<HashMap><database>GEO</database><file_versions><headers><Content-Type>application/xml</Content-Type></headers><body><files><Other>ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE310nnn/GSE310711/</Other></files><type>primary</type></body><statusCode>OK</statusCode><statusCodeValue>200</statusCodeValue></file_versions><scores/><additional><omics_type>Transcriptomics</omics_type><species>Mus musculus</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=GSE310711</full_dataset_link><repository>GEO</repository><entry_type>GSE</entry_type></additional><is_claimable>false</is_claimable><name>Bifidobacteria infantis and human milk oligosaccharides have independent effects on immune response and amino acid metabolism in germ-free mouse models</name><description>Early-life microbial colonization is essential for gut and immune development. Human milk oligosaccharides (HMO) support the growth of Bifidobacterium infantis (BI), a keystone infant species. Herein, we studied the individual and combined effects of BI and HMO on immune and colon transcriptomes, and the serum metabolome. Germ-free mice were randomly assigned to four groups [10-14/group: HMO, BI, BI+HMO and control (no HMO or BI)]. HMO and BI+HMO groups received 5 mg/d each of 2′-fucosyllactose, lacto-N-tetraose and 3′-sialyllactose for 14 d. BI and BI+HMO received B. infantis ATCC 15697 (1x10^9 CFU/d) on days 1, 4, and 9. Mono-colonization with BI increased monocytes, macrophages, B cells, CD4+ T cells, and Treg cells in mesenteric lymph nodes (MLN) relative to control. In the spleen, BI alone increased B cells, dendritic cells, Th17 cells, and ILC3 cells, and enriched serum amino acid metabolism pathways. Additionally, BI influenced colonocyte gene expression, and modulated serum metabolites regulating circadian rhythms. BI+HMO increased MLN Th17 cells and spleen monocytes compared to HMO alone. Collectively, the results of this study highlight the complex interplay between host-microbe-diet interactions and emphasize the importance of considering these interactions when designing strategies to modulate infant health during early life.</description><dates><publication>2026/06/01</publication></dates><accession>GSE310711</accession><cross_references><GSM>GSM9307344</GSM><GSM>GSM9307333</GSM><GSM>GSM9307332</GSM><GSM>GSM9307343</GSM><GSM>GSM9307335</GSM><GSM>GSM9307346</GSM><GSM>GSM9307334</GSM><GSM>GSM9307345</GSM><GSM>GSM9307337</GSM><GSM>GSM9307336</GSM><GSM>GSM9307339</GSM><GSM>GSM9307338</GSM><GSM>GSM9307340</GSM><GSM>GSM9307342</GSM><GSM>GSM9307341</GSM><GPL>34290</GPL><GSE>310711</GSE><taxon>Mus musculus</taxon></cross_references></HashMap>