Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.1.1.37 (DNA methyltransferase)
 4,983 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Paratuberculosis is an infectious, chronic, and incurable disease that affects ruminants, caused by Mycobacterium avium subsp. paratuberculosis. This bacterium is shed primarily through feces of infected cows but can be also excreted in colostrum and milk and might survive pasteurization. Since an association of genomic sequences of M. avium subsp. paratuberculosis in patients with Crohn's disease has been described; it is of interest to rapidly detect M. avium subsp. paratuberculosis in milk for human consumption. IS900 insertion is used as a target for PCR amplification to identify the presence of M. avium subsp. paratuberculosis in biological samples. Two target sequences were selected: IS1 (155 bp) and IS2 (94 bp). These fragments have a 100% identity among all M. avium subsp. paratuberculosis strains sequenced. M. avium subsp. paratuberculosis was specifically concentrated from milk samples by immunomagnetic separation prior to performing PCR. The amplicons were characterized using DNA methylase Genotyping, i.e., the amplicons were methylated with 6-methyl-adenine and digested with restriction enzymes to confirm their identity. The methylated amplicons from 100 CFU of M. avium subsp. paratuberculosis can be visualized in a Western blot format using an anti-6-methyl-adenine monoclonal antibody. The use of DNA methyltransferase genotyping coupled to a scintillation proximity assay allows for the detection of up to 10 CFU of M. avium subsp. paratuberculosis per ml of milk. This test is rapid and sensitive and allows for automation and thus multiple samples can be tested at the same time.
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PMID:Rapid and sensitive method to identify Mycobacterium avium subsp. paratuberculosis in cow's milk by DNA methylase genotyping. 2327 11

The gut microbiota is a central player in the etiology of inflammatory bowel diseases. As such, there is intense scientific interest in elucidating the specific group/s of bacteria responsible for driving barrier damage and perpetuating the chronic inflammation that results in disease. Because of their ability to colonize close to the surface of the host intestinal epithelium, mucosa-associated bacteria are considered key players in the initiation and development of both Crohn's disease and ulcerative colitis. The leading bacterial candidates include adherent and invasive Escherichia coli, Helicobacter, Fusobacteria, Mycobacteria, and Campylobacter species. Of these, a member of the Campylobacter genus, Campylobacter concisus, has recently emerged as a putative player in the pathogenesis of inflammatory bowel diseases. Current research indicates that this bacterium possesses extraordinarily diverse pathogenic capacities as well as unique genetic and functional signatures that are defined by their ability to adhere to and invade host cells, secrete toxins, and the presence of a virulence-associated restriction-modification system. These characteristics enable the potential classification of C. concisus into distinct pathotypes, which we have named adherent and invasive C. concisus and adherent and toxinogenic C. concisus. In this review, we evaluate evidence for the role of emerging Campylobacter species in the pathogenesis of inflammatory bowel diseases.
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PMID:Role of emerging Campylobacter species in inflammatory bowel diseases. 2487 62

Inflammation causes proliferation of intestinal smooth muscle cells (ISMC), contributing to a thickened intestinal wall and to stricture formation in Crohn's disease. Proliferation of ISMC in vitro and in vivo caused decreased expression of marker proteins, but the underlying cause is unclear. Since epigenetic change is important in other systems, we used immunocytochemistry, immunoblotting, and quantitative PCR to examine epigenetic modification in cell lines from rat colon at low passage or after extended growth to evaluate phenotype. Exposure to the histone deacetylase (HDAC) inhibitor trichostatin A or the DNA methyltransferase inhibitor 5-azacytidine reversed the characteristic loss of phenotypic markers among high-passage cell lines of ISMC. Expression of smooth muscle actin and smooth muscle protein 22, as well as functional expression of the neurotrophin glial cell line-derived neurotrophic factor, was markedly increased. Increased expression of muscarinic receptor 3 and myosin light chain kinase was correlated with an upregulated response to cholinergic stimulation. In human ISMC (hISMC) lines from the terminal ileum, phenotype was similarly affected by extended proliferation. However, in hISMC from resected Crohn's strictures, we observed a significantly reduced contractile phenotype compared with patient-matched intrinsic controls that was associated with increased patient-specific expression of DNA methyltransferase 1, HDAC2, and HDAC5. Therefore, protracted growth causes epigenetic alterations that account for an altered phenotype of ISMC. A similar process may promote stricture formation in Crohn's disease, where the potential for halting progression, or even reversal, of disease through control of phenotypic modulation may become a novel treatment option.
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PMID:Epigenetic modification of intestinal smooth muscle cell phenotype during proliferation. 3011 May 65