口腔菌群与胰腺疾病的关系

陈嘉芳; 庄铭泉; 林振和

doi:10.12449/JCH250837

口腔菌群与胰腺疾病的关系

DOI: 10.12449/JCH250837

陈嘉芳¹,
庄铭泉¹,
林振和^{1, 2, , ,}

1.
福建医科大学研究生院，福州 350122
2.
厦门大学附属中山医院消化内科，福建厦门 361004

基金项目:

2024年厦门市医疗卫生指导性项目 (3502Z20244ZD1096)

利益冲突声明：本文不存在任何利益冲突。

作者贡献声明：陈嘉芳负责文章的构思与设计，撰写论文；庄铭泉负责论文的修订；林振和负责文章的质量控制及审校，对文章整体负责、监督管理。

详细信息

通信作者:
林振和， zhenhelin@163.com （ORCID： 0000-0002-9590-8999）

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出版历程
- 收稿日期: 2024-12-23
- 录用日期: 2025-01-14
- 出版日期: 2025-08-25

Association between oral flora and pancreatic diseases

1.
Graduate School of Fujian Medical University，Fuzhou 350122，China
2.
Department of Gastroenterology，Zhongshan Hospital，Xiamen University，Xiamen，Fujian 361004，China

Research funding:

2024 Xiamen Medical and Health Guidance Project (3502Z20244ZD1096)

More Information

Corresponding author: LIN Zhenhe， zhenhelin@163.com （ORCID： 0000-0002-9590-8999）

摘要

摘要: 口腔微生物群在人类健康和疾病状态中发挥着重要作用，相关研究已逐渐拓展至消化系统疾病领域。从胰腺组织中分离出的微生物群落在组成上与口腔菌群具有一定相似性，提示二者之间存在潜在生物学联系。基于口腔菌群采样方式无创、操作简便、储存成本低等优势，获取口腔菌群信息并识别其特征性变化具有可行性。这不仅有助于深入理解胰腺疾病的发病机制，还为开发新型诊断工具和个性化治疗方案奠定基础。本文系统综述了口腔菌群与胰腺疾病的关系，旨在为探索口腔菌群在胰腺疾病的早期诊断、预后评估及治疗中的潜在应用价值提供新思路。
- 口腔菌群 /
- 胰腺疾病 /
- 胰腺炎 /
- 胰腺肿瘤
Abstract: Oral flora plays a vital role in human health and disease， and related studies have extended to the field of gastrointestinal diseases. Evidence has shown that microbial communities isolated from pancreatic tissue have a similar composition to oral flora， indicating a potential biological connection between them. Due to the advantages of noninvasiveness， simple operation， and low storage costs of collecting oral flora samples， it is feasible to obtain the information on oral flora and identify its characteristic changes. This approach not only helps to gain a deeper understanding of the pathogenesis of pancreatic diseases， but also lays a foundation for developing novel diagnostic tools and personalized treatment regimens. This article systematically reviews the research advances in the association between oral flora and pancreatic diseases， in order to provide new ideas for exploring the potential application value of oral flora in the early diagnosis， prognostic evaluation， and treatment of pancreatic diseases.
- Oral Flora /
- Pancreatic Disease /
- Pancreatitis /
- Pancreatic Neoplasms

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参考文献(45)

[1]	THOMAS C, MINTY M, VINEL A, et al. Oral microbiota: A major player in the diagnosis of systemic diseases[J]. Diagnostics(Basel), 2021, 11( 8): 1376. DOI: 10.3390/diagnostics11081376.
[2]	KITAMOTO S, NAGAO-KITAMOTO H, HEIN R, et al. The bacterial connection between the oral cavity and the gut diseases[J]. J Dent Res, 2020, 99( 9): 1021- 1029. DOI: 10.1177/0022034520924633.
[3]	FLEMER B, WARREN RD, BARRETT MP, et al. The oral microbiota in colorectal cancer is distinctive and predictive[J]. Gut, 2018, 67( 8): 1454- 1463. DOI: 10.1136/gutjnl-2017-314814.
[4]	ZHANG S, KONG C, YANG YZ, et al. Human oral microbiome dysbiosis as a novel non-invasive biomarker in detection of colorectal cancer[J]. Theranostics, 2020, 10( 25): 11595- 11606. DOI: 10.7150/thno.49515.
[5]	YU T, GUO FF, YU YN, et al. Fusobacterium nucleatum promotes chemoresistance to colorectal cancer by modulating autophagy[J]. Cell, 2017, 170( 3): 548- 563. e 16. DOI: 10.1016/j.cell.2017.07.008.
[6]	HUI BQ, ZHOU CC, XU YT, et al. Exosomes secreted by Fusobacterium nucleatum-infected colon cancer cells transmit resistance to oxaliplatin and 5-FU by delivering hsa_circ_0004085[J]. J Nanobiotechnology, 2024, 22( 1): 62. DOI: 10.1186/s12951-024-02331-9.
[7]	YEE JC. Are the view of Helicobacter pylori colonized in the oral cavity an illusion?[J]. Exp Mol Med, 2017, 49( 11): e397. DOI: 10.1038/emm.2017.225.
[8]	WANG ZM. Relationship between oral microecological imbalance and general health[J]. Chin J Stomatol, 2019, 54( 3): 145- 150. DOI: 10.3760/cma.j.issn.1002-0098.2019.03.001. 王左敏. 口腔微生态失衡与全身健康的关系[J]. 中华口腔医学杂志, 2019, 54( 3): 145- 150. DOI: 10.3760/cma.j.issn.1002-0098.2019.03.001.
[9]	RISELY A. Applying the core microbiome to understand host-microbe systems[J]. J Anim Ecol, 2020, 89( 7): 1549- 1558. DOI: 10.1111/1365-2656.13229.
[10]	RUAN XW, LUO JQ, ZHANG PZ, et al. The salivary microbiome shows a high prevalence of core bacterial members yet variability across human populations[J]. NPJ Biofilms Microbiomes, 2022, 8( 1): 85. DOI: 10.1038/s41522-022-00343-7.
[11]	WADE WG. Resilience of the oral microbiome[J]. Periodontol 2000, 2021, 86( 1): 113- 122. DOI: 10.1111/prd.12365.
[12]	LAZAREVIC V, WHITESON K, HERNANDEZ D, et al. Study of inter- and intra-individual variations in the salivary microbiota[J]. BMC Genom, 2010, 11( 1): 523. DOI: 10.1186/1471-2164-11-523.
[13]	ZAURA E, BRANDT BW, TEIXEIRA de MATTOS MJ, et al. Same exposure but two radically different responses to antibiotics: Resilience of the salivary microbiome versus long-term microbial shifts in feces[J]. mBio, 2015, 6( 6): e01693-15. DOI: 10.1128/mBio.01693-15.
[14]	CABRAL DJ, WURSTER JI, FLOKAS ME, et al. The salivary microbiome is consistent between subjects and resistant to impacts of short-term hospitalization[J]. Sci Rep, 2017, 7( 1): 11040. DOI: 10.1038/s41598-017-11427-2.
[15]	TAN Q, MA X, YANG B, et al. Periodontitis pathogen Porphyromonas gingivalis promotes pancreatic tumorigenesis via neutrophil elastase from tumor-associated neutrophils[J]. Gut Microbes, 2022, 14( 1): 2073785. DOI: 10.1080/19490976.2022.2073785.
[16]	SABA E, FARHAT M, DAOUD A, et al. Oral bacteria accelerate pancreatic cancer development in mice[J]. Gut, 2024, 73( 5): 770- 786. DOI: 10.1136/gutjnl-2023-330941.
[17]	LIU YT, LIU H, RONG YP, et al. Alterations of oral microbiota are associated with the development and severity of acute pancreatitis[J]. J Oral Microbiol, 2023, 15( 1): 2264619. DOI: 10.1080/20002297.2023.2264619.
[18]	SUN Z, XIONG CL, TEH SW, et al. Mechanisms of oral bacterial virulence factors in pancreatic cancer[J]. Front Cell Infect Microbiol, 2019, 9: 412. DOI: 10.3389/fcimb.2019.00412.
[19]	RUBINSTEIN MR, WANG XW, LIU W, et al. Fusobacterium nucleatum promotes colorectal carcinogenesis by modulating E-cadherin/β‍-catenin signaling via its FadA adhesin[J]. Cell Host Microbe, 2013, 14( 2): 195- 206. DOI: 10.1016/j.chom.2013.07.012.
[20]	YILMAZ O, YAO LY, MAEDA K, et al. ATP scavenging by the intracellular pathogen Porphyromonas gingivalis inhibits P2X7-mediated host-cell apoptosis[J]. Cell Microbiol, 2008, 10( 4): 863- 875. DOI: 10.1111/j.1462-5822.2007.01089.x.
[21]	YILMAZ O, JUNGAS T, VERBEKE P, et al. Activation of the phosphatidylinositol 3-kinase/Akt pathway contributes to survival of primary epithelial cells infected with the periodontal pathogen Porphyromonas gingivalis[J]. Infect Immun, 2004, 72( 7): 3743- 3751. DOI: 10.1128/IAI.72.7.3743-3751.2004.
[22]	MOFFATT CE, LAMONT RJ. Porphyromonas gingivalis induction of microRNA-203 expression controls suppressor of cytokine signaling 3 in gingival epithelial cells[J]. Infect Immun, 2011, 79( 7): 2632- 2637. DOI: 10.1128/IAI.00082-11.
[23]	IKEZAWA K, HIKITA H, SHIGEKAWA M, et al. Increased bcl-xL expression in pancreatic neoplasia promotes carcinogenesis by inhibiting senescence and apoptosis[J]. Cell Mol Gastroenterol Hepatol, 2017, 4( 1): 185- 200. e 1. DOI: 10.1016/j.jcmgh.2017.02.001.
[24]	NOURI Z, CHOI SW, CHOI IJ, et al. Exploring connections between oral microbiota, short-chain fatty acids, and specific cancer types: A study of oral cancer, head and neck cancer, pancreatic cancer, and gastric cancer[J]. Cancers(Basel), 2023, 15( 11): 2898. DOI: 10.3390/cancers15112898.
[25]	GUR C, IBRAHIM Y, ISAACSON B, et al. Binding of the Fap2 protein of fusobacterium nucleatum to human inhibitory receptor TIGIT protects tumors from immune cell attack[J]. Immunity, 2015, 42( 2): 344- 355. DOI: 10.1016/j.immuni.2015.01.010.
[26]	SEGATA N, HAAKE SK, MANNON P, et al. Composition of the adult digestive tract bacterial microbiome based on seven mouth surfaces, tonsils, throat and stool samples[J]. Genome Biol, 2012, 13( 6): R42. DOI: 10.1186/gb-2012-13-6-r42.
[27]	ELEY BM, COX SW. Proteolytic and hydrolytic enzymes from putative periodontal pathogens: Characterization, molecular genetics, effects on host defenses and tissues and detection in gingival crevice fluid[J]. Periodontol 2000, 2003, 31: 105- 124. DOI: 10.1034/j.1600-0757.2003.03107.x.
[28]	NAKAJIMA M, ARIMATSU K, KATO T, et al. Oral administration of P. gingivalis induces dysbiosis of gut microbiota and impaired barrier function leading to dissemination of enterobacteria to the liver[J]. PLoS One, 2015, 10( 7): e0134234. DOI: 10.1371/journal.pone.0134234.
[29]	ARIMATSU K, YAMADA H, MIYAZAWA H, et al. Oral pathobiont induces systemic inflammation and metabolic changes associated with alteration of gut microbiota[J]. Sci Rep, 2014, 4: 4828. DOI: 10.1038/srep04828.
[30]	THOMAS RM, JOBIN C. Microbiota in pancreatic health and disease: The next frontier in microbiome research[J]. Nat Rev Gastroenterol Hepatol, 2020, 17( 1): 53- 64. DOI: 10.1038/s41575-019-0242-7.
[31]	HERREMANS KM, RINER AN, CAMERON ME, et al. The oral microbiome, pancreatic cancer and human diversity in the age of precision medicine[J]. Microbiome, 2022, 10( 1): 93. DOI: 10.1186/s40168-022-01262-7.
[32]	FARRELL JJ, ZHANG L, ZHOU H, et al. Variations of oral microbiota are associated with pancreatic diseases including pancreatic cancer[J]. Gut, 2012, 61( 4): 582- 588. DOI: 10.1136/gutjnl-2011-300784.
[33]	TORRES PJ, FLETCHER EM, GIBBONS SM, et al. Characterization of the salivary microbiome in patients with pancreatic cancer[J]. PeerJ, 2015, 3: e1373. DOI: 10.7717/peerj.1373.
[34]	MICHAUD DS, IZARD J, WILHELM-BENARTZI CS, et al. Plasma antibodies to oral bacteria and risk of pancreatic cancer in a large European prospective cohort study[J]. Gut, 2013, 62( 12): 1764- 1770. DOI: 10.1136/gutjnl-2012-303006.
[35]	FAN XZ, ALEKSEYENKO AV, WU J, et al. Human oral microbiome and prospective risk for pancreatic cancer: A population-based nested case-control study[J]. Gut, 2018, 67( 1): 120- 127. DOI: 10.1136/gutjnl-2016-312580.
[36]	TRIKUDANATHAN G, PHILIP A, DASANU CA, et al. Association between Helicobacter pylori infection and pancreatic cancer. A cumulative meta-analysis[J]. JOP, 2011, 12( 1): 26- 31.
[37]	LU HF, LI A, ZHANG T, et al. Disordered oropharyngeal microbial communities in H7N9 patients with or without secondary bacterial lung infection[J]. Emerg Microbes Infect, 2017, 6( 12): e112. DOI: 10.1038/emi.2017.101.
[38]	AMMER-HERRMENAU C, ANTWEILER KL, ASENDORF T, et al. Gut microbiota predicts severity and reveals novel metabolic signatures in acute pancreatitis[J]. Gut, 2024, 73( 3): 485- 495. DOI: 10.1136/gutjnl-2023-330987.
[39]	LARSEN JM. The immune response to Prevotella bacteria in chronic inflammatory disease[J]. Immunology, 2017, 151( 4): 363- 374. DOI: 10.1111/imm.12760.
[40]	AMMER-HERRMENAU C, LINGENS CHM, RATEI CS, et al. Whole 16S rRNA sequencing of the oral microbiome predicts postoperative pancreatic fistula: Prospective observational cohort study[J]. Br J Surg, 2023, 110( 10): 1279- 1283. DOI: 10.1093/bjs/znad129.
[41]	ESKANDARI A, MAHMOUDPOUR A, ABOLFAZLI N, et al. Detection of Helicobacter pylori using PCR in dental plaque of patients with and without gastritis[J]. Med Oral Patol Oral Cir Bucal, 2010, 15( 1): e28-31. DOI: 10.4317/medoral.15.e28.
[42]	GUARNERI F, GUARNERI C, BENVENGA S. Helicobacter pylori and autoimmune pancreatitis: Role of carbonic anhydrase via molecular mimicry?[J]. J Cell Mol Med, 2005, 9( 3): 741- 744. DOI: 10.1111/j.1582-4934.2005.tb00506.x.
[43]	FRULLONI L, LUNARDI C, SIMONE R, et al. Identification of a novel antibody associated with autoimmune pancreatitis[J]. N Engl J Med, 2009, 361( 22): 2135- 2142. DOI: 10.1056/NEJMoa0903068.
[44]	PAWLACZYK-KAMIEŃSKA T, BORYSEWICZ-LEWICKA M, BATURA-GABRYEL H. Salivary biomarkers and oral microbial load in relation to the dental status of adults with cystic fibrosis[J]. Microorganisms, 2019, 7( 12): 692. DOI: 10.3390/microorganisms7120692.
[45]	GOLDBERG JB, PIER GB. The role of the CFTR in susceptibility to Pseudomonas aeruginosa infections in cystic fibrosis[J]. Trends Microbiol, 2000, 8( 11): 514- 520. DOI: 10.1016/s0966-842x(00)01872-2.