<HashMap><database>GEO</database><file_versions><headers><Content-Type>application/xml</Content-Type></headers><body><files><Xlsx>ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE281nnn/GSE281635/suppl/GSE281635_DESeq2analysis.xlsx</Xlsx><Txt>ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE281nnn/GSE281635/suppl/GSE281635_rawCountMatrix.txt.gz</Txt><Other>ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE281nnn/GSE281635/</Other></files><type>primary</type></body><statusCode>OK</statusCode><statusCodeValue>200</statusCodeValue></file_versions><scores/><additional><omics_type>Transcriptomics</omics_type><species>Homo sapiens</species><gds_type>Expression profiling by high throughput sequencing</gds_type><full_dataset_link>https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE281635</full_dataset_link><repository>GEO</repository><entry_type>GSE</entry_type></additional><is_claimable>false</is_claimable><name>Molecular Profiling of the Appendix in Pediatric Inflammatory Bowel Diseases</name><description>Clinical studies suggest a critical role for the appendix in the pathogenesis of inflammatory bowel diseases (IBD), including Crohn disease (CD) and ulcerative colitis (UC), as indicated by the presence of peri-appendicular patches in UC and the beneficial effects of appendectomy in UC. However, the underlying mechanisms remain unclear. To address this gap, we characterized microbial species, associated patterns, and host-microbiota interactions in the appendix and non-inflamed regions of the colon tissue and mucus from pediatric IBD and non-IBD patients (n=15). Metagenomic analyses revealed an enrichment of Proteobacteria (p-value=0.0061) and reduced bacterial diversity in IBD patients’ appendix compared to controls. Strong correlations between host tissue and mucus microbial pathways of IBD patients highlighted a link between microbial communities and host gene expression, contributing to immune activation and inflammation in the appendix. Our findings thus provide valuable insights and a basis for mechanistic hypotheses regarding the appendix’s role in IBD pathogenesis.</description><dates><publication>2026/07/14</publication></dates><accession>GSE281635</accession><cross_references><GSM>GSM8625163</GSM><GSM>GSM8625164</GSM><GSM>GSM8625165</GSM><GSM>GSM8625166</GSM><GSM>GSM8625170</GSM><GSM>GSM8625160</GSM><GSM>GSM8625171</GSM><GSM>GSM8625161</GSM><GSM>GSM8625162</GSM><GSM>GSM8625167</GSM><GSM>GSM8625157</GSM><GSM>GSM8625168</GSM><GSM>GSM8625158</GSM><GSM>GSM8625169</GSM><GSM>GSM8625159</GSM><GPL>34281</GPL><GSE>281635</GSE><taxon>Homo sapiens</taxon></cross_references></HashMap>