<HashMap><database>biostudies-arrayexpress</database><scores/><additional><omics_type>Metabolomics</omics_type><omics_type>Unknown</omics_type><omics_type>Transcriptomics</omics_type><omics_type>Genomics</omics_type><omics_type>Proteomics</omics_type><submitter>Sajeev Batra</submitter><study_type>transcription profiling by array</study_type><organism>Homo sapiens</organism><species>Homo sapiens</species><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/E-GEOD-25277</full_dataset_link><description>Helminth infection may have the potential to suppress intestinal inflammation in inflammatory bowel diseases. Ulcerative colitis is more common in developed countries than in developing countries endemic for helminth infections. There are animal models, as well as clinical trials, suggesting therapeutic effects of experimental helminth infection. Here, we provide a comprehensive molecular portrait of dynamic changes in the intestinal mucosa of an individual who infected himself with Trichuris trichiura to treat his symptoms of ulcerative colitis. Genes involved in carbohydrate and lipid metabolism were upregulated in helminth-colonized tissue, while tissues with active colitis showed upregulation of proinflammatory genes such as IL-17, IL13RA2, and CHI3L1. T. trichiura colonization of the intestine may reduce symptomatic colitis by promoting goblet cell hyperplasia and mucus production through TH2 cytokines and IL-22. By better understanding the physiological effects of helminth infection, new therapies for ulcerative colitis could be identified. This is the third (out of three) series of arrays from this patient from a colonoscopy in 2009 when the patient was in remission. We analyzed 12 HEEBO arrays on which were hybridized RNA amplified from pinch biopsies collected from different regions of the colon. 4 samples were from the ascending colon, which was colonized by worms at the time. 3 samples were from the transverse colon, which appeared normal at the time. 3 samples were from the recto-sigmoid colon, which had recovered from colitis at the time. 2 samples were from the terminal ileum, which was unaffected by worms or colitis.</description><repository>biostudies-arrayexpress</repository><sample_protocol>Labeling - RNA extracted from the 12 samples was amplified separately using Amino Allyl MessageAmp II aRNA kit from Ambion and then pooled. The pooled amplified material was then coupled to Cy3.</sample_protocol><sample_protocol>Labeling - RNA extracted from the samples was amplified using Amino Allyl MessageAmp II aRNA kit from Ambion. The amplified material was then coupled to Cy5.</sample_protocol><sample_protocol>Nucleic Acid Extraction - Trizol reagent and Invitrogen Purelink RNA purification system</sample_protocol><sample_protocol>Hybridization - Labeled samples were hybridized to the HEEBO array in 3x SSC at 65C 16 hours.</sample_protocol><figure_sub>MIAME Score</figure_sub><figure_sub>Raw Data</figure_sub><figure_sub>Organization</figure_sub><figure_sub>Assays and Data</figure_sub><figure_sub>Processed Data</figure_sub><figure_sub>Additional Files</figure_sub><figure_sub>MAGE-TAB Files</figure_sub><figure_sub>Array Designs</figure_sub><pubmed_authors>Vikram Kashyap</pubmed_authors><pubmed_authors>Mara Broadhurst</pubmed_authors><pubmed_authors>P'ng Loke</pubmed_authors><pubmed_authors>Sajeev Batra</pubmed_authors><pubmed_authors>Joseph McCune</pubmed_authors><pubmed_authors>James McKerrow</pubmed_authors><pubmed_authors>Jacqueline Leung</pubmed_authors><pubmed_authors>Uma Mahadevan</pubmed_authors><data_protocol>Feature Extraction - Spot analysis was performed with Spotreader and stored in a relational database (Acuity).</data_protocol><data_protocol>Assay Data Transformation - ID_REF = &lt;br>VALUE = log2 of the normalized Ratio Of Medians (635/532) with values that did not pass filtering removed</data_protocol><data_protocol>Image Adquisition - HEEBO arrays were scanned with an Axon 4000B scanner (Axon Instruments, Union City, CA, USA) and gridded using the Spotreader program (Niles Scientific, Portola Valley, CA. USA)</data_protocol></additional><is_claimable>false</is_claimable><name>Gene expression patterns of biopsies from a colonoscopy taken in 2009 of an ulcerative colitis patient infected with Trichuris trichiura</name><description>Helminth infection may have the potential to suppress intestinal inflammation in inflammatory bowel diseases. Ulcerative colitis is more common in developed countries than in developing countries endemic for helminth infections. There are animal models, as well as clinical trials, suggesting therapeutic effects of experimental helminth infection. Here, we provide a comprehensive molecular portrait of dynamic changes in the intestinal mucosa of an individual who infected himself with Trichuris trichiura to treat his symptoms of ulcerative colitis. Genes involved in carbohydrate and lipid metabolism were upregulated in helminth-colonized tissue, while tissues with active colitis showed upregulation of proinflammatory genes such as IL-17, IL13RA2, and CHI3L1. T. trichiura colonization of the intestine may reduce symptomatic colitis by promoting goblet cell hyperplasia and mucus production through TH2 cytokines and IL-22. By better understanding the physiological effects of helminth infection, new therapies for ulcerative colitis could be identified. This is the third (out of three) series of arrays from this patient from a colonoscopy in 2009 when the patient was in remission. We analyzed 12 HEEBO arrays on which were hybridized RNA amplified from pinch biopsies collected from different regions of the colon. 4 samples were from the ascending colon, which was colonized by worms at the time. 3 samples were from the transverse colon, which appeared normal at the time. 3 samples were from the recto-sigmoid colon, which had recovered from colitis at the time. 2 samples were from the terminal ileum, which was unaffected by worms or colitis.</description><dates><release>2010-11-20T00:00:00Z</release><modification>2022-11-27T14:23:26.738Z</modification><creation>2022-03-04T18:25:02.418Z</creation></dates><accession>E-GEOD-25277</accession><cross_references><GEO>GSE25277</GEO><EFO>EFO_0002768</EFO></cross_references></HashMap>