赤峰地区蒙古族人溃疡性结肠炎患者肠道菌群分析
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摘要
目的：
研究赤峰地区蒙古族溃疡性结肠炎患者活动期和缓解期肠道优势菌群的变化,探讨UC患者肠道优势菌群的变化与疾病发生、发展的关系,为临床治疗UC提供依据。
方法：
病例采集及菌群分析法
1.收集2008年10月-2009年12月我地区两家三级医院消化内科收治的蒙古族溃疡性结肠炎确诊患者32例,根据Sourtherland疾病活动指数(DAI),将病例分为UC活动期和UC缓解期两组。
2.选取来我院正常体检的蒙古族人员18例作为正常对照组。
3.采集病例组与对照组人员粪便进行肠杆菌、肠球菌、葡萄球菌、酵母菌、类杆菌、双歧杆菌、消化球菌、乳酸杆菌、优杆菌和梭菌10种肠道优势菌群定量分析。
结果：
1.与正常对照组比较,活动期溃疡性结肠炎患者肠道菌群中肠杆菌(9.00±0.19,p<0.01)、肠球菌(8.04±0.38,p<0.01)的数量明显增加,梭杆菌(6.83±0.34,p<0.05)的数量略有增加;双歧杆菌(7.34±0.29,p<0.01)的数量明显下降,其他细菌无明显变化。
2.缓解期溃疡性结肠炎患者肠道菌群中肠杆菌(8.54±0.24,P<0.05)仍呈增加趋势,双歧杆菌、优杆菌数量略有下降,但无显著性差异,其他细菌无明显变化。
结论：
1.赤峰地区蒙古族溃疡性结肠炎患者均不同程度存在优势菌群失调。
2.不同分期的UC患者肠道优势菌群的改变与UC的活动性具有相关性。
Objective:
Studying the alteration of intestinal flor in active ulcerative colitis, ulcerative colitis in remission patinents and the change of pathology for Mongolian in Chifeng region.To explor the relationship between the change of ulcerative colitis (UC)intestinal flora and occurrence and development of disease. To provide the basis for clinical treatment of UC.
Methods:
Case collection and analysis method of Fecal Flora
1.Collecting 32 cases Mongolian (UC) Ulcerative Colitis patients who were treated from two third level hospitals from October 2008 to December 2009, in accordance with Sourtherland DAI,individed into two groups,UC active and UC remission.
2.Choosing 18 Mongolian cases of physical examination from our hospital as control group.
3.Collecting excrement of the cases and control groups for Enterobacteria,Enterococcus,Staphylococcus, Yeast,Bacteroides,bifidobacte rium,peptococcus,lactobacillus, eubacterium and Clostridium,above 10 kinds of intestinal predominant flor make quantitative analysis of the flora.
Results
1. Comparing with the control group, the quantity of Enterobacteria (9.00±0.19, p<0.01) in the Intestinal Flora with active (UC) Ulcerative Colitis patients, Enterococcus (8.04±0.38, p<0.01) increases obviously,the quantity of fusiformis (6.83±0.34, p<0.05) increase slightly,the quantity of Bacillus Bifidus (7.34±0.29, p<0.01) decrease obviously and other Bacteriums do not change obviously.
2. Enterobacteria (8.54±0.24, P<0.05) in remission (UC) Ulcerative Colitis patinents is the trend of increasment, the quantity of Bacillus Bifidus and Eubacterium decrease slightly,but it is not obvious difference. Other Bacterias do not change obviously.
Conclusions
1, The Mongolian Ulcerative Coliti patients of ChiFeng exist flora imblanceIn different degrees.,
2, the different stages (UC) Ulcerative Colitis patinents, it has the relevant connections between the UC patients with changes in intestinal predominant flora and the activity of UC.
研究赤峰地区蒙古族溃疡性结肠炎患者活动期和缓解期肠道优势菌群的变化,探讨UC患者肠道优势菌群的变化与疾病发生、发展的关系,为临床治疗UC提供依据。
方法：
病例采集及菌群分析法
1.收集2008年10月-2009年12月我地区两家三级医院消化内科收治的蒙古族溃疡性结肠炎确诊患者32例,根据Sourtherland疾病活动指数(DAI),将病例分为UC活动期和UC缓解期两组。
2.选取来我院正常体检的蒙古族人员18例作为正常对照组。
3.采集病例组与对照组人员粪便进行肠杆菌、肠球菌、葡萄球菌、酵母菌、类杆菌、双歧杆菌、消化球菌、乳酸杆菌、优杆菌和梭菌10种肠道优势菌群定量分析。
结果：
1.与正常对照组比较,活动期溃疡性结肠炎患者肠道菌群中肠杆菌(9.00±0.19,p<0.01)、肠球菌(8.04±0.38,p<0.01)的数量明显增加,梭杆菌(6.83±0.34,p<0.05)的数量略有增加;双歧杆菌(7.34±0.29,p<0.01)的数量明显下降,其他细菌无明显变化。
2.缓解期溃疡性结肠炎患者肠道菌群中肠杆菌(8.54±0.24,P<0.05)仍呈增加趋势,双歧杆菌、优杆菌数量略有下降,但无显著性差异,其他细菌无明显变化。
结论：
1.赤峰地区蒙古族溃疡性结肠炎患者均不同程度存在优势菌群失调。
2.不同分期的UC患者肠道优势菌群的改变与UC的活动性具有相关性。
Objective:
Studying the alteration of intestinal flor in active ulcerative colitis, ulcerative colitis in remission patinents and the change of pathology for Mongolian in Chifeng region.To explor the relationship between the change of ulcerative colitis (UC)intestinal flora and occurrence and development of disease. To provide the basis for clinical treatment of UC.
Methods:
Case collection and analysis method of Fecal Flora
1.Collecting 32 cases Mongolian (UC) Ulcerative Colitis patients who were treated from two third level hospitals from October 2008 to December 2009, in accordance with Sourtherland DAI,individed into two groups,UC active and UC remission.
2.Choosing 18 Mongolian cases of physical examination from our hospital as control group.
3.Collecting excrement of the cases and control groups for Enterobacteria,Enterococcus,Staphylococcus, Yeast,Bacteroides,bifidobacte rium,peptococcus,lactobacillus, eubacterium and Clostridium,above 10 kinds of intestinal predominant flor make quantitative analysis of the flora.
Results
1. Comparing with the control group, the quantity of Enterobacteria (9.00±0.19, p<0.01) in the Intestinal Flora with active (UC) Ulcerative Colitis patients, Enterococcus (8.04±0.38, p<0.01) increases obviously,the quantity of fusiformis (6.83±0.34, p<0.05) increase slightly,the quantity of Bacillus Bifidus (7.34±0.29, p<0.01) decrease obviously and other Bacteriums do not change obviously.
2. Enterobacteria (8.54±0.24, P<0.05) in remission (UC) Ulcerative Colitis patinents is the trend of increasment, the quantity of Bacillus Bifidus and Eubacterium decrease slightly,but it is not obvious difference. Other Bacterias do not change obviously.
Conclusions
1, The Mongolian Ulcerative Coliti patients of ChiFeng exist flora imblanceIn different degrees.,
2, the different stages (UC) Ulcerative Colitis patinents, it has the relevant connections between the UC patients with changes in intestinal predominant flora and the activity of UC.
引文
1. Satsangi J, Parkes M, Louis E, et al. [J]. Nat Genet,1996.14(2):199-202.
2. Leong RW, Lee Y, Ching JY, et al. [J]. Liment Pharmacol Ther,2003, 17(5):711-718.
3. Wills-Karp M, Santeliz J, Karp Cl. The germless theory of allergic disease: revisiting the hypothesis. Nature Rev,2001,1:69-75.
4. Baumgart DC, Carding SR. Inflammatory bowel disease:cause and immunobiology. Lancet,2007,369 (9573):1627-1640.
5. Orholm M, Binder V, S"rensen TI, et al. Concordance of inflammatory bowel disease among Danish twins. Results of a nationwide study. Scand J Gastroenterol,2000,35(10):1075-1081.
6. Hugot JP, Chamaillard M, Zouali H, et al. Association of NOD2 leucine-rich repeat variants with susceptibility to Crohn's disease.Nature,2001,411:599-603.
7. Duerr RH, Barmada MU, Zhang L, et al. High density genome scan in Crohn disease shows confirmed linkage to chromosone 14qll-2=12. Am J Hum Genet,2000,66:1257-1262.
8. 刘重阳.肠道菌群在炎症性肠病发病中的作用.重庆医学2009；38：1251-1253
9. 白爱平.炎症性肠病发病机制的微生物因素.世界华人消化杂志2006；14：645-645
10. Sellon PK, Tonkonogy S, Schuitz M, et al. Resident enteric bacteria are necessary for development of spontaneous colitis and immune system activation in interleukiw10-deficient mice[J]. Infect Immun,1998,66:5224.
11. Taurog JD, Richardson JA, Croft JT, et al. The germfree state prevents development of gut and joint inflammatory disease in HLA-B27 transgenic rats[J]. J Exp Med,1994,180:2359.
12. 熊德鑫.现代微生态学.北京：中国科学技术出版社,2000,252.255.
13. 崔海宏,陈村龙,孙勇,王亚东,张耀东,杨玉捷,王群英,潘令嘉.炎症性肠病患者肠粘膜菌群改变及抗体反应.胃肠病学和肝病学杂志(Chin J Gastro Hcpa)2003,12(3):276—278
14. Linskens RK, Huijsdens XW, Savelkoul PH, Vandenbroucke-Grauls-CM, Meuwissen SG. The bacterial flora in inflammatory bowel disease:current insights in pathogenesis and the influence of antibiotics and probiotics. Scand J Gastroenterol Suppl 2001; 29-40
15. Dickinson RJ, Varian SA, Axon AT, et al. Increased incidence of faecal coilforms with in vitro adhesive and invasive properties in patients with uleerative colitis. Gut 1980;21:787-792.
16. Swidsinski A, Weber J, Loening-Baucke V, Hale LP, Lochs H. Spatial Organization and Composition of the Mucosal Flora in Patients with Inflammatory bowel disease. J Clin Microbiol 2005; 43:3380-3389.
17. Klessen B, Kroesen AJ, Buhr HJ, Blaut M. Mucosal andinvading bacteria in patients with inflammatory bowel disease compared with controls. Scand J Gastroenterol 2002; 37:1034-1041.
18. 李润美,韩英,王继恒,等.炎症性肠病患者肠道菌丛结构特征的指纹图谱分析[J].中华内科杂志,2007,46(2)：96-98.
19. Duchmann R, Schmitt E, Knolle P. Meyer zum Buschenfelde KH, Neurath M. Tolerance towards resident intestinal flora in mice is abrogated in experimental colitis and restored by treatment with Interleukin-10 or antibodies to interleukin-12. Eur J, immunol 1996:26:934-938
20. Bouma G, Strober W. The immunological and genetic basis of inflammatory bowel disease. Nat Rev Immunol,2003,3:521-533.
21. Monteleone I, Vavassori P, Biancone L, et al. Immunoregulation in the gut: success and failures in human disease. Gut,2002,50(Suppl III):60-64.
22. Brown SJ, Mayer L. The immune response in inflammatory bawel disease. Am J Gastroenterol.2007,102(9):2058-2069.
23. Yen D, Cheung J, Seheerens H, et al. IL-23 is essential for T cell-mediated coliris and promotes inflammation via IL-17 and IL-6 J Clin Invest, 2006,116:1310-1316.
24. Iwakura Y, Ishigame H. The IL-23/IL-17 axis in inflammation. J Clin Invest,2006,116(5):1218-1222.
25. Swidsinski A, Ladhoff A, Pernthaler A, et al. Mucosal flora in inflammatory bowel disease. Gastroenterology,2002,122:44-54.
26. Guandalini S. Use of lactobacillus-GG in paediatric Crohn's disease. Dig liver Dis,2002,34 Suppl 2:S63-S65.
27. Schultz Z, Sartorh B.Probiotics and inflammatory bowel diseases J.Am J Castroenterol 2000,95(1 Suppl):19-21
28. Borody TJ, Warren EF, Leis S, Surace R, Ashman o. Treatment of ulcerative colitis using fecal bacteriotherapy. J Clin Gastroeterol 2003; 37:42-47
29. Gionchetti P, Rizzello F, Venturi A. Brigidi P, Matteuzzi D. Bazzocchi G, Poggioli G, Miglioli M, Campieri M. Oral bacteriotherapy as maintenance treatment in patients with chronic pouchitis:a double-blind, placebo-controlled trial. Gastmenterology,2000,119:305-309.
1. Satsangi J, Parkes M, Louis E, et al. [J]. Nat Genet,1996,14(2):199-202.
2. Leong RW, Lee Y, Ching JY, et al. [J]. Liment Pharmacol Ther,2003,17(5): 711-718.
3. Swidsinski A LadhoffA PemthalerA Swidsinski S, Loening-Baucke V, Ortner M, et al. (2002)Mucosal flora in inflammatory bowel disease. Gastroenterology 122: 44-54
4. Kim PH, Ko KJ. Bifidobacterium is a strong stimulant for IgA antibody production by mucosal B lymphocytes [J],1998,12:5278.
5.中华医学会消化病学分会炎症性肠病协作组.对我国炎症性肠病诊断治疗规范的共识意见.中华消化杂志,2007,27(8)：545-550.
6. Gordon J I, et al. Epithelial cell growth and differentiation:promoting diversity in the intestine:conversations between the microflora, epithelium, and diffuse GALT. Am J Physiol,1997,273:G565-570.
7. Sartor R(2004)Therapeutic manipulation of the enteriemieroflom in inflammatory bowel diseases:antibiotics, probiotics, and prebiotics. Gastroenterology 126: 1620-1633
8. Bullock NR, Booth JC, Gibson GR. Comparative composition of bacteria in the human intestinal microfiom during remission and active ulcerative colitis. Curr Issues Intest Microbiol,2004,5:59-64.
9.熊德鑫.现代微生态学[M]。北京：中国科学技术出版社,2000。
10.王占国,张皓,陈洁,杨建平等.补硒对克山病区儿童肠道菌群影响的研究[J].中国预防医学理论与实践,1991,185-289.
11. Wills-Karp M, Santeliz J, Karp C1. The germless theory of allergic disease: revisiting the hypothesis. Nature Rev,2001,1:69-75.
12. Seksik P. Sokol H, Lepage P. et al. Review article:the role of bacteria in onset and perpetuation of inflammatory bowel disease. Aliment Pharmacot Ther.2006,24 Suppl 3:11-18.
13. Sokol H, Scksik P,Rigottier-Gois L,et al. Speeificities of the fecal microbiota in inflammatory bowel disease. Inflamm Bowel Dis.2006,12:106-111.
14.Zhang M, Liu B. Zhang Y, et al. Structural shifts of mucosaassociated lactobacilli and Clostridium leptum subgroup in patients with ulcerative colitis. J Clin Microbiol,2007.45:496—500.
15.刘重阳.肠道菌群在炎症性肠病发病中的作用.重庆医学2009；38：1251-1253
16.白爱平.炎症性肠病发病机制的微生物因素.世界华人消化杂志2006；14：645-645
17.陈渝萍.肠道菌群状态在溃疡性结肠炎患者中的价值探讨[J]。右江医学,2006,34(5)：499-500.
18. Kim PH, Ko KJ. Bifidobacterium is a strong stimulant for IgA antibody production by mucosal B lymphoeytes[J]. FEBJ,1998,12:5278。
19.崔海宏,陈村龙.生态制剂在炎症性肠病中的作用[J].临床消化病杂志,2002,14(4)： 187-189.
20. Mantzaris GJ, Petraki K,Archavlis, et al.A prospective randomized controlled trial of intravenous ciproflaxacin as all adjunct to corticosteroids in acute, severe ulcerative colitis. Scand J Gastroenterol JT,2001,36(9):971-974
21. Guandalini S. Use of lactobacillus-GG in paediatric Crohn's disease. Dig liver Dis,2002,34 Suppl 2:S63-S65.
22. Schultz Z, Sartorh B.Probiotics and inflammatory bowel diseases.J.Am J Castroenterol 2000,95 (1 Suppl):19-21
23. Borody TJ, Warren EF, Leis S, Surace R, Ashman o. Treatment of ulcerative colitis using fecal bacteriotherapy. J Clin Gastroeterol 2003; 37:42-47
24. SonnenbergA. Seasonal variation of enterons and inflammatory bowel disease. Inflamm Bowel Dis.2008,4:955-959.
25. Sellon PK, Tonkonogy S, Schuitz M, et al. Resident entericbacteria are necessary for development of spontaneous colitis and immune system activation in interleukiwl0-deficient mice[J]. Infect Immun,1998,66:5224.
26. Machoonald TT, Monteleone G, Render SL. Recent developments in immunology of Inflammatory bowel disease [J].Scand J Immounol,2000,51(1):2-9
2. Leong RW, Lee Y, Ching JY, et al. [J]. Liment Pharmacol Ther,2003, 17(5):711-718.
3. Wills-Karp M, Santeliz J, Karp Cl. The germless theory of allergic disease: revisiting the hypothesis. Nature Rev,2001,1:69-75.
4. Baumgart DC, Carding SR. Inflammatory bowel disease:cause and immunobiology. Lancet,2007,369 (9573):1627-1640.
5. Orholm M, Binder V, S"rensen TI, et al. Concordance of inflammatory bowel disease among Danish twins. Results of a nationwide study. Scand J Gastroenterol,2000,35(10):1075-1081.
6. Hugot JP, Chamaillard M, Zouali H, et al. Association of NOD2 leucine-rich repeat variants with susceptibility to Crohn's disease.Nature,2001,411:599-603.
7. Duerr RH, Barmada MU, Zhang L, et al. High density genome scan in Crohn disease shows confirmed linkage to chromosone 14qll-2=12. Am J Hum Genet,2000,66:1257-1262.
8. 刘重阳.肠道菌群在炎症性肠病发病中的作用.重庆医学2009；38：1251-1253
9. 白爱平.炎症性肠病发病机制的微生物因素.世界华人消化杂志2006；14：645-645
10. Sellon PK, Tonkonogy S, Schuitz M, et al. Resident enteric bacteria are necessary for development of spontaneous colitis and immune system activation in interleukiw10-deficient mice[J]. Infect Immun,1998,66:5224.
11. Taurog JD, Richardson JA, Croft JT, et al. The germfree state prevents development of gut and joint inflammatory disease in HLA-B27 transgenic rats[J]. J Exp Med,1994,180:2359.
12. 熊德鑫.现代微生态学.北京：中国科学技术出版社,2000,252.255.
13. 崔海宏,陈村龙,孙勇,王亚东,张耀东,杨玉捷,王群英,潘令嘉.炎症性肠病患者肠粘膜菌群改变及抗体反应.胃肠病学和肝病学杂志(Chin J Gastro Hcpa)2003,12(3):276—278
14. Linskens RK, Huijsdens XW, Savelkoul PH, Vandenbroucke-Grauls-CM, Meuwissen SG. The bacterial flora in inflammatory bowel disease:current insights in pathogenesis and the influence of antibiotics and probiotics. Scand J Gastroenterol Suppl 2001; 29-40
15. Dickinson RJ, Varian SA, Axon AT, et al. Increased incidence of faecal coilforms with in vitro adhesive and invasive properties in patients with uleerative colitis. Gut 1980;21:787-792.
16. Swidsinski A, Weber J, Loening-Baucke V, Hale LP, Lochs H. Spatial Organization and Composition of the Mucosal Flora in Patients with Inflammatory bowel disease. J Clin Microbiol 2005; 43:3380-3389.
17. Klessen B, Kroesen AJ, Buhr HJ, Blaut M. Mucosal andinvading bacteria in patients with inflammatory bowel disease compared with controls. Scand J Gastroenterol 2002; 37:1034-1041.
18. 李润美,韩英,王继恒,等.炎症性肠病患者肠道菌丛结构特征的指纹图谱分析[J].中华内科杂志,2007,46(2)：96-98.
19. Duchmann R, Schmitt E, Knolle P. Meyer zum Buschenfelde KH, Neurath M. Tolerance towards resident intestinal flora in mice is abrogated in experimental colitis and restored by treatment with Interleukin-10 or antibodies to interleukin-12. Eur J, immunol 1996:26:934-938
20. Bouma G, Strober W. The immunological and genetic basis of inflammatory bowel disease. Nat Rev Immunol,2003,3:521-533.
21. Monteleone I, Vavassori P, Biancone L, et al. Immunoregulation in the gut: success and failures in human disease. Gut,2002,50(Suppl III):60-64.
22. Brown SJ, Mayer L. The immune response in inflammatory bawel disease. Am J Gastroenterol.2007,102(9):2058-2069.
23. Yen D, Cheung J, Seheerens H, et al. IL-23 is essential for T cell-mediated coliris and promotes inflammation via IL-17 and IL-6 J Clin Invest, 2006,116:1310-1316.
24. Iwakura Y, Ishigame H. The IL-23/IL-17 axis in inflammation. J Clin Invest,2006,116(5):1218-1222.
25. Swidsinski A, Ladhoff A, Pernthaler A, et al. Mucosal flora in inflammatory bowel disease. Gastroenterology,2002,122:44-54.
26. Guandalini S. Use of lactobacillus-GG in paediatric Crohn's disease. Dig liver Dis,2002,34 Suppl 2:S63-S65.
27. Schultz Z, Sartorh B.Probiotics and inflammatory bowel diseases J.Am J Castroenterol 2000,95(1 Suppl):19-21
28. Borody TJ, Warren EF, Leis S, Surace R, Ashman o. Treatment of ulcerative colitis using fecal bacteriotherapy. J Clin Gastroeterol 2003; 37:42-47
29. Gionchetti P, Rizzello F, Venturi A. Brigidi P, Matteuzzi D. Bazzocchi G, Poggioli G, Miglioli M, Campieri M. Oral bacteriotherapy as maintenance treatment in patients with chronic pouchitis:a double-blind, placebo-controlled trial. Gastmenterology,2000,119:305-309.
1. Satsangi J, Parkes M, Louis E, et al. [J]. Nat Genet,1996,14(2):199-202.
2. Leong RW, Lee Y, Ching JY, et al. [J]. Liment Pharmacol Ther,2003,17(5): 711-718.
3. Swidsinski A LadhoffA PemthalerA Swidsinski S, Loening-Baucke V, Ortner M, et al. (2002)Mucosal flora in inflammatory bowel disease. Gastroenterology 122: 44-54
4. Kim PH, Ko KJ. Bifidobacterium is a strong stimulant for IgA antibody production by mucosal B lymphocytes [J],1998,12:5278.
5.中华医学会消化病学分会炎症性肠病协作组.对我国炎症性肠病诊断治疗规范的共识意见.中华消化杂志,2007,27(8)：545-550.
6. Gordon J I, et al. Epithelial cell growth and differentiation:promoting diversity in the intestine:conversations between the microflora, epithelium, and diffuse GALT. Am J Physiol,1997,273:G565-570.
7. Sartor R(2004)Therapeutic manipulation of the enteriemieroflom in inflammatory bowel diseases:antibiotics, probiotics, and prebiotics. Gastroenterology 126: 1620-1633
8. Bullock NR, Booth JC, Gibson GR. Comparative composition of bacteria in the human intestinal microfiom during remission and active ulcerative colitis. Curr Issues Intest Microbiol,2004,5:59-64.
9.熊德鑫.现代微生态学[M]。北京：中国科学技术出版社,2000。
10.王占国,张皓,陈洁,杨建平等.补硒对克山病区儿童肠道菌群影响的研究[J].中国预防医学理论与实践,1991,185-289.
11. Wills-Karp M, Santeliz J, Karp C1. The germless theory of allergic disease: revisiting the hypothesis. Nature Rev,2001,1:69-75.
12. Seksik P. Sokol H, Lepage P. et al. Review article:the role of bacteria in onset and perpetuation of inflammatory bowel disease. Aliment Pharmacot Ther.2006,24 Suppl 3:11-18.
13. Sokol H, Scksik P,Rigottier-Gois L,et al. Speeificities of the fecal microbiota in inflammatory bowel disease. Inflamm Bowel Dis.2006,12:106-111.
14.Zhang M, Liu B. Zhang Y, et al. Structural shifts of mucosaassociated lactobacilli and Clostridium leptum subgroup in patients with ulcerative colitis. J Clin Microbiol,2007.45:496—500.
15.刘重阳.肠道菌群在炎症性肠病发病中的作用.重庆医学2009；38：1251-1253
16.白爱平.炎症性肠病发病机制的微生物因素.世界华人消化杂志2006；14：645-645
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