更新于：2024-09-19

NLRP6

更新于：2024-09-19

基本信息

别名

Angiotensin II/vasopressin receptor、CLR11.4、NACHT, leucine rich repeat and PYD containing 6

+ [8]

简介

Acts as the sensor component of the NLRP6 inflammasome, which mediates inflammasome activation in response to various pathogen-associated signals, leading to maturation and secretion of IL1B and IL18 (PubMed:30392956, PubMed:34678144). Inflammasomes are supramolecular complexes that assemble in the cytosol in response to pathogens and other damage-associated signals and play critical roles in innate immunity and inflammation (PubMed:30674671). Acts as a recognition receptor (PRR): recognizes and binds specific pathogens and other damage-associated signals, such as lipoteichoic acid (LTA), a cell-wall component of Gram-positive bacteria, or double stranded RNA (dsRNA) (PubMed:30392956, PubMed:34678144, PubMed:33377178). May also recognize and bind lipopolysaccharide (LPS), a major component of the outer membrane of Gram-negative bacteria; however, LPS is probably not a major activator of the NLRP6 inflammasome (PubMed:31932628, PubMed:34678144). Following LTA- or dsRNA-binding, NLRP6 undergoes liquid-liquid phase separation (LLPS), enhancing multivalent interactions, an essential step for the formation of the NLRP6 inflammasome polymeric complex (PubMed:34678144). The NLRP6 inflammasome acts by promoting recruitment of effector pro-inflammatory caspases (CASP1 and/or CASP4) that catalyze maturation and secretion of IL1B and IL18 in the extracellular milieu (PubMed:30674671, PubMed:12387869, PubMed:30392956, PubMed:34678144). The NLRP6 inflammasome plays a central role in the maintenance of epithelial integrity and host defense against microbial infections in the intestine (PubMed:30392956). Required to restrict infection against Gram-positive bacteria by recognizing lipoteichoic acid (LTA), leading to recruitment of CASP4 and CASP1, and subsequent maturation and secretion of IL1B and IL18 (PubMed:30392956, PubMed:33377178). Involved in intestinal antiviral innate immunity together with DHX15: recognizes and binds viral dsRNA to restrict infection by enteric viruses through the interferon pathway and GSDMD-dependent release of IL18 (PubMed:34678144, PubMed:34161762). Required to prevent infection by the apicomplexan parasite Cryptosporidium in enterocytes by promoting GSDMD-dependent release of IL18 (By similarity). The NLRP6 inflammasome may also regulate the gut microbiota composition by acting as a sensor of microbiota-associated metabolites to form a PYCARD/ASC-dependent inflammasome for downstream IL18 release and secretion of antimicrobial peptides (By similarity). Essential for gut mucosal self-renewal and proliferation (By similarity). Regulate mucus secretion in an inflammasome- and autophagy-dependent manner to prevent invasion by enteric bacteria, (By similarity). During systemic bacterial infections, the NLRP6 inflammasome negatively regulates neutrophil recruitment and neutrophil extracellular traps (NETs) formation (By similarity). May promote peripheral nerve recovery following injury via an inflammasome-independent mechanism (By similarity).

关联

100 项与 NLRP6 相关的临床结果

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100 项与 NLRP6 相关的转化医学

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0 项与 NLRP6 相关的专利（医药）

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277

项与 NLRP6 相关的文献（医药）

2024-12-01·Molecular Biology Reports

The role of NLRP6 in the development and progression of neurological diseases

Review

作者: Yan, Mengyu ; Guo, Yiming ; Huang, Lihong ; Lü, Yang ; Yu, Weihua ; Chen, Yingxi ; Liu, Jiarui ; He, Yurou ; Song, Jiaqi

The nervous system possesses the remarkable ability to undergo changes in order to store information; however, it is also susceptible to damage caused by invading pathogens or neurodegenerative processes. As a member of nucleotide-binding oligomerization domain-like receptor (NLR) family, the NLRP6 inflammasome serves as a cytoplasmic innate immune sensor responsible for detecting microbe-associated molecular patterns. Upon activation, NLRP6 can recruit the adapter protein apoptosis-associated speck-like protein (ASC) and the inflammatory factors caspase-1 or caspase-11. Consequently, inflammasomes are formed, facilitating the maturation and secretion of pro-inflammatory cytokines such as inflammatory factors-18 (IL-18) and inflammatory factors-1β (IL-1β). Precise regulation of NLRP6 is crucial for maintaining tissue homeostasis, as dysregulated inflammasome activation can contribute to the development of various diseases. Furthermore, NLRP6 may also play a role in the regulation of extraintestinal diseases. In cells of the brain, such as astrocytes and neurons, NLRP6 inflammasome are also present. Here, the assembly and subsequent activation of caspase-1 mediated by NLRP6 contribute to disease progression. This review aims to discuss the structure and function of NLRP6, explain clearly the mechanisms that induce and activate NLRP6, and explore its role within the central and peripheral nervous system.

2024-12-01·Cellular and Molecular Life Sciences

Decreased expression of the NLRP6 inflammasome is associated with increased intestinal permeability and inflammation in obesity with type 2 diabetes

Article

作者: Moncada, Rafael ; Silva, Camilo ; Gómez-Ambrosi, Javier ; Reina, Gabriel ; Ramírez, Beatriz ; Casado, Marcos ; Mentxaka, Amaia ; Frühbeck, Gema ; Escalada, Javier ; Baixauli, Jorge ; Valentí, Víctor ; Rodríguez, Amaia ; Catalán, Victoria ; Becerril, Sara

AbstractBackgroundObesity-associated dysfunctional intestinal permeability contributes to systemic chronic inflammation leading to the development of metabolic diseases. The inflammasomes constitute essential components in the regulation of intestinal homeostasis. We aimed to determine the impact of the inflammasomes in the regulation of gut barrier dysfunction and metabolic inflammation in the context of obesity and type 2 diabetes (T2D).MethodsBlood samples obtained from 80 volunteers (n = 20 normal weight, n = 21 OB without T2D, n = 39 OB with T2D) and a subgroup of jejunum samples were used in a case–control study. Circulating levels of intestinal damage markers and expression levels of inflammasomes as well as their main effectors (IL-1β and IL-18) and key inflammation-related genes were analyzed. The impact of inflammation-related factors, different metabolites and Akkermansia muciniphila in the regulation of inflammasomes and intestinal integrity genes was evaluated. The effect of blocking NLRP6 by using siRNA in inflammation was also studied.ResultsIncreased circulating levels (P < 0.01) of the intestinal damage markers endotoxin, LBP, and zonulin in patients with obesity decreased (P < 0.05) after weight loss. Patients with obesity and T2D exhibited decreased (P < 0.05) jejunum gene expression levels of NLRP6 and its main effector IL18 together with increased (P < 0.05) mRNA levels of inflammatory markers. We further showed that while NLRP6 was primarily localized in goblet cells, NLRP3 was localized in the intestinal epithelial cells. Additionally, decreased (P < 0.05) mRNA levels of Nlrp1, Nlrp3 and Nlrp6 in the small intestinal tract obtained from rats with diet-induced obesity were found. NLRP6 expression was regulated by taurine, parthenolide and A. muciniphila in the human enterocyte cell line CCL-241. Finally, a significant decrease (P < 0.01) in the expression and release of MUC2 after the knockdown of NLRP6 was observed.ConclusionsThe increased levels of intestinal damage markers together with the downregulation of NLRP6 and IL18 in the jejunum in obesity-associated T2D suggest a defective inflammasome sensing, driving to an impaired epithelial intestinal barrier that may regulate the progression of multiple obesity-associated comorbidities.

2024-09-01·Veterinary Microbiology

The suppressive role of NLRP6 in host defense against Streptococcus suis infection

Article

作者: Lu, Yi ; Yu, Xiaoying ; Fang, Rendong ; Xiong, Qiuting ; Jia, Kaixiang ; Hu, Xiaoxiang

Streptococcus suis (S. suis) disease is a prevalent zoonotic infectious threat that elicits a systemic inflammatory response in both swine and humans, frequently culminating in high mortality rates. The excessive inflammation triggered by S. suis infection can precipitate tissue damage and sudden death; however, a comprehensive strategy to mitigate this inflammatory response remains elusive. Our study examines the role of NLRP6 in S. suis infection, with a particular focus on its involvement in pathogen regulation. A marked upregulation of NLRP6 was observed in peritoneal macrophages post-infection with S. suis SC19 strain, consequently activating the NLRP6 inflammasome. Furthermore, SC19 infection was found to augment the secretion of pro-inflammatory cytokines IL-1β via NLRP6 activation, while NLRP6 deficiency mitigates the invasion and adhesion of SC19 to macrophages. In vivo models revealed that NLRP6 deletion enhanced survival rates of SC19-infected mice, alongside a reduction in tissue bacterial load and inflammatory cytokine levels. NLRP6^-/- mice were shown to exhibit attenuated inflammatory responses in pulmonary, hepatic, and splenic tissues post-SC19 infection, as evidenced by lower inflammation scores. Flow cytometry analyses further substantiated that NLRP6 is involved in modulating macrophage and neutrophil recruitment during infection. Our findings suggest that NLRP6 negatively regulates host resistance against S. suis infection; its absence results in reduced mortality, bacterial colonization, and a milder inflammatory response. Elucidating the mechanism of NLRP6 in S. suis-induced inflammation provides novel insights and theoretical underpinnings for the prophylaxis and therapeutics of S. suis diseases.

项与 NLRP6 相关的新闻（医药）

2024-02-06

·今日头条

王军+崔玉涛等：疫情期间，儿童"消失"不少肠道微生物

02月06日的《热心肠日报》，我们解读了 15 篇文献，关注：儿童肠道菌群，双歧杆菌，丁酸，生命早期，IBD，抗感染，动物模型，厌食症，生殖健康，饮食，蜜蜂，信达生物，LimmaTech Biologics，杰毅生物，安邦，Adipo Therapeutics。该篇日报由R·AI辅助创作生成，人工审核校对。王军+崔玉涛等：疫情对婴儿和儿童肠道菌群有何影响？ Science China Life Sciences——[10.372] ① 中科院微生物所王军、北京崔玉涛诊所崔玉涛与热心肠研究院及团队，对比分析了新冠疫情前后1126名未感染的婴儿和儿童的肠道菌群（疫情前队列906人，疫情后队列220人）；② 肠道菌群组成在疫情前后呈现显著差异，拟杆菌肠型占比从30.46%增加到35.45%，7个关键分类群的细菌载量降低（降低幅度19.58%~91.69%）；③ 定量微生物组分析表明疫情后队列的肠道菌群载量减少，20个主要属中有15个的细菌载量显著下降，且疫情对菌群变化的解释度超过了性别；④ 使用疫情前菌群数据构建的随机森林年龄预测器显示，疫情后儿童肠道菌群成熟度较低，平均年龄特征较实际年龄年轻约1.86岁；⑤ 此外，疫情后婴儿的体重和身高与疫情前相比有显著下降，与肠道细菌载量减少相关；⑥ 这些发现表明疫情相关举措（如社交减少和过度消毒等生活习惯变化）可能影响了婴儿/儿童肠道菌群结构和发育。【原文信息】 The Missing Microbes in Infants and Children in the COVID-19 Pandemic: a Study of 1,126 Participants in Beijing, China 2024-02-04 , doi: 10.1007/s11427-023-2488-0 Nature子刊：母乳低聚糖与婴儿双歧杆菌定植有何关系？ Nature Communications——[16.6] ① 纳入21对母婴组成的纵向队列，利用一种高通量方法来定量测定长双歧杆菌婴儿亚种（BL. infantis，一种擅长利用母乳低聚糖HMO的肠菌），并分析母乳HMO组成；② 婴儿肠道菌群在几个月的时间内发生了显著变化，而母乳中的HMO组成保持相对稳定；③ 虽然双歧杆菌种类显著影响样本差异，但没有特定的HMO与双歧杆菌种丰度相关；④ BL. infantis在婴儿肠道的定植发生在哺乳期末期；⑤ 这些发现强调了母乳HMO组成与婴儿肠道菌群演变之间的复杂关系，为研究婴儿肠道微生物群的发育提供重要参考。【原文信息】 Longitudinal quantification of Bifidobacterium longum subsp. infantis reveals late colonization in the infant gut independent of maternal milk HMO composition 2024-01-30 , doi: 10.1038/s41467-024-45209-y Cell子刊：丁酸抑制tuft细胞分化进而调节2型免疫反应 Immunity——[32.4] ① 文章聚焦肠道菌群对肠道tuft细胞的影响，定义了干细胞受共生代谢物影响，进而调控tuft细胞分化的机制，揭示了肠道菌群调节肠道2型免疫反应的途径；② 产短链脂肪酸的共生菌限制了肠道tuft细胞诱导的2型免疫反应；③ 丁酸盐通过抑制组蛋白去乙酰化酶3（HDAC3），进而抑制小鼠和人tuft细胞发育；④ 上皮内HDAC3的表达对于激活tuft细胞-ILC2通路和促进蠕虫感染相关2型免疫反应是必需的；⑤ 丁酸盐和产丁酸盐的共生菌限制tuft细胞的分化，肠道干细胞中HDAC3的靶向缺失阻断tuft细胞的分化和下游ILC2反应。【原文信息】 Microbiota-derived butyrate restricts tuft cell differentiation via histone deacetylase 3 to modulate intestinal type 2 immunity 2024-01-24 , doi: 10.1016/j.immuni.2024.01.002 1岁时期饮食质量影响炎症性肠病发病 Gut——[24.5] ① 这项研究分析了斯堪的纳维亚出生队列，发现生命早期（1岁）的高质量饮食和鱼类的摄入与较低的炎症性肠病（IBD）风险相关；② 在1,304,433人年的随访期内，对81,280名参与者从出生到童年和青少年时期进行随访，其中307人被诊断为IBD；③ 与饮食质量低相比，1岁时中等和高饮食质量与较低的IBD风险相关，aHR分别是0.75、0.75；④ 1岁时鱼类摄入高与鱼类摄入低相比，IBD的汇总aHR为0.70，并显示出与溃疡性结肠炎（UC）风险降低的关联，1岁时更高的蔬菜摄入与IBD的风险降低相关，饮用含糖饮料与IBD风险增加相关；⑤ 3岁时的饮食质量与IBD无关联；⑥ 早期饮食可能对预防儿童炎症性肠病具有潜在的重要作用，值得进一步关注和研究。【原文信息】 Early-life diet and risk of inflammatory bowel disease: a pooled study in two Scandinavian birth cohorts 2024-01-30 , doi: 10.1136/gutjnl-2023-330971 首次揭示新生儿肠道上皮细胞对沙门氏菌感染防御机制 Journal of Experimental Medicine——[15.3] ① 本研究首次揭示新生儿宿主中邻近上皮细胞通过非专职吞噬作用清除沙门氏菌感染的肠上皮细胞，为新生儿抗微生物宿主防御机制提供了新见解；② 新生儿和成年细胞单层的肠上皮干细胞类器官共培养实验证实肠上皮细胞吞噬作用具有年龄依赖性，且需要适配器磷脂酰丝氨酸和C1q、“吃我”受体CD51和CD36的参与；③ 沙门氏菌感染的新生儿患者体内有大量上皮细胞膜突出、与凋亡细胞接触部位CD36积累；④ 本研究发现了一种维持屏障完整性的先前未被报道的新生儿抗菌宿主防御方式。【原文信息】 Non-professional efferocytosis of Salmonella-infected intestinal epithelial cells in the neonatal host 2024-02-02 , doi: 10.1084/jem.20231237 朱书等：构建小鼠模型，区分NLRP6介导的炎症小体依赖和非依赖性功能 PNAS——[11.1] ① NLRP6在肠上皮细胞中作为微生物双链RNA或脂肪酸类胞壁酸（LTA）的感知器，启动多条途径，包括炎症小体途径、I型干扰素（IFN）途径以及调控NF-κB和MAPK途径，中国科技大学朱书团队与合作者的这项研究，构建了突变小鼠来区分NLRP6介导的各个途径对体内生理和病理的贡献；② 小鼠NLRP6蛋白结构域PYD中的Arg39和Trp50残基对ASC的招募和炎症小体激活是必需的，但对RNA结合和PYD非依赖性的NLRP6寡聚化并不重要；③ 构建 Nlrp6R39E&W50E 突变小鼠，其在稳态肠道或病毒感染期间炎症小体激活减少，但I型IFN产生仍然正常；④ NLRP6介导的炎症小体激活或IFN-I产生在对抗不同类型的RNA病毒的防御反应中发挥着不同的作用。【原文信息】 A mouse model to distinguish NLRP6-mediated inflammasome-dependent and -independent functions 2024-01-30 , doi: 10.1073/pnas.2321419121 纵向分析厌食症青少年肠道菌群变化及临床相关因素 Gut Microbes——[12.2] ① 纳入57名厌食症（AN）青少年患者及34名健康对照（HCs），对其肠道菌群进行长达一年的纵向观察；② 与HCs相比，AN患者肠道菌群组成在疾病进程中呈现动态变化，尤其是在急性饥饿期和低体重阶段存在明显差异，但差异随着体重增加逐渐减小；③ 疾病持续时间和先前体重减轻与患者入院时的菌群组成密切相关，而治疗期间的菌群变化与摄入热量、体重增加和激素恢复相关；④ 入院时的菌群组成可预测住院复发，而 Sutterella 的丰度与1年后的体重增加正相关；⑤ 本研究揭示了肠道菌群在厌食症中的潜在作用，为厌食症的治疗提供了新的思路和靶点。【原文信息】 Longitudinal analysis of the gut microbiome in adolescent patients with anorexia nervosa: microbiome-related factors associated with clinical outcome 2024-01-31 , doi: 10.1080/19490976.2024.2304158 男性生育力与饮食（综述） Human Reproduction Update——[13.3] ① 纳入37项随机对照试验和观察性研究，评估饮食在受孕前期对男性临床生育能力和生殖结果的影响；② 主要结果包括男性受孕前饮食对临床结果的影响，如受孕、怀孕率和活产率，次要结果包括受孕时间和精子参数；③ 随机对照试验未评估临床结果，但发现番茄汁可能有益于精子活力，在观察性研究中，一些证据表明增加鱼类摄入或减少含糖饮料、加工肉类或总脂肪摄入可能改善受孕能力；④ 对于妊娠率或活产率，显示出与谷物、大豆和乳制品摄入无关，与红肉或“健康饮食”模式摄入关系不一致；⑤ 对于改善精子参数，有限的证据支持增加鱼类、脂肪/脂肪酸、碳水化合物和乳制品摄入，减少加工肉类摄入，而水果、蔬菜、谷物、豆类、鸡蛋、红肉和蛋白质的证据不一致。【原文信息】 Assessing the influence of preconception diet on male fertility: a systematic scoping review 2024-01-17 , doi: 10.1093/humupd/dmad035 孕前及孕期营养干预对婴儿BMI和体重增长的影响 BMC Medicine——[9.3] ① 孕前和孕期补充肌醇、益生菌和额外微量营养素可降低子代快速体重增长和肥胖风险，对儿童健康成长具有重要意义；② 两岁时，干预组子代平均BMI呈下降趋势，且较少出现BMI>95th百分位数；③ 干预组子代在出生后第一年和前两年的快速/持续体重增长风险分别降低24%和45%，且有更多子代保持稳定的正常体重增长轨迹；④ 这些结果表明孕前和孕期营养干预对儿童健康成长具有积极影响，为孕期营养干预在儿童肥胖预防领域提供了重要的临床证据支持。【原文信息】 Impact of preconception and antenatal supplementation with myo-inositol, probiotics, and micronutrients on offspring BMI and weight gain over the first 2 years 2024-01-30 , doi: 10.1186/s12916-024-03246-w Nature子刊：蜜蜂微生物组及其对宿主健康的影响（综述） Nature Reviews Microbiology——[88.1] ① 蜜蜂是全球农业的主要传粉媒介，目前也越来越多地被用作菌群的研究模型，本综述总结了蜜蜂微生物组的研究方法、现有菌群-宿主-营养互作知识、菌株进化、共生和拮抗等内容；② 目前蜜蜂微生物组研究方法包括减菌蜜蜂、特定人工群落定植蜜蜂、抗生素扰动、荧光标记工程菌株、异源表达菌群来源酶、标记重捕、测序和体外实验等，基于这些研究方法获得了蜜蜂菌群的空间分布、微生物动力学、以及菌群-宿主-营养互作机制；③ 蜜蜂微生物组内存在代谢交叉互养，也存在直接拮抗（如T6SS），菌群介导对蜜蜂病原体的定植抗性，包括免疫激活、营养/空间竞争、活性抑菌物质分泌和肠屏障维持；④ 菌群参与蜜蜂发育和行为调节，同时介导营养代谢和解毒，农用化学品或抗生素施用会对蜜蜂及共生菌群产生直接的负面影响。【原文信息】 The honeybee microbiota and its impact on health and disease 2023-12-04 , doi: 10.1038/s41579-023-00990-3 信达生物启动IBI343治疗胃癌3期临床研究 ① 近日，信达生物启动了IBI343单药治疗Claudin18.2阳性、HER2阴性的胃或胃食管交界处腺癌患者3期临床G-HOPE-001研究；② G-HOPE-001研究是一项随机、多中心、开放标签试验，计划招募450例患者；③ IBI343是一种针对Claudin18.2的重组人源化抗体偶联药物（ADC），通过与肿瘤细胞结合释放毒素药物引起肿瘤细胞凋亡；④ 国内外关于Claudin18.2靶点的研发竞争激烈，目前信达生物的IBI343在同类药物中进展最快。【原文信息】首个！信达生物CLDN18.2 ADC启动III期临床 2024-02-05 , 医药魔方「LimmaTech Biologics」获得300万美元融资，剑指耐药问题 ① 2月1日，瑞士生物技术公司LimmaTech Biologics宣布，在A轮融资中获得了第二笔300万美元（约合人民币2158万元）资金，总融资额来到了4000万美元；② 资金将用于推进LimmaTech Biologics公司耐药性细菌感染疫苗技术平台开发，加速其疫苗候选产品的临床前和临床研究；③ LimmaTech Biologics公司致力于解决耐药菌感染问题，包括金黄色葡萄球菌、志贺氏菌和引起性传播疾病的耐药菌；④ LimmaTech Biologics公司计划在2024年启动针对金黄色葡萄球菌候选疫苗的1期临床试验，以及针对志贺氏菌候选疫苗的2期临床试验。【原文信息】 LimmaTech Biologics Adds Additional $3 Million in Series A Second Closing Bringing Total Raised to $40 Million 2024-02-01 , businesswire 感染病原分子诊断公司「杰毅生物」完成数亿元C+轮融资 ① 近日，杭州杰毅生物技术有限公司（Matridx）宣布，完成了数亿元人民币C+轮融资；② 本轮投资方包括昆泰基金、余杭国投集团及其它产业投资者；③ 融资将用于杰毅生物产品管线研发、医疗器械产品注册及商业化应用战略落地；④ 杰毅生物致力于感染病原分子诊断技术创新，自主研发了一系列自动化检测仪器、诊断试剂和生物信息学分析平台，能够提供全场景化的创新分子诊断解决方案。【原文信息】杰毅生物（Matridx）完成数亿元C+轮融资 2024-02-02 , 微创投生物医药公司「安邦生技」完成1250万美元A轮融资 ① 2月1日，安邦生技宣布获得1250万美元（约合人民币8997.3万元）的A轮融资，中华开发（CDIB）公司领衔了本次投资；② 资金将用于推进安邦生技旗下两款候选抗癌药物ABT-101与ABT-301的临床开发；③ 候选药物ABT-101为针对HER2的标靶药物，在1b期临床试验中显示出优异的安全性和抗癌潜力，安邦生技正探索其治疗大肠癌的可行性；④ ABT-301已完成1期临床试验，与免疫检查点抑制剂联用时在大肠癌模型中显示出高度协同作用。【原文信息】安邦完成A輪融資一千兩百五十萬美元，推動精準腫瘤學藥物研發的進展 2024-02-01 , 安邦生物制药公司「Adipo」获得190万美元种子轮融资 ① 1月31日，Adipo Therapeutics公司宣布完成了190万美元（约合人民币1366.6万元）的种子轮融资，② 截至目前，Adipo Therapeutics公司已累计筹集了400万美元的资金；③ 此次主要投资者包括Purdue Research Foundation和Elevate Ventures等公司，融资将用于推进其针对肥胖和2型糖尿病治疗管线药物ADPO-002的临床开发；④ 管线药物ADPO-002可以将储能的白色脂肪组织转化为燃烧能量的棕色脂肪组织，从而实现减肥功效并改善血糖控制水平。【原文信息】 Adipo Therapeutics completes $1.9M seed funding bridge to advance obesity and Type 2 diabetes treatment 2024-01-31 , Purdue University 感谢本期日报的审核者：mildbreeze，章台柳，RZN，圆圈儿，九卿臣，Johnson，Richard 点击阅读过去10天的日报： 0205 | 糖尿病如何促肝癌？Nature揭示新机制 0204 | 大型研究再证：饮食血糖指数/负荷与慢性疾病的关联 0203 | Nature新闻：人类肠菌中古怪的微小RNA 0202 | 流感肆虐，高分Cell子刊揭示肠菌如何影响呼吸道感染 0201 | 1月，最值得看的40篇肠道健康文献！ 0131 | 今日Cell：于君/沈祖尧团队发现新的促胃癌菌 0130 | 炎症性肠病如何进行营养治疗？胃肠病学顶刊发出最新专家建议 0129 | 国内团队24页综述详解瘤内菌群——肿瘤研究新前沿 0128 | 32分综述详解：饮食如何通过菌群代谢物影响免疫？ 0127 | 今日Cell双发聚焦肠道！揭示肠道免疫和肠肝轴新机制

微生物疗法临床研究