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12 records – page 1 of 2.

Alpha-methylacyl-CoA racemase from Mycobacterium tuberculosis. Mutational and structural characterization of the active site and the fold.

https://arctichealth.org/en/permalink/ahliterature69307
Source
J Biol Chem. 2005 Apr 1;280(13):12611-20
Publication Type
Article
Date
Apr-1-2005
Author
Kalle Savolainen
Prasenjit Bhaumik
Werner Schmitz
Tiina J Kotti
Ernst Conzelmann
Rik K Wierenga
J Kalervo Hiltunen
Author Affiliation
Biocenter Oulu and Department of Biochemistry, University of Oulu, Linnanmaa, P. O. Box 3000, FIN-90014 University of Oulu, Finland.
Source
J Biol Chem. 2005 Apr 1;280(13):12611-20
Date
Apr-1-2005
Language
English
Publication Type
Article
Keywords
Alanine - chemistry
Amino Acid Sequence
Animals
Bile Acids and Salts - metabolism
Binding Sites
Catalysis
Circular Dichroism
Cloning, Molecular
Crystallography, X-Ray
Dimerization
Escherichia coli - metabolism
Models, Chemical
Models, Molecular
Molecular Sequence Data
Mutation
Mycobacterium tuberculosis - enzymology - genetics
Protein Conformation
Protein Folding
Protein Structure, Secondary
Racemases and Epimerases - chemistry - genetics
Rats
Research Support, Non-U.S. Gov't
Sequence Homology, Amino Acid
Substrate Specificity
Ultraviolet Rays
Abstract
Alpha-methylacyl-CoA racemase (Amacr) catalyzes the racemization of alpha-methyl-branched CoA esters. Sequence comparisons have shown that this enzyme is a member of the family III CoA transferases. The mammalian Amacr is involved in bile acid synthesis and branched-chain fatty acid degradation. In human, mutated variants of Amacr have been shown to be associated with disease states. Amino acid sequence alignment of Amacrs and its homologues from various species revealed 26 conserved protic residues, assumed to be potential candidates as catalytic residues. Amacr from Mycobacterium tuberculosis (MCR) was taken as a representative of the racemases. To determine their importance for efficient catalysis, each of these 26 protic residues of MCR was mutated into an alanine, respectively, and the mutated variants were overexpressed in Escherichia coli. It was found that four variants (R91A, H126A, D156A, and E241A) were properly folded but had much decreased catalytic efficiency. Apparently, Arg91, His126, Asp156, and Glu241 are important catalytic residues of MCR. The importance of these residues for catalysis can be rationalized by the 1.8 A resolution crystal structure of MCR, which shows that the catalytic site is at the interface between the large and small domain of two different subunits of the dimeric enzyme. This crystal structure is the first structure of a complete enzyme of the bile acid synthesis pathway. It shows that MCR has unique structural features, not seen in the structures of the sequence related formyl-CoA transferases, suggesting that the family III CoA transferases can be subdivided in at least two classes, being racemases and CoA transferases.
PubMed ID
15632186 View in PubMed
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Biliary lipid output and bile acid kinetics in cholesterol gallstone disease. Evidence for an increased hepatic secretion of cholesterol in Swedish patients.

https://arctichealth.org/en/permalink/ahliterature238500
Source
Gastroenterology. 1985 Aug;89(2):287-93
Publication Type
Article
Date
Aug-1985
Author
K. Nilsell
B. Angelin
L. Liljeqvist
K. Einarsson
Source
Gastroenterology. 1985 Aug;89(2):287-93
Date
Aug-1985
Language
English
Publication Type
Article
Keywords
Adult
Aged
Bile - metabolism - secretion
Bile Acids and Salts - metabolism
Cholelithiasis - metabolism
Cholesterol - secretion
Female
Humans
Kinetics
Lipid Metabolism
Liver - secretion
Male
Middle Aged
Sweden
Abstract
Sweden has one of the highest incidences of gallstone disease in the Western world. It is therefore important to characterize the mechanisms responsible for the formation of cholesterol gallstones in this population. In the present study, we have determined the kinetics of the two primary bile acids, cholic acid and chenodeoxycholic acid, and the hepatic secretion rates of the biliary lipids in 21 normolipidemic, nonobese gallstone patients (13 with functioning and 8 with nonfunctioning gallbladder) and in 23 healthy controls. The cholesterol saturation of fasting gallbladder bile averaged 110% in the gallstone patients with functioning gallbladder and 82% in the controls. The pool sizes of cholic acid and chenodeoxycholic acid were reduced by about 40% in the two groups of gallstone patients, whereas the rates of synthesis were close to normal. The fractional catabolic rate of both bile acids was increased in both groups of gallstone patients. The gallstone patients with functioning gallbladder had an increased (about 50%) cholesterol secretion but normal bile acid and phospholipid secretion rates. In the gallstone patients with nonfunctioning gallbladder the secretion rates of biliary lipids were not significantly different from those of the controls. The ratio between cholesterol and bile acids was about 50% higher in the gallstone patients with functioning gallbladder than in the controls or in those with nonfunctioning gallbladder. The results indicate that the hepatic secretion of cholesterol is an important determinant for the development of saturated gallbladder bile in Swedish gallstone patients.
PubMed ID
4007420 View in PubMed
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[Effect of stimulation and inhibition of macrophage functions on hypercholesterolemia in rats]

https://arctichealth.org/en/permalink/ahliterature45980
Source
Vopr Med Khim. 2002 Mar-Apr;48(2):180-8
Publication Type
Article
Author
P O Kuznetsov
A F Safina
Ia Sh Shvarts
D D Tsyrendorzhiev
A A Zubakhin
M I Dushkin
Author Affiliation
Institute of Internal Medicine, Siberian Division of the Russian Academy of Medical Sciences, Vladimirovski st. 2a, Novosibirsk 630003, Russia.
Source
Vopr Med Khim. 2002 Mar-Apr;48(2):180-8
Language
Russian
Publication Type
Article
Keywords
Animals
Bile Acids and Salts - metabolism
Biological Transport
Cholesterol - blood - metabolism
Cholesterol Esterase - metabolism
Cholesterol Esters - blood
Depression, Chemical
English Abstract
Gadolinium - pharmacology
Hypercholesterolemia - chemically induced - metabolism
Kupffer Cells - drug effects - pathology
Lipoproteins, LDL - blood
Lipoproteins, VLDL - blood
Liver - drug effects - metabolism - pathology
Macrophages, Peritoneal - drug effects - metabolism
Male
Phagocytosis - drug effects
Prodigiozan - pharmacology
Rats
Rats, Wistar
Sterol O-Acyltransferase - metabolism
Stimulation, Chemical
Zymosan - pharmacology
Abstract
In this study we investigated the effects of zymosan and prodigiozan, the macrophage stimulators, and GdCl3, a macrophage inhibitor, on blood lipoprotein composition, activities of liver cholesterly ester (CE) metabolising enzymes, incorporation of [14C]cholesterol (C) into bile acids and accumulation and synthesis of CE in peritoneal macrophages (PM) of rats fed with C-enriched diet for 7 days. The increase of number of phagocyte cells quantity in liver and blood colony-stimulating activity in rats pretreated with intravenous injection of zymosan and prodigiozan was accompanied by reduced C content in blood low density and very low density lipoproteins (LDL and VLDL), increase of liver lysosomal CE hydrolase activity (without change of acyl-CoA:C acyltransferase and cytoplasmatic CE hydrolase activities) and incorporation of labeled C into bile acids and decrease of CE formation and accumulation in PM in rats with hypercholesterolemia. In contrast, reduction of phagocyte population in liver caused by intravenous injection of GdCl3 was accompanied by enhancement of C and CE level in blood LDL and VLDL and decrease of lysosomal CE hydrolase activity and incorporation of C into bile acids in liver of C-feeding rats. The data obtained suggest that the stimulation of mononuclear phagocyte system may lead to a decrease of plasma C via activation of LDL and VLDL catabolism and induction of bile acid synthesis in liver.
PubMed ID
12189625 View in PubMed
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Effects of fructo-oligosaccharides ingestion on fecal bifidobacteria and selected metabolic indexes of colon carcinogenesis in healthy humans.

https://arctichealth.org/en/permalink/ahliterature213341
Source
Nutr Cancer. 1996;26(1):21-9
Publication Type
Article
Date
1996
Author
Y. Bouhnik
B. Flourié
M. Riottot
N. Bisetti
M F Gailing
A. Guibert
F. Bornet
J C Rambaud
Author Affiliation
Hôpital Saint-Lazare, Institut National de la Santé et de la Recherche Médicale, Paris, France.
Source
Nutr Cancer. 1996;26(1):21-9
Date
1996
Language
English
Publication Type
Article
Keywords
Adult
Bifidobacterium - drug effects - enzymology - growth & development
Bile Acids and Salts - metabolism
Colonic Neoplasms - metabolism
Feces - microbiology
Female
Fructose - administration & dosage - pharmacology
Glucuronidase - metabolism
Glycoside Hydrolases - metabolism
Humans
Hydrogen-Ion Concentration
Male
NADH, NADPH Oxidoreductases - metabolism
Nitroreductases - metabolism
Oligosaccharides - administration & dosage - pharmacology
Placebos
Sterols - metabolism
beta-Fructofuranosidase
Abstract
Fructo-oligosaccharides (FOS) are a mixture of oligosaccharides consisting of glucose linked to fructose units. They are not digested in the human small intestine but fermented in the colon, where they could specifically promote the growth of some species of the indigenous microflora, especially bifidobacteria. We assessed in healthy humans the effects of FOS ingestion in fecal bifidobacteria and selected metabolic indexes potentially involved in colonic carcinogenesis. Twenty volunteers randomly divided into two groups were studied for three consecutive 12-day periods. During the ingestion period, they received 12.5 g/day FOS or placebo (saccharose) in three oral doses. Stools were regularly collected and analyzed. FOS ingestion led to an increase in fecal bifidobacterial counts [7.9 +/- 0.5 to 9.1 +/- 0.3 (SE) log colony-forming units/g wet wt, p
PubMed ID
8844718 View in PubMed
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Fecal sterols and bacterial beta-glucuronidase activity: a preliminary metabolic epidemiology study of healthy volunteers from Umea, Sweden, and metropolitan New York.

https://arctichealth.org/en/permalink/ahliterature27126
Source
Nutr Cancer. 1982;4(2):120-7
Publication Type
Article
Date
1982
Author
L. Domellof
L. Darby
D. Hanson
L. Mathews
B. Simi
B S Reddy
Source
Nutr Cancer. 1982;4(2):120-7
Date
1982
Language
English
Publication Type
Article
Keywords
Bacteria - enzymology
Bile Acids and Salts - metabolism
Colonic Neoplasms - etiology
Comparative Study
Diet
Dietary Fats - adverse effects
Dietary Fiber - pharmacology
Feces - analysis - microbiology
Female
Glucuronidase - metabolism
Humans
Male
Middle Aged
New York City
Risk
Sterols - metabolism
Sweden
Abstract
The dietary pattern, fecal bile acid and neutral sterol concentrations, and the bacterial beta-glucuronidase activity of 2 population groups with a varied risk for colon cancer development (i.e., a high-risk population in the metropolitan New York area and an intermediate-risk population in Umea, Sweden) were investigated. The average daily intake of dietary protein was the same in the 2 groups, but the fat intake was higher in Umea than in New York. The daily total fiber intake was also higher in Umea, as was the daily total stool output. The concentration of fecal secondary bile acids and beta-glucuronidase activity was lower in Umea than in New York, but the total daily excretion of these constituents was the same in both groups. The data suggest that one of the factors contributing to the lower risk of colon cancer in Umea, despite the high dietary fat intake, is the high intake of dietary whole grain and cereal fiber, which leads to an increase in stool bulk, thus diluting and/or binding promoters.
PubMed ID
6298751 View in PubMed
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Fiber, Fat, and Colorectal Cancer: New Insight into Modifiable Dietary Risk Factors.

https://arctichealth.org/en/permalink/ahliterature307900
Source
Curr Gastroenterol Rep. 2019 Dec 02; 21(11):62
Publication Type
Journal Article
Review
Date
Dec-02-2019
Author
Soeren Ocvirk
Annette S Wilson
Corynn N Appolonia
Timothy K Thomas
Stephen J D O'Keefe
Author Affiliation
Division of Gastroenterology, Hepatology and Nutrition, Department of Medicine, University of Pittsburgh, W1112 Biomedical Science Tower, 200 Lothrop Street, Pittsburgh, PA, 15213, USA.
Source
Curr Gastroenterol Rep. 2019 Dec 02; 21(11):62
Date
Dec-02-2019
Language
English
Publication Type
Journal Article
Review
Keywords
Bile Acids and Salts - metabolism
Colorectal Neoplasms - etiology - metabolism - microbiology - prevention & control
Diet, High-Fat - adverse effects
Dietary Fats - administration & dosage - adverse effects - pharmacology
Dietary Fiber - administration & dosage
Gastrointestinal Microbiome - drug effects - physiology
Humans
Risk factors
Abstract
To review recent data on the role and interactions of fiber and fat as dietary risk factors associated with colorectal cancer (CRC) risk in humans.
Fiber intake shows convincing and linear dose-response negative correlation with CRC risk. Dietary fiber stimulates butyrogenic activity of the gut microbiota, providing high amounts of butyrate that shows extensive anti-neoplastic effects. A high-fat diet promotes CRC risk through stimulated bile acid metabolism, facilitating bile acid conversion by the gut microbiota to tumor-promoting deoxycholic acid. Comprehensive interactions of these microbial metabolites are likely to underlie mechanisms driving diet-dependent CRC risk in different populations, but require further experimental investigation. Dietary fiber and fat shape the composition and metabolic function of the gut microbiota, resulting in altered amounts of butyrate and deoxycholic acid in the colon. Fiber supplementation and restriction of fat intake represent promising strategies to reduce CRC risk in healthy individuals.
PubMed ID
31792624 View in PubMed
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Source
Dig Dis Sci. 1986 Sep;31(9 Suppl):147S-162S
Publication Type
Article
Date
Sep-1986
Author
G L Simon
S L Gorbach
Source
Dig Dis Sci. 1986 Sep;31(9 Suppl):147S-162S
Date
Sep-1986
Language
English
Publication Type
Article
Keywords
Animals
Bacteria - drug effects - growth & development - metabolism
Bacterial Physiological Phenomena
Bile Acids and Salts - metabolism
Carcinogens - metabolism
Colonic Neoplasms - epidemiology - etiology
Diarrhea - microbiology
Diet
Enterohepatic Circulation
Gonadal Steroid Hormones - metabolism
Humans
Intestines - microbiology
Sprue, Tropical - microbiology
Abstract
The major host defense mechanisms against bacterial overgrowth in the small bowel are the normal propulsive activity of the bowel itself and gastric acid secretion. Microbial interactions are a major factor in regulating the indigenous bacterial flora. Studies of the bacterial enzymes of the gut suggest that changes in diet may lead to marked changes in the colonic flora. Antibiotics affect the composition of the colonic microflora. The microflora also influence the degradation of mucin, the conversion of urobilin to urobilinogen, of cholesterol to coprostanol, and the production of short chain fatty acids. Current interests are focused on the bacterial flora of tropical sprue, the role of bacteria in colorectal cancer, and the involvement of intestinal microflora in the enterohepatic circulation of sex steroid hormones.
PubMed ID
3731990 View in PubMed
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Indolepropionic acid and novel lipid metabolites are associated with a lower risk of type 2 diabetes in the Finnish Diabetes Prevention Study.

https://arctichealth.org/en/permalink/ahliterature296231
Source
Sci Rep. 2017 04 11; 7:46337
Publication Type
Journal Article
Research Support, Non-U.S. Gov't
Date
04-11-2017
Author
Vanessa D de Mello
Jussi Paananen
Jaana Lindström
Maria A Lankinen
Lin Shi
Johanna Kuusisto
Jussi Pihlajamäki
Seppo Auriola
Marko Lehtonen
Olov Rolandsson
Ingvar A Bergdahl
Elise Nordin
Pirjo Ilanne-Parikka
Sirkka Keinänen-Kiukaanniemi
Rikard Landberg
Johan G Eriksson
Jaakko Tuomilehto
Kati Hanhineva
Matti Uusitupa
Author Affiliation
Institute of Public Health and Clinical Nutrition, Department of Clinical Nutrition, University of Eastern Finland, Kuopio, Finland.
Source
Sci Rep. 2017 04 11; 7:46337
Date
04-11-2017
Language
English
Publication Type
Journal Article
Research Support, Non-U.S. Gov't
Keywords
Aged
Amino Acids - metabolism
Bile Acids and Salts - metabolism
Biomarkers
C-Reactive Protein - metabolism
Diabetes Mellitus, Type 2 - epidemiology - etiology - metabolism
Dietary Fiber
Female
Finland - epidemiology
Humans
Indoles - adverse effects
Insulin - secretion
Life Style
Lipid Metabolism
Lipids - adverse effects
Male
Metabolomics - methods
Middle Aged
Population Surveillance
Risk assessment
Risk factors
Abstract
Wide-scale profiling technologies including metabolomics broaden the possibility of novel discoveries related to the pathogenesis of type 2 diabetes (T2D). By applying non-targeted metabolomics approach, we investigated here whether serum metabolite profile predicts T2D in a well-characterized study population with impaired glucose tolerance by examining two groups of individuals who took part in the Finnish Diabetes Prevention Study (DPS); those who either early developed T2D (n?=?96) or did not convert to T2D within the 15-year follow-up (n?=?104). Several novel metabolites were associated with lower likelihood of developing T2D, including indole and lipid related metabolites. Higher indolepropionic acid was associated with reduced likelihood of T2D in the DPS. Interestingly, in those who remained free of T2D, indolepropionic acid and various lipid species were associated with better insulin secretion and sensitivity, respectively. Furthermore, these metabolites were negatively correlated with low-grade inflammation. We replicated the association between indolepropionic acid and T2D risk in one Finnish and one Swedish population. We suggest that indolepropionic acid, a gut microbiota-produced metabolite, is a potential biomarker for the development of T2D that may mediate its protective effect by preservation of ß-cell function. Novel lipid metabolites associated with T2D may exert their effects partly through enhancing insulin sensitivity.
Notes
Cites: Diabetes Care. 2014 Jun;37(6):1751-8 PMID 24812433
Cites: Eur J Clin Nutr. 2013 Mar;67(3):259-63 PMID 23388668
Cites: Adv Nutr. 2016 Jul 15;7(4):730-4 PMID 27422507
Cites: Diabetes Care. 2013 Mar;36(3):648-55 PMID 23129134
Cites: J Appl Bacteriol. 1996 Sep;81(3):288-302 PMID 8810056
Cites: Cytokine. 2016 Oct;86:100-9 PMID 27498215
Cites: Nature. 2012 Oct 4;490(7418):55-60 PMID 23023125
Cites: Nature. 2016 Jul 21;535(7612):376-81 PMID 27409811
Cites: J Biol Chem. 2009 Dec 4;284(49):33833-40 PMID 19815546
Cites: Nat Commun. 2015 Jul 21;6:7715 PMID 26197299
Cites: J Clin Endocrinol Metab. 2013 Jun;98(6):E1060-5 PMID 23633210
Cites: J Chromatogr B Analyt Technol Biomed Life Sci. 2015 Sep 1;1000:120-9 PMID 26218771
Cites: J Cell Biochem. 2001;81(3):507-13 PMID 11255233
Cites: Cell Rep. 2014 Nov 20;9(4):1202-8 PMID 25456122
Cites: PeerJ. 2013 Feb 26;1:e32 PMID 23638368
Cites: Front Neurosci. 2015 Jun 16;9:216 PMID 26136651
Cites: Diabetes Care. 2012 Aug;35(8):1749-56 PMID 22563043
Cites: Diabetologia. 2013 Feb;56(2):284-93 PMID 23093136
Cites: Anal Chem. 2006 Feb 1;78(3):779-87 PMID 16448051
Cites: Diabetologia. 2015 Jul;58(7):1394-408 PMID 26021487
Cites: Scand J Prim Health Care. 2012 Jun;30(2):81-7 PMID 22643152
Cites: Diabetes Care. 2011 May;34 Suppl 2:S258-63 PMID 21525465
Cites: Immunity. 2014 Aug 21;41(2):296-310 PMID 25065623
Cites: Eur J Endocrinol. 2014 Aug;171(2):R47-65 PMID 24760535
Cites: Curr Opin Gastroenterol. 2014 May;30(3):332-8 PMID 24625896
Cites: Molecules. 2015 Jan 30;20(2):2425-44 PMID 25647578
Cites: Nutr Metab Cardiovasc Dis. 2015 Jul;25(7):635-42 PMID 25921846
Cites: Diabetes. 2009 May;58(5):1212-21 PMID 19223598
Cites: Gut Microbes. 2012 Jul-Aug;3(4):279-88 PMID 22572877
Cites: J Clin Endocrinol Metab. 2016 Jan;101(1):233-42 PMID 26505825
Cites: Diabetes. 2013 Dec;62(12):4184-91 PMID 23884887
Cites: Diabetes. 2013 Feb;62(2):639-48 PMID 23043162
Cites: Gut. 2016 Feb;65(2):330-9 PMID 26338727
Cites: Gut. 2016 Nov;65(11):1812-1821 PMID 26416813
Cites: Microb Ecol. 1997 Apr;33(3):180-8 PMID 9115181
Cites: Proc Natl Acad Sci U S A. 2009 Mar 10;106(10):3698-703 PMID 19234110
Cites: Circ Res. 2015 Oct 9;117(9):817-24 PMID 26358192
Cites: Nat Med. 2011 Apr;17(4):448-53 PMID 21423183
Cites: Diabetes Care. 2012 Feb;35(2):211-7 PMID 22210578
Cites: N Engl J Med. 2001 May 3;344(18):1343-50 PMID 11333990
Cites: J Nutr. 2015 Jan;145(1):7-17 PMID 25527657
Cites: Diabetes Care. 2013 Jan;36(1):166-75 PMID 23264288
Cites: J Biol Chem. 1999 Jul 30;274(31):21937-42 PMID 10419516
Cites: Biochem Biophys Res Commun. 2005 Jan 28;326(4):744-51 PMID 15607732
Cites: PLoS One. 2013 Sep 27;8(9):e74341 PMID 24086336
Cites: Mol Syst Biol. 2012;8:615 PMID 23010998
Cites: Curr Diab Rep. 2014;14(5):482 PMID 24623198
Cites: Am J Clin Nutr. 2015 Dec;102(6):1563-73 PMID 26561617
Cites: Am J Clin Nutr. 2015 Jun;101(6):1241-50 PMID 25948672
Cites: Metabolomics. 2016;12 (11):173 PMID 27746707
Cites: Diabetes Care. 2014 Sep;37(9):2508-14 PMID 24947790
Cites: Diabetes. 2013 Dec;62(12):4270-6 PMID 23884885
Cites: Diabetologia. 2015 Nov;58(11):2533-44 PMID 26277381
PubMed ID
28397877 View in PubMed
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Intermittent intrahepatic cholestasis of unknown etiology in five young males from the Faroe Islands.

https://arctichealth.org/en/permalink/ahliterature110032
Source
Acta Med Scand. 1969 Jun;185(6):523-30
Publication Type
Article
Date
Jun-1969

Role of the intestinal microbiota in resistance to colonization by Clostridium difficile.

https://arctichealth.org/en/permalink/ahliterature105040
Source
Gastroenterology. 2014 May;146(6):1547-53
Publication Type
Article
Date
May-2014
Author
Robert A Britton
Vincent B Young
Author Affiliation
Department of Microbiology and Molecular Genetics, Michigan State University, East Lansing, Michigan.
Source
Gastroenterology. 2014 May;146(6):1547-53
Date
May-2014
Language
English
Publication Type
Article
Keywords
Animals
Anti-Bacterial Agents - adverse effects
Bile Acids and Salts - metabolism
Biological Therapy - methods
Clostridium difficile - growth & development - metabolism - pathogenicity
Disease Models, Animal
Dysbiosis
Enterocolitis, Pseudomembranous - metabolism - microbiology - prevention & control
Feces - microbiology
Host-Pathogen Interactions
Humans
Intestines - drug effects - metabolism - microbiology
Microbiota - drug effects
Probiotics - therapeutic use
Abstract
Antibiotic-associated infection with the bacterial pathogen Clostridium difficile is a major cause of morbidity and increased health care costs. C difficile infection follows disruption of the indigenous gut microbiota by antibiotics. Antibiotics create an environment within the intestine that promotes C difficile spore germination, vegetative growth, and toxin production, leading to epithelial damage and colitis. Studies of patients with C difficile infection and animal models have shown that the indigenous microbiota can inhibit expansion and persistence of C difficile. Although the specific mechanisms of these processes are not known, they are likely to interfere with key aspects of the pathogen's physiology, including spore germination and competitive growth. Increasing our understanding of how the intestinal microbiota manage C difficile could lead to better means of controlling this important nosocomial pathogen.
PubMed ID
24503131 View in PubMed
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12 records – page 1 of 2.