<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Liu T</submitter><funding>NIAID NIH HHS</funding><funding>NHLBI NIH HHS</funding><funding>U.S. Department of Health &amp; Human Services | NIH | National Institute of Allergy and Infectious Diseases (NIAID)</funding><funding>U.S. Department of Health &amp; Human Services | NIH | National Heart, Lung, and Blood Institute (NHLBI)</funding><funding>NIH HHS</funding><pagination>1837</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC12749005</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>8(1)</volume><pubmed_abstract>Influenza-associated bacterial super-infections in the lung lead to increased morbidity and mortality. Previous studies have investigated how preceding viral infection causes dysregulation of the innate and adaptive immune systems, leading to increased susceptibility of developing secondary bacterial pneumonia. However, these previous studies cannot account for the spatial context of immune cells in lung. In our study, we employ a spatial transcriptomics platform (10X Genomics Visium) to systematically characterize the coordination of immune cells during super-infection. We compare deconvoluted spatial transcriptomics data between super-infection and single influenza and methicillin-resistant Staphylococcus aureus infections. Consequently, we find that the recruitment of neutrophils and in</pubmed_abstract><journal>Communications biology</journal><pubmed_title>Influenza virus and Staphylococcus aureus super-infection disrupts spatially coordinated cellular immunity in the mouse lung.</pubmed_title><pmcid>PMC12749005</pmcid><funding_grant_id>P01 AI106684</funding_grant_id><funding_grant_id>HL167449</funding_grant_id><funding_grant_id>S10 OD028483</funding_grant_id><funding_grant_id>T32 AI060525</funding_grant_id><funding_grant_id>R01 HL107380</funding_grant_id><funding_grant_id>R01 HL167449</funding_grant_id><funding_grant_id>AI060525</funding_grant_id><funding_grant_id>AI106684</funding_grant_id><funding_grant_id>HL107380</funding_grant_id><pubmed_authors>Rangel-Garcia A</pubmed_authors><pubmed_authors>Rangel-Moreno J</pubmed_authors><pubmed_authors>Alcorn JF</pubmed_authors><pubmed_authors>Zhao C</pubmed_authors><pubmed_authors>Miller LM</pubmed_authors><pubmed_authors>Dresden BP</pubmed_authors><pubmed_authors>Chen W</pubmed_authors><pubmed_authors>Garcia-Hernandez ML</pubmed_authors><pubmed_authors>Liu T</pubmed_authors><pubmed_authors>Pillai Y</pubmed_authors></additional><is_claimable>false</is_claimable><name>Influenza virus and Staphylococcus aureus super-infection disrupts spatially coordinated cellular immunity in the mouse lung.</name><description>Influenza-associated bacterial super-infections in the lung lead to increased morbidity and mortality. Previous studies have investigated how preceding viral infection causes dysregulation of the innate and adaptive immune systems, leading to increased susceptibility of developing secondary bacterial pneumonia. However, these previous studies cannot account for the spatial context of immune cells in lung. In our study, we employ a spatial transcriptomics platform (10X Genomics Visium) to systematically characterize the coordination of immune cells during super-infection. We compare deconvoluted spatial transcriptomics data between super-infection and single influenza and methicillin-resistant Staphylococcus aureus infections. Consequently, we find that the recruitment of neutrophils and in</description><dates><release>2025-01-01T00:00:00Z</release><publication>2025 Nov</publication><modification>2026-06-06T09:45:51.638Z</modification><creation>2026-05-28T03:12:25.186Z</creation></dates><accession>S-EPMC12749005</accession><cross_references><pubmed>41276707</pubmed><doi>10.1038/s42003-025-09268-1</doi></cross_references></HashMap>