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Human inflammatory bowel disease does not associate with Lawsonia intracellularis infection
BACKGROUND: There is increasing evidence that bacterial infection of the intestinal mucosa may contribute to the pathogenesis of inflammatory bowel diseases (IBD). In pigs, an obligate intracellular bacterium, Lawsonia intracellularis (LI), was shown to cause proliferative enteropathy (PE) of which...
Autores principales: | , , , , , , , |
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Formato: | Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2006
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1590022/ https://www.ncbi.nlm.nih.gov/pubmed/16984651 http://dx.doi.org/10.1186/1471-2180-6-81 |
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author | Michalski, Christoph W Di Mola, Fabio Francesco Kümmel, Klaus Wendt, Michael Köninger, Jörg S Giese, Thomas Giese, Nathalia A Friess, Helmut |
author_facet | Michalski, Christoph W Di Mola, Fabio Francesco Kümmel, Klaus Wendt, Michael Köninger, Jörg S Giese, Thomas Giese, Nathalia A Friess, Helmut |
author_sort | Michalski, Christoph W |
collection | PubMed |
description | BACKGROUND: There is increasing evidence that bacterial infection of the intestinal mucosa may contribute to the pathogenesis of inflammatory bowel diseases (IBD). In pigs, an obligate intracellular bacterium, Lawsonia intracellularis (LI), was shown to cause proliferative enteropathy (PE) of which some forms display histological and clinical similarities to human IBD. Since LI-similar Desulfovibrio spp. may infect human cells, we hypothesized that LI might be associated with the development of human IBD. RESULTS: In human intestinal tissue samples, PCR using LLG, 50SL27, LSA and strictly LI-specific 16SII primers, yielded either no amplicons or products with weak homology to human genomic sequences. Sequencing of these amplicons revealed no specificity for LI. However, amplification of DNA with less specific 16SI primers resulted in products bearing homology to certain Streptococcus species. These 16SI-amplified products were present in healthy and diseased specimens, without obvious prevalence. CONCLUSION: LI is not associated with the pathogenesis of UC or CD. Whether an immunologic response to commensal bacteria such as streptococci may contribute to the chronic inflammatory condition in IBD, remained to be determined. |
format | Text |
id | pubmed-1590022 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2006 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-15900222006-10-05 Human inflammatory bowel disease does not associate with Lawsonia intracellularis infection Michalski, Christoph W Di Mola, Fabio Francesco Kümmel, Klaus Wendt, Michael Köninger, Jörg S Giese, Thomas Giese, Nathalia A Friess, Helmut BMC Microbiol Research Article BACKGROUND: There is increasing evidence that bacterial infection of the intestinal mucosa may contribute to the pathogenesis of inflammatory bowel diseases (IBD). In pigs, an obligate intracellular bacterium, Lawsonia intracellularis (LI), was shown to cause proliferative enteropathy (PE) of which some forms display histological and clinical similarities to human IBD. Since LI-similar Desulfovibrio spp. may infect human cells, we hypothesized that LI might be associated with the development of human IBD. RESULTS: In human intestinal tissue samples, PCR using LLG, 50SL27, LSA and strictly LI-specific 16SII primers, yielded either no amplicons or products with weak homology to human genomic sequences. Sequencing of these amplicons revealed no specificity for LI. However, amplification of DNA with less specific 16SI primers resulted in products bearing homology to certain Streptococcus species. These 16SI-amplified products were present in healthy and diseased specimens, without obvious prevalence. CONCLUSION: LI is not associated with the pathogenesis of UC or CD. Whether an immunologic response to commensal bacteria such as streptococci may contribute to the chronic inflammatory condition in IBD, remained to be determined. BioMed Central 2006-09-19 /pmc/articles/PMC1590022/ /pubmed/16984651 http://dx.doi.org/10.1186/1471-2180-6-81 Text en Copyright © 2006 Michalski et al; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/2.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( (http://creativecommons.org/licenses/by/2.0) ), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Research Article Michalski, Christoph W Di Mola, Fabio Francesco Kümmel, Klaus Wendt, Michael Köninger, Jörg S Giese, Thomas Giese, Nathalia A Friess, Helmut Human inflammatory bowel disease does not associate with Lawsonia intracellularis infection |
title | Human inflammatory bowel disease does not associate with Lawsonia intracellularis infection |
title_full | Human inflammatory bowel disease does not associate with Lawsonia intracellularis infection |
title_fullStr | Human inflammatory bowel disease does not associate with Lawsonia intracellularis infection |
title_full_unstemmed | Human inflammatory bowel disease does not associate with Lawsonia intracellularis infection |
title_short | Human inflammatory bowel disease does not associate with Lawsonia intracellularis infection |
title_sort | human inflammatory bowel disease does not associate with lawsonia intracellularis infection |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1590022/ https://www.ncbi.nlm.nih.gov/pubmed/16984651 http://dx.doi.org/10.1186/1471-2180-6-81 |
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