<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Peng X</submitter><funding>BLRD VA</funding><funding>NCATS NIH HHS</funding><funding>NHLBI NIH HHS</funding><pagination>1314-1322</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9523490</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>209(7)</volume><pubmed_abstract>Postviral bacterial infections are a major health care challenge in coronavirus infections, including COVID-19; however, the coronavirus-specific mechanisms of increased host susceptibility to secondary infections remain unknown. In humans, coronaviruses, including SARS-CoV-2, infect lung immune cells, including alveolar macrophages, a phenotype poorly replicated in mouse models of SARS-CoV-2. To overcome this, we used a mouse model of native murine β-coronavirus that infects both immune and structural cells to investigate coronavirus-enhanced susceptibility to bacterial infections. Our data show that coronavirus infection impairs the host ability to clear invading bacterial pathogens and potentiates lung tissue damage in mice. Mechanistically, coronavirus limits the bacterial killing abil</pubmed_abstract><journal>Journal of immunology (Baltimore, Md. : 1950)</journal><pubmed_title>Coronavirus Lung Infection Impairs Host Immunity against Secondary Bacterial Infection by Promoting Lysosomal Dysfunction.</pubmed_title><pmcid>PMC9523490</pmcid><funding_grant_id>I01 BX004661</funding_grant_id><funding_grant_id>T32 HL007778</funding_grant_id><funding_grant_id>UL1 TR001863</funding_grant_id><funding_grant_id>R01 HL126094</funding_grant_id><pubmed_authors>Peng X</pubmed_authors><pubmed_authors>Audia JP</pubmed_authors><pubmed_authors>Korde A</pubmed_authors><pubmed_authors>Mankowski MC</pubmed_authors><pubmed_authors>Agaronyan K</pubmed_authors><pubmed_authors>Kim J</pubmed_authors><pubmed_authors>Wang L</pubmed_authors><pubmed_authors>Sharma L</pubmed_authors><pubmed_authors>Liu X</pubmed_authors><pubmed_authors>Ishibe S</pubmed_authors><pubmed_authors>Takyar SS</pubmed_authors><pubmed_authors>Voth S</pubmed_authors><pubmed_authors>Habet V</pubmed_authors><pubmed_authors>Chang</pubmed_authors><pubmed_authors>Tian X</pubmed_authors><pubmed_authors>Gupta G</pubmed_authors><pubmed_authors>Kang MJ</pubmed_authors><pubmed_authors>Cai Y</pubmed_authors><pubmed_authors>Wilen CB</pubmed_authors><pubmed_authors>Dela Cruz CS</pubmed_authors><pubmed_authors>Shin HJ</pubmed_authors><pubmed_authors>Compton S</pubmed_authors></additional><is_claimable>false</is_claimable><name>Coronavirus Lung Infection Impairs Host Immunity against Secondary Bacterial Infection by Promoting Lysosomal Dysfunction.</name><description>Postviral bacterial infections are a major health care challenge in coronavirus infections, including COVID-19; however, the coronavirus-specific mechanisms of increased host susceptibility to secondary infections remain unknown. In humans, coronaviruses, including SARS-CoV-2, infect lung immune cells, including alveolar macrophages, a phenotype poorly replicated in mouse models of SARS-CoV-2. To overcome this, we used a mouse model of native murine β-coronavirus that infects both immune and structural cells to investigate coronavirus-enhanced susceptibility to bacterial infections. Our data show that coronavirus infection impairs the host ability to clear invading bacterial pathogens and potentiates lung tissue damage in mice. Mechanistically, coronavirus limits the bacterial killing abil</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022 Oct</publication><modification>2025-04-04T21:10:02.936Z</modification><creation>2025-04-04T21:10:02.936Z</creation></dates><accession>S-EPMC9523490</accession><cross_references><pubmed>36165196</pubmed><doi>10.4049/jimmunol.2200198</doi></cross_references></HashMap>