The precise etiology of Inflammatory Bowel Disease (IBD) remains unclear and several factors are believed to play a role in its development and progression, including the composition of microbial communities resident in the gastrointestinal tract. Human intestinal microbiota are extensive with at least 15.000-36.000 bacterial species. However, thanks to the new development in sequencing and molecular taxonomic methodologies, our understanding of the microbiota population composition, dynamics, and ecology has greatly increased. Intestinal microbiota play a critical role in the maintenance of the host intestinal barrier homeostasis, while dysbiosis, which involves reduction in the microbiome diversity, can lead to progression of the inflammatory disorders, such as IBD and colorectal cancer. It is hypothesized that fingerprinting characterization of the microbiota community composition is the first step in the study of this complex bacterial ecosystem and a crucial step in the targeted therapy. Molecular fingerprinting of human gastrointestinal tract microbiota could be performed by different techniques including the semi quantitation, 16srRNA, the DNA-microarray as well as other relatively new methods which were developed to study many complex bacterial ecosystem. These techniques provide individual data of the human intestinal microbiota and provide estimation of the relative presence of the microbial target groups within each individual. such personalized information serves as a remarkable and unprecedented opportunity to improve targeted medical treatment and probably develop strategies to prfevent disease.

Tomasello, G., Mazzola, M., Jurjus, A., Cappello, F., Carini, F., Damiani, P., et al. (2017). THE FINGERPRINT OF THE HUMAN GASTROINTESTINAL TRACT MICROBIOTA: A HYPOTHESIS OF MOLECULAR MAPPING. JOURNAL OF BIOLOGICAL REGULATORS & HOMEOSTATIC AGENTS, 31(1), 245-249.

THE FINGERPRINT OF THE HUMAN GASTROINTESTINAL TRACT MICROBIOTA: A HYPOTHESIS OF MOLECULAR MAPPING

TOMASELLO, Giovanni
Supervision
;
CAPPELLO, Francesco
Validation
;
CARINI, Francesco
Membro del Collaboration Group
;
LEONE, Angelo
2017-01-01

Abstract

The precise etiology of Inflammatory Bowel Disease (IBD) remains unclear and several factors are believed to play a role in its development and progression, including the composition of microbial communities resident in the gastrointestinal tract. Human intestinal microbiota are extensive with at least 15.000-36.000 bacterial species. However, thanks to the new development in sequencing and molecular taxonomic methodologies, our understanding of the microbiota population composition, dynamics, and ecology has greatly increased. Intestinal microbiota play a critical role in the maintenance of the host intestinal barrier homeostasis, while dysbiosis, which involves reduction in the microbiome diversity, can lead to progression of the inflammatory disorders, such as IBD and colorectal cancer. It is hypothesized that fingerprinting characterization of the microbiota community composition is the first step in the study of this complex bacterial ecosystem and a crucial step in the targeted therapy. Molecular fingerprinting of human gastrointestinal tract microbiota could be performed by different techniques including the semi quantitation, 16srRNA, the DNA-microarray as well as other relatively new methods which were developed to study many complex bacterial ecosystem. These techniques provide individual data of the human intestinal microbiota and provide estimation of the relative presence of the microbial target groups within each individual. such personalized information serves as a remarkable and unprecedented opportunity to improve targeted medical treatment and probably develop strategies to prfevent disease.
2017
Tomasello, G., Mazzola, M., Jurjus, A., Cappello, F., Carini, F., Damiani, P., et al. (2017). THE FINGERPRINT OF THE HUMAN GASTROINTESTINAL TRACT MICROBIOTA: A HYPOTHESIS OF MOLECULAR MAPPING. JOURNAL OF BIOLOGICAL REGULATORS & HOMEOSTATIC AGENTS, 31(1), 245-249.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/10447/225301
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