是非常重要的性器官,并存在一个微生物群落[56]。研究表明,细菌可能通过肠道相关黏膜组织中的树突状细胞和巨噬细胞,经内化作用由胃肠道传播到乳腺系统,与乳腺系统感染相关的病原菌可能通过该途径在微生物-肠道-乳腺轴之间移位[52]。乳腺炎是常见的奶用反刍动物炎性疾病,与氧化应激有关,胃肠道菌群可能在乳腺炎中充当重要角色。有关奶牛的研究发现,乳腺炎期间,瘤胃中与炎症相关的细菌增加,产生VFA的细菌和益生菌减少,并伴随着瘤胃代谢物的改变,其中与氧化应激有关代谢物和促炎细胞因子还与瘤胃菌群之间存在显著相关性,这提示了瘤胃菌群与乳腺氧化应激的重要联系[57-58]。

2.2.3 微生物-肠道-生殖器轴

关于胃肠道菌群和生殖器及菌群之间存在的相互作用,可被称为微生物-肠道-生殖器轴。目前,胃肠道微生物区系和生殖系统之间的具体关系仍然未知。与胃肠道菌群相同的是,生殖器菌群在疾病状态下也会出现生态失调[52]。反刍动物的子宫炎主要发生在能量代谢负平衡条件下,与氧化应激的增加有关。研究表明,反刍动物瘤胃菌群产生的LPS可在亚急性酸中毒期间诱发子宫炎症[59]。肠道菌群的失调还会增强金黄色葡萄球菌(Staphylococcus aureus)引起的子宫炎的易感性[60]。此外,肠道菌群可通过分泌β-葡萄糖醛酸酶来调节雌激素,进而影响子宫炎和代谢综合征等疾病[61]。
最近的研究发现,在氧化应激的调节过程中,胃肠道微生物区系可能通过代谢物、诱导ROS、新陈代谢和营养摄入等途径影响睾丸的功能,这对未完全定义的微生物-肠道-睾丸轴提供了一个新的认识[62]。研究报道,胃肠道菌群释放的内毒素可引发全身慢性炎症,从而对睾丸中的睾丸间质细胞造成伤害,导致雄性的性腺功能减退[63]。此外,有关绵羊的研究发现,口服黄曲霉毒素可引起的瘤胃菌群失调,并通过激活谷胱甘肽过氧化物酶3介导的氧化途径破坏绵羊抗氧化防御系统,激活B细胞淋巴瘤/白血病-2(Bcl-2)/B细胞淋巴瘤/白血病-2相关X蛋白(Bax)信号通路,导致睾丸损伤和功能障碍[64],说明饮食诱导的胃肠道菌群的失调可能与睾丸的氧化应激损伤有关。不过,目前的报道仍不足以完全证实微生物-肠道-睾丸轴,有必要进一步研究胃肠道菌群与雄性动物氧化应激之间的联系。

3 胃肠道菌群和抗氧化与反刍动物效率的联系

氧化应激被认为是导致反刍动物生产效率差异的生理机制之一,高效反刍动物对氧化应激的耐受性更高[65]。动物机体的抗氧化防御机制基于大量生物抗氧化剂的合成,包括抗氧化酶、谷胱甘肽、硫氧还蛋白、辅酶Q和维生素E等,但在压力条件下,动物仅靠内部抗氧化网络系统无法应对过量ROS的形成,需要通过饲料或饮水补充抗氧化剂获得额外的帮助[2]。益生菌等饲料添加剂的供应可通过调控胃肠道菌群,提高反刍动物的抗氧化能力,预防或对抗氧化应激[66]。最近的研究强调,反刍动物效率与胃肠道菌群的之间存在联系。高效反刍动物胃肠道菌群的丰富度和多样性较高,致病菌丰度较低[67-68]。胃肠道菌群与反刍动物效率的联系更好地诠释了其对宿主生理的重要意义,未来有必要以提高反刍动物的生产效率为目标,进一步研究胃肠道菌群与机体抗氧化能力两者的关系。

4 小结

综上所述,反刍动物的胃肠道菌群与氧化应激之间存在联系,但相关具体的调控机制仍有待阐述。目前的有关胃肠道菌群调控氧化应激的研究主要集中在人和小鼠,而有关反刍动物的研究相对较少。考虑到反刍动物具有十分复杂的胃肠道消化系统和微生物区系,未来的工作应基于多组学平台和生物信息学等技术,更全面地研究反刍动物胃肠道微生态系统与宿主健康的关系,这对规模逐渐扩大的畜牧业发展十分重要。

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