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                <identifier>oai:data.mendeley.com/7pn4pwj3td.1</identifier>
                <datestamp>2025-04-02T09:49:03Z</datestamp>
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            <metadata><oai_dc:dc xsi:schemaLocation="http://www.openarchives.org/OAI/2.0/oai_dc/ http://www.openarchives.org/OAI/2.0/oai_dc.xsd" xmlns:oai_dc="http://www.openarchives.org/OAI/2.0/oai_dc/" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance">
    <dc:creator>Ferraro, Mariola</dc:creator>
    <dc:title>Gut Microbiome Profiles in CB2R-Knockout and Wild-Type Mice With and Without Salmonella Infection</dc:title>
    <dc:publisher>Mendeley Data</dc:publisher>
    <dc:description>This dataset examines how genetic deletion of cannabinoid receptor 2 (CB2R) impacts gut microbiome composition during Salmonella enterica serovar Typhimurium infection. CB2R is a G protein-coupled receptor involved in regulating immune responses and intestinal homeostasis. Its expression in immune cells and the gastrointestinal tract suggests a potential role in shaping host-microbiota interactions.

To investigate whether CB2R deficiency alters microbial dynamics in a way that influences susceptibility to infection, we compared CB2R knockout (CB2R-KO) mice with wild-type (WT) littermate controls in an oral Salmonella challenge model. Fecal samples were collected at two time points: pre-infection (baseline) and four days post-infection. Samples were subjected to shallow shotgun metagenomic sequencing (1×150 bp, Illumina). Raw reads were filtered using Vsearch to remove low-quality sequences and short fragments. Taxonomic classification was performed with Kraken2, and processed data were analyzed using R (phyloseq, ALDEx2, microbiome packages).

Alpha diversity analysis showed no significant difference in species richness or evenness between genotypes. However, CB2R-KO mice exhibited distinct shifts in microbial composition following infection. These findings suggest that CB2R contributes to maintaining a balanced gut microbial ecosystem and that its absence may promote dysbiosis during enteric infection, potentially increasing host susceptibility.

</dc:description>
    <dc:subject>Gut Microbiome</dc:subject>
    <dc:contributor>Barker, Hailey</dc:contributor>
    <dc:contributor>Roesch, Luiz</dc:contributor>
    <dc:type>Dataset</dc:type>
    <dc:identifier>doi:10.17632/7pn4pwj3td.1</dc:identifier>
    <dc:identifier>oai:data.mendeley.com/7pn4pwj3td.1</dc:identifier>
    <dc:rights>Creative Commons Attribution 4.0 International</dc:rights>
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    <dc:date>2025-04-02T09:49:03Z</dc:date>
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