Genes of intestinal Escherichia coli and their relation to the inflammatory activity in patients with ulcerative colitis and Crohn's disease
Jazyk angličtina Země Spojené státy americké Médium print-electronic
Typ dokumentu časopisecké články
PubMed
21877213
PubMed Central
PMC3189319
DOI
10.1007/s12223-011-0051-z
Knihovny.cz E-zdroje
- MeSH
- antibakteriální látky terapeutické užití MeSH
- Crohnova nemoc komplikace farmakoterapie imunologie mikrobiologie patologie MeSH
- dospělí MeSH
- Escherichia coli genetika imunologie MeSH
- infekce vyvolané Escherichia coli komplikace farmakoterapie imunologie mikrobiologie patologie MeSH
- interleukin-10 biosyntéza MeSH
- interleukin-6 biosyntéza MeSH
- interleukin-8 biosyntéza MeSH
- lidé středního věku MeSH
- lidé MeSH
- polymerázová řetězová reakce MeSH
- proteiny fimbrií genetika izolace a purifikace MeSH
- senioři MeSH
- střeva imunologie mikrobiologie patologie MeSH
- studie případů a kontrol MeSH
- techniky typizace bakterií MeSH
- TNF-alfa biosyntéza MeSH
- ulcerózní kolitida komplikace farmakoterapie imunologie mikrobiologie patologie MeSH
- zánět komplikace farmakoterapie imunologie mikrobiologie patologie MeSH
- Check Tag
- dospělí MeSH
- lidé středního věku MeSH
- lidé MeSH
- mužské pohlaví MeSH
- senioři MeSH
- ženské pohlaví MeSH
- Publikační typ
- časopisecké články MeSH
- Geografické názvy
- Česká republika MeSH
- Názvy látek
- antibakteriální látky MeSH
- fimbrillin MeSH Prohlížeč
- interleukin-10 MeSH
- interleukin-6 MeSH
- interleukin-8 MeSH
- proteiny fimbrií MeSH
- TNF-alfa MeSH
Escherichia coli gene fimA was the most frequent gene that occurred in the intestine of all investigated groups. All subjects with fimA gene had significantly higher values of tumor necrosis factor alpha (TNF-α) and CRP than those with other E. coli genes. There was also a tendency to increased serum interleukin (IL)-6 levels in patients carrying the fimA gene; however, no relation was observed to serum IL-8 and IL-10. Patients with Crohn's disease had significantly higher IL-6 than those with ulcerative colitis (UC) and controls. The highest levels of TNF-α were detected in the UC group. There were no significant differences in serum IL-8 and IL-10 between all three groups. The presence of E. coli gene fimA in the large bowel of patients with IBD is related to the immunological activity of the disease which may be important from the aspect of therapeutical strategy.
Zobrazit více v PubMed
Best WR, Becktel JM, Singleton JW, et al. Development of a Crohn’s disease activity index. National Cooperative Crohn’s Disease Study. Gastroenterology. 1976;70:439–444. PubMed
Boudeau J, Barnich N, Darfeuille-Michaud A. Type 1 pili-mediated adherence of E. coli strain LF82 isolated from Crohn’s disease is involved in bacterial invasion of intestinal epithelial cells. Mol Microbiol. 2001;39:1272–1284. doi: 10.1111/j.1365-2958.2001.02315.x. PubMed DOI
Chamberli WM, Naser SA. Integrating theories of the etiology of Crohn’s disease: questioning the hypotheses. Med Sci Monit. 2006;12:27–33. PubMed
Denis MA, Reenaers C, Fontaine F, et al. Assessment of endoscopic activity index and biological inflammatory markers in clinically active Crohn’s disease with normal C-reactive protein serum level. Inflamm Bowel Dis. 2007;13:1100–1105. doi: 10.1002/ibd.20178. PubMed DOI
Dignass AU, Baumgart DC, Sturm A. Review article: the etiopathogenesis of inflammatory bowel disease—immunology and repair mechanisms. Aliment Pharmacol Ther. 2004;20(Suppl. V):9–17. doi: 10.1111/j.1365-2036.2004.02047.x. PubMed DOI
Dogan B, Simpson KW. Microflora in Crohn’s disease: the emergence of adherent and invasive Escherichia coli. Expert Rev Clin Immunol. 2008;4:133–137. doi: 10.1586/1744666X.4.2.133. PubMed DOI
Douda T, Bureš J, Rejchrt S. Mean platelet volume in Crohn’s disease patients. Cas Lek Cesk. 2006;145:870–873. PubMed
Fantini MC, Monteleone G, MacDonald TT. New players in the cytokine orchestra of inflammatory bowel disease. Inflamm Bowel Dis. 2007;13:1–5. doi: 10.1002/ibd.20212. PubMed DOI
Florin TH, Paterson EW, Fowler EV. Clinically active Crohn’s disease in the presence of a low C reactive protein. Scand J Gastroenterol. 2006;41:306–311. doi: 10.1080/00365520500217118. PubMed DOI
Guarner F, Malagelada JR. Role of bacteria in experimental colitis. Best Pract Res Clin Gastroenterol. 2003;17:793–804. doi: 10.1016/S1521-6918(03)00068-4. PubMed DOI
Irving PM, Pasi KJ, Rampton DS. Thrombosis and inflammatory bowel disease. Clin Gastroenterol Hepatol. 2005;3:617–628. doi: 10.1016/S1542-3565(05)00154-0. PubMed DOI
Kuhnert P, Hacker J, Muhldorfer I, et al. Detection system for Escherichia coli-specific virulence genes: absence of virulence determinants in B and C strains. Appl Environ Microbiol. 1997;63:703–709. PubMed PMC
Liptáková A, Sehnálková H, Sabol M, et al. Detection of shiga-like toxin producing Escherichia coli by multiplex PCR. Biologia Bratislava. 2001;56:65–68.
Macfarlane S, Steed H, Macfarlane GT. Intestinal bacteria and inflammatory bowel disease. Crit Rev Clin Lab Sci. 2009;46:25–54. doi: 10.1080/10408360802485792. PubMed DOI
Martin HM, Campbell BJ, Hart CA, et al. Enhanced E. coli adherence and invasion in Crohn’s disease and colon cancer. Gastroenterology. 2004;127:1649–1650. doi: 10.1053/j.gastro.2004.09.072. PubMed DOI
Mitsuyama K, Tomiyasu N, Takaki K. IL-10 in the pathophysiology of inflammatory bowel disease: increased serum concentrations during the recovery phase. Med Inflamm. 2006;1:1–7. doi: 10.1155/MI/2006/26875. PubMed DOI PMC
Mudter J, Neurath MF. IL-6 signaling in inflammatory bowel disease: pathophysiology role and clinical relevance. Inflamm Bowel Dis. 2007;13:1016–1023. doi: 10.1002/ibd.20148. PubMed DOI
Nielsen OH, Rudiger N, Gaustadnes M, et al. Intestinal interleukin-8 concentration and gene expression in inflammatory bowel disease. Scand J Gastroenterol. 1997;32:1028–1034. doi: 10.3109/00365529709011220. PubMed DOI
Reinecker HC, Steffen M, Witthoeft T, et al. Enhanced secretion of tumour necrosis factor-α, IL-6, and IL-1β by isolated lamina propria mononuclear cells from patients with ulcerative colitis and Crohn’s disease. Clin Exp Immunol. 1993;94:174–181. doi: 10.1111/j.1365-2249.1993.tb05997.x. PubMed DOI PMC
Sanchez-Muñoz F, Dominguez-Lopez A, Yamamoto Furusho JK. Role of cytokines in inflammatory bowel disease. World J Gastroenterol. 2008;14:4280–4288. doi: 10.3748/wjg.14.4280. PubMed DOI PMC
Sansonetti PJ, Arondel J, Huerre M. IL-8 controls bacterial transepithelial translocation at cost of epithelial destruction in experimental shigellosis. Infect Immun. 1999;67:1471–1480. PubMed PMC
Sasaki M, Sitaraman SV, Babbin BA, et al. Invasive Escherichia coli are a feature of Crohn’s disease. Lab Invest. 2007;87:1042–1054. doi: 10.1038/labinvest.3700661. PubMed DOI
Scaldaferri F, Fiocchi C. Inflammatory bowel disease: progress and current concepts of etiopathogenesis. J Dig Dis. 2007;8:1–9. doi: 10.1111/j.1751-2980.2007.00310.x. PubMed DOI
Schroeder KW, Tremaine WJ, Ilstrup DM. Coated oral 5-aminosalicylic acid therapy for mildly to moderately active ulcerative colitis: a randomised study. New Engl J Med. 1987;317:1625–1629. doi: 10.1056/NEJM198712243172603. PubMed DOI
Vermèire S, van Assche G, Rutgeerts P. Laboratory markers in IBD: useful, magic, or unnecessary toys? Gut. 2006;55:426–431. doi: 10.1136/gut.2005.069476. PubMed DOI PMC
Yamamoto S, Terai A, Yuri K, et al. Detection of virulence factors in Escherichia coli by multiplex polymerase chain reaction. FEMS Immunol Med Microbiol. 1995;12:85–90. doi: 10.1111/j.1574-695X.1995.tb00179.x. PubMed DOI