Oral microbiota and inflammatory bowel disease

doi:10.7518/hxkq.2019.04.020

Abstract

Abstract:

Inflammatory bowel disease (IBD) is a chronic inflammatory disease of the gastrointestinal tract with a high incidence but a poor therapeutic outcome. However, IBD is generally caused by complicated interactions between environmental factors and gut microflora in genetically susceptible individuals. In view of a series of oral manifestations in patients with IBD and a high detection rate of oral bacteria among this population, oral microbiota may play an important role in the development of IBD. This article reviews the relationship between oral microbiota and IBD.

Key words: inflammatory bowel disease, oral microbiota, ulcerative colitis, Crohn’s disease;

CLC Number:

R780.2

Haonan Zhang,Xuedong Zhou,Xin Xu,Yan Wang. Oral microbiota and inflammatory bowel disease[J]. West China Journal of Stomatology, 2019, 37(4): 443-449.

References 67

[1]	Malik TA . Inflammatory bowel disease: historical perspective, epidemiology, and risk factors[J]. Surg Clin North Am, 2015,95(6):1105-1122.
[2]	Molodecky NA, Soon IS, Rabi DM , et al. Increasing incidence and prevalence of the inflammatory bowel diseases with time, based on systematic review[J]. Gastroenterology, 2012,142(1):46-54.
[3]	Mulder DJ, Noble AJ, Justinich CJ , et al. A tale of two diseases: the history of inflammatory bowel disease[J]. J Crohns Colitis, 2014,8(5):341-348.
[4]	Zhang YZ, Li YY . Inflammatory bowel disease: pathogenesis[J]. World J Gastroenterol, 2014,20(1):91-99.
[5]	Adams SM, Bornemann PH . Ulcerative colitis[J]. Am Fam Physician, 2013,87(10):699-705.
[6]	Jostins L, Ripke S, Weersma RK , et al. Host-microbe interactions have shaped the genetic architecture of inflammatory bowel disease[J]. Nature, 2012,491(7422):119-124.
[7]	张静, 韩英, 王继恒 , 等. 炎症性肠病与肠道细菌研究进展[J]. 世界华人消化杂志, 2007,15(12):1406-1410.
	Zhang J, Han Y, Wang JH , et al. Advance on the relationship between inflammatory bowel disease and intestinal bacteria[J]. World Chin J Digestol, 2007,15(12):1406-1410.
[8]	白爱平 . 炎症性肠病发病机制的微生物因素[J]. 世界华人消化杂志, 2006,14(7):645-649.
	Bai AP . Biological factors in pathogenesis of inflammatory bowel disease[J]. World Chin J Digestol, 2006,14(7):645-649.
[9]	Scaldaferri F, Gerardi V, Lopetuso LR , et al. Gut microbial flora, prebiotics, and probiotics in IBD: their current usage and utility[J]. Biomed Res Int, 2013,2013:435268.
[10]	Willing BP, Dicksved J, Halfvarson J , et al. A pyrosequencing study in twins shows that gastrointestinal microbial profiles vary with inflammatory bowel disease phenotypes[J]. Gastroenterology, 2010,139(6):1844-1854.
[11]	Maloy KJ, Powrie F . Intestinal homeostasis and its breakdown in inflammatory bowel disease[J]. Nature, 2011,474(7351):298-306.
[12]	牛润章, 张兰兰, 司依馨 . 炎症性肠病的病因及诊治研究进展[J]. 实用医药杂志, 2014,31(5):461-463.
	Niu RZ, Zhang LL, Si YX . Etiology, diagnosis and treatment of inflammatory bowel disease[J]. Pract J Med Pharm, 2014,31(5):461-463.
[13]	Yang Y, Weng W, Peng J , et al. Fusobacterium nucleatum increases proliferation of colorectal cancer cells and tumor development in mice by activating Toll-like receptor 4 signaling to nuclear factor-κB, and up-regulating expression of MicroRNA-21[J]. Gastroenterology, 2017,152(4):851-866.
[14]	Bashir A, Miskeen AY, Bhat A , et al. Fusobacterium nucleatum: an emerging bug in colorectal tumorigenesis[J]. Eur J Cancer Prev, 2015,24(5):373-385.
[15]	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.
[16]	Bashir A, Miskeen AY, Hazari YM , et al. Fusobacterium nucleatum, inflammation, and immunity: the fire within human gut[J]. Tumour Biol, 2016,37(3):2805-2810.
[17]	Rogers MB, Brower-Sinning R, Firek B , et al. Acute appendicitis in children is associated with a local expansion of fusobacteria[J]. Clin Infect Dis, 2016,63(1):71-78.
[18]	Guinane CM, Tadrous A, Fouhy F , et al. Microbial composition of human appendices from patients following appendectomy[J]. MBio, 2013, 4(1). pii:e00366-12. doi: 10.1128/mBio.00366-12.
[19]	Singhal S, Dian D, Keshavarzian A , et al. The role of oral hygiene in inflammatory bowel disease[J]. Dig Dis Sci, 2011,56(1):170-175.
[20]	Habashneh RA, Khader YS, Alhumouz MK , et al. The association between inflammatory bowel disease and periodontitis among Jordanians: a case-control study[J]. J Periodontal Res, 2012,47(3):293-298.
[21]	Ricart E, Panaccione R, Loftus EV Jr , et al. Autoimmune disorders and extraintestinal manifestations in first-degree familial and sporadic inflammatory bowel disease: a case-control study[J]. Inflamm Bowel Dis, 2004,10(3):207-214.
[22]	Veloso FT, Carvalho J, Magro F . Immune-related systemic manifestations of inflammatory bowel disease. A prospective study of 792 patients[J]. J Clin Gastroenterol, 1996,23(1):29-34.
[23]	Lakatos L, Pandur T, David G , et al. Association of extraintestinal manifestations of inflammatory bowel disease in a province of western Hungary with disease phenotype: results of a 25-year follow-up study[J]. World J Gastroenterol, 2003,9(10):2300-2307.
[24]	Muhvić-Urek M, Tomac-Stojmenović M, Mijandrušić-Sinčić B . Oral pathology in inflammatory bowel disease[J]. World J Gastroenterol, 2016,22(25):5655-5657.
[25]	Mills CC, Amin M, Manisali M . Salivary duct fistula and recurrent buccal space infection: a complication of Crohn’s disease[J]. J Oral Maxillofac Surg, 2003,61(12):1485-1487.
[26]	李敏, 宋文婷, 林梅 , 等. 炎症性肠病的口腔损害及其诊断[J]. 国际口腔医学杂志, 2010,37(3):330-332. doi: 10.3969/j.issn.1673-5749.2010.
	Li M, Song WT, Lin M , et al. Oral lesion of inflammatory bowel disease and its diagnosis[J]. Int J Stomatol, 2010,37(3):330-332. doi: 10.3969/j.issn.1673-5749.2010.
[27]	Lankarani KB, Sivandzadeh GR, Hassanpour S . Oral manifestation in inflammatory bowel disease: a review[J]. World J Gastroenterol, 2013,19(46):8571-8579.
[28]	Said HS, Suda W, Nakagome S , et al. Dysbiosis of salivary microbiota in inflammatory bowel disease and its association with oral immunological biomarkers[J]. DNA Res, 2014,21(1):15-25.
[29]	Szczeklik K, Owczarek D, Pytko-Polończyk J , et al. Proinflammatory cytokines in the saliva of patients with active and non-active Crohn’s disease[J]. Pol Arch Med Wewn, 2012,122(5):200-208.
[30]	Rathnayake N, Åkerman S, Klinge B , et al. Salivary biomarkers for detection of systemic diseases[J]. PLoS One, 2013,8(4):e61356.
[31]	Wescombe PA, Hale JD, Heng NC , et al. Developing oral probiotics from Streptococcus salivarius[J]. Future Microbiol, 2012,7(12):1355-1371.
[32]	Teughels W, Kinder Haake S, Sliepen I , et al. Bacteria interfere with A. actinomycetemcomitans colonization[J]. J Dent Res, 2007,86(7):611-617.
[33]	Kaci G, Lakhdari O, Doré J , et al. Inhibition of the NF-kappaB pathway in human intestinal epithelial cells by commensal Streptococcus salivarius[J]. Appl Environ Microbiol, 2011,77(13):4681-4684.
[34]	Cosseau C, Devine DA, Dullaghan E , et al. The commensal Streptococcus salivarius K12 downregulates the innate immune responses of human epithelial cells and promotes host-microbe homeostasis[J]. Infect Immun, 2008,76(9):4163-4175.
[35]	Kaci G, Goudercourt D, Dennin V , et al. Anti-inflammatory properties of Streptococcus salivarius, a commensal bacterium of the oral cavity and digestive tract[J]. Appl Environ Microbiol, 2014,80(3):928-934.
[36]	Fujiwara T, Nakano K, Kawaguchi M , et al. Biochemical and genetic characterization of serologically untypable Streptococcus mutans strains isolated from patients with bacteremia[J]. Eur J Oral Sci, 2001,109(5):330-334.
[37]	Nakano K, Nomura R, Nakagawa I , et al. Demonstration of Streptococcus mutans with a cell wall polysaccharide specific to a new serotype, k, in the human oral cavity[J]. J Clin Microbiol, 2004,42(1):198-202.
[38]	Kojima A, Nakano K, Wada K , et al. Infection of specific strains of Streptococcus mutans, oral bacteria, confers a risk of ulcerative colitis[J]. Sci Rep, 2012,2:332.
[39]	Kojima A, Nomura R, Naka S , et al. Aggravation of inflammatory bowel diseases by oral streptococci[J]. Oral Dis, 2014,20(4):359-366.
[40]	Liu P, Liu Y, Wang J , et al. Detection of Fusobacterium nucleatum and fadA adhesin gene in patients with orthodontic gingivitis and non-orthodontic periodontal inflammation[J]. PLoS One, 2014,9(1):e85280.
[41]	Nosho K, Sukawa Y, Adachi Y , et al. Association of Fusobacterium nucleatum with immunity and molecular alterations in colorectal cancer[J]. World J Gastroenterol, 2016,22(2):557-566.
[42]	Strauss J, Kaplan GG, Beck PL , et al. Invasive potential of gut mucosa-derived Fusobacterium nucleatum positively correlates with IBD status of the host[J]. Inflamm Bowel Dis, 2011,17(9):1971-1978.
[43]	Liu H, Redline RW, Han YW . Fusobacterium nucleatum induces fetal death in mice via stimulation of TLR4-mediated placental inflammatory response[J]. J Immunol, 2007,179(4):2501-2508.
[44]	Kostic AD, Chun E, Robertson L , et al. Fusobacterium nucleatum potentiates intestinal tumorigenesis and modulates the tumor-immune microenvironment[J]. Cell Host Microbe, 2013,14(2):207-215.
[45]	Sears CL, Garrett WS . Microbes, microbiota, and colon cancer[J]. Cell Host Microbe, 2014,15(3):317-328.
[46]	Irrazábal T, Belcheva A, Girardin SE , et al. The multifaceted role of the intestinal microbiota in colon cancer[J]. Mol Cell, 2014,54(2):309-320.
[47]	Zhang L, Budiman V, Day AS , et al. Isolation and detection of Campylobacter concisus from saliva of healthy individuals and patients with inflammatory bowel disease[J]. J Clin Microbiol, 2010,48(8):2965-2967.
[48]	Nielsen HL, Ejlertsen T, Engberg J , et al. High incidence of Campylobacter concisus in gastroenteritis in North Jutland, Denmark: a population-based study[J]. Clin Microbiol Infect, 2013,19(5):445-450.
[49]	Mukhopadhya I, Thomson JM, Hansen R , et al. Detection of Campylobacter concisus and other Campylobacter species in colonic biopsies from adults with ulcerative colitis[J]. PLoS One, 2011,6(6):e21490.
[50]	Underwood AP, Kaakoush NO, Sodhi N , et al. Campylobacter concisus pathotypes are present at significant levels in patients with gastroenteritis[J]. J Med Microbiol, 2016,65(3):219-226.
[51]	Man SM, Kaakoush NO, Leach ST , et al. Host attachment, invasion, and stimulation of proinflammatory cytokines by Campylobacter concisus and other non-Campylobacter jejuni Campylobacter species[J]. J Infect Dis, 2010,202(12):1855-1865.
[52]	Kalischuk LD, Inglis GD . Comparative genotypic and pathogenic examination of Campylobacter concisus isolates from diarrheic and non-diarrheic humans[J]. BMC Microbiol, 2011,11:53.
[53]	Ismail Y, Lee H, Riordan SM , et al. The effects of oral and enteric Campylobacter concisus strains on expression of TLR4, MD-2, TLR2, TLR5 and COX-2 in HT-29 cells[J]. PLoS One, 2013,8(2):e56888.
[54]	Nielsen HL, Nielsen H, Ejlertsen T , et al. Oral and fecal Campylobacter concisus strains perturb barrier function by apoptosis induction in HT-29/B6 intestinal epithelial cells[J]. PLoS One, 2011,6(8):e23858.
[55]	Zhang L, Lee H, Grimm MC , et al. Campylobacter concisus and inflammatory bowel disease[J]. World J Gastroenterol, 2014,20(5):1259-1267.
[56]	Waldor MK, Mekalanos JJ . Lysogenic conversion by a filamentous phage encoding cholera toxin[J]. Science, 1996,272(5270):1910-1914.
[57]	Fasano A, Baudry B, Pumplin DW , et al. Vibrio cholerae produces a second enterotoxin, which affects intestinal tight junctions[J]. Proc Natl Acad Sci U S A, 1991,88(12):5242-5246.
[58]	Kaakoush NO, Mitchell HM, Man SM . Role of emerging Campylobacter species in inflammatory bowel diseases[J]. Inflamm Bowel Dis, 2014,20(11):2189-2197.
[59]	王林峰, 王选锭 . 肺炎克雷伯氏菌耐药机制研究进展[J]. 中国抗生素杂志, 2004,29(6):324-328.
	Wang LF, Wang XD . Advances in the mechanism of drug resistance of Klebsiella pneumoniae[J]. Chin J Antibiot, 2004,29(6):324-328.
[60]	Pamer EG . Resurrecting the intestinal microbiota to combat antibiotic-resistant pathogens[J]. Science, 2016,352(6285):535-538.
[61]	Atarashi K, Suda W, Luo C , et al. Ectopic colonization of oral bacteria in the intestine drives TH1 cell induction and inflammation[J]. Science, 2017,358(6361):359-365.
[62]	Cao XT . Intestinal inflammation induced by oral bacteria[J]. Science, 2017,358(6361):308-309.
[63]	Inohara N . Route connection: mouth to intestine in colitis[J]. Cell Host Microbe, 2017,22(6):730-731.
[64]	Poulain D . Candida albicans, plasticity and pathogenesis[J]. Crit Rev Microbiol, 2015,41(2):208-217.
[65]	Standaertvitse A, Sendid B, Joossens M , et al. Candida albicans colonization and ASCA in familial Crohn’s disease[J]. Am J Gastroenterol, 2009,104(7):1745-1753.
[66]	Zwolinska-Wcislo M, Brzozowski T, Budak A , et al. Effect of Candida colonization on human ulcerative colitis and the healing of inflammatory changes of the colon in the experimental model of colitis ulcerosa[J]. J Physiol Pharmacol, 2009,60(1):107-118.
[67]	Forcione DG, Rosen MJ, Kisiel JB , et al. Anti-Saccharomyces cerevisiae antibody (ASCA) positivity is associated with increased risk for early surgery in Crohn’s disease[J]. Gut, 2004,53(8):1117-1122.