<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Rao C</submitter><funding>Army Medical University Foundations</funding><funding>MOST | National Natural Science Foundation of China (NSFC)</funding><funding>National Natural Science Foundation of China</funding><funding>National Natural Science Foundation of China (NSFC)</funding><funding>MOST | National Natural Science Foundation of China</funding><pagination>e0045324</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC11580396</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>9(11)</volume><pubmed_abstract>Melioidosis is a serious infectious disease caused by the Gram-negative bacterium &lt;i>Burkholderia pseudomallei&lt;/i>. Recently, Rab32-dependent immune vesicles emerge as a critical defense pathway to restrict the intracellular &lt;i>B. pseudomallei&lt;/i>. However, &lt;i>B. pseudomallei&lt;/i> can evade host immune vesicles and survive in the cytoplasm, although this mechanism is not well understood. In this study, we found Rab32-dependent vesicles could effectively combat &lt;i>B. pseudomallei&lt;/i> infection, but not all intracellular &lt;i>B. pseudomallei&lt;/i> were encapsulated in Rab32-positive vesicles. To explore how &lt;i>B. pseudomallei&lt;/i> counteracted the Rab32-dependent defense pathway, transcriptomic profiling of &lt;i>B. pseudomallei&lt;/i> was performed to characterize the response dynamics during infection</pubmed_abstract><journal>mSphere</journal><pubmed_title>&lt;i>Burkholderia pseudomallei&lt;/i> BopE suppresses the Rab32-dependent defense pathway to promote its intracellular replication and virulence.</pubmed_title><pmcid>PMC11580396</pmcid><funding_grant_id>2021-2018-098,2020XQN06</funding_grant_id><funding_grant_id>82402640</funding_grant_id><funding_grant_id>32270190,82272350</funding_grant_id><pubmed_authors>Wen Y</pubmed_authors><pubmed_authors>Liao Y</pubmed_authors><pubmed_authors>Yan J</pubmed_authors><pubmed_authors>Huang J</pubmed_authors><pubmed_authors>Hu Z</pubmed_authors><pubmed_authors>Nan D</pubmed_authors><pubmed_authors>Wu P</pubmed_authors><pubmed_authors>Zheng S</pubmed_authors><pubmed_authors>Li Q</pubmed_authors><pubmed_authors>Wang L</pubmed_authors><pubmed_authors>Liu W</pubmed_authors><pubmed_authors>Rao C</pubmed_authors><pubmed_authors>Zhang Z</pubmed_authors><pubmed_authors>Wang S</pubmed_authors><pubmed_authors>Yao C</pubmed_authors><pubmed_authors>Mao X</pubmed_authors><pubmed_authors>Qiao J</pubmed_authors></additional><is_claimable>false</is_claimable><name>&lt;i>Burkholderia pseudomallei&lt;/i> BopE suppresses the Rab32-dependent defense pathway to promote its intracellular replication and virulence.</name><description>Melioidosis is a serious infectious disease caused by the Gram-negative bacterium &lt;i>Burkholderia pseudomallei&lt;/i>. Recently, Rab32-dependent immune vesicles emerge as a critical defense pathway to restrict the intracellular &lt;i>B. pseudomallei&lt;/i>. However, &lt;i>B. pseudomallei&lt;/i> can evade host immune vesicles and survive in the cytoplasm, although this mechanism is not well understood. In this study, we found Rab32-dependent vesicles could effectively combat &lt;i>B. pseudomallei&lt;/i> infection, but not all intracellular &lt;i>B. pseudomallei&lt;/i> were encapsulated in Rab32-positive vesicles. To explore how &lt;i>B. pseudomallei&lt;/i> counteracted the Rab32-dependent defense pathway, transcriptomic profiling of &lt;i>B. pseudomallei&lt;/i> was performed to characterize the response dynamics during infection</description><dates><release>2024-01-01T00:00:00Z</release><publication>2024 Nov</publication><modification>2026-06-03T01:07:47.483Z</modification><creation>2025-04-04T12:00:29.891Z</creation></dates><accession>S-EPMC11580396</accession><cross_references><pubmed>39431830</pubmed><doi>10.1128/msphere.00453-24</doi></cross_references></HashMap>