<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Ghimire S</submitter><funding>NHLBI NIH HHS</funding><pagination>105920</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC12466150</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>120</volume><pubmed_abstract>&lt;h4>Background&lt;/h4>Treatments available to prevent progression of virus-induced lung diseases, including coronavirus disease 2019 (COVID-19) are of limited benefit once respiratory failure occurs. The efficacy of approved and emerging cytokine signalling-modulating antibodies is variable and is affected by disease course and patient-specific inflammation patterns. Therefore, understanding the role of inflammation on the viral infectious cycle is critical for effective use of cytokine-modulating agents.&lt;h4>Methods&lt;/h4>The role of the type 2 cytokine IL-13 on SARS-CoV-2 binding/entry, replication, and host response was investigated in primary HAE cells in vitro and in a model of mouse-adapted SARS-CoV-2 infection in vivo using single-cell and bulk RNA-sequencing approaches. Additionally, the</pubmed_abstract><journal>EBioMedicine</journal><pubmed_title>IL-13 decreases susceptibility to airway epithelial SARS-CoV-2 infection but increases disease severity in vivo via eicosanoid signalling.</pubmed_title><pmcid>PMC12466150</pmcid><funding_grant_id>R01 HL163024</funding_grant_id><pubmed_authors>Necker GC</pubmed_authors><pubmed_authors>Xue B</pubmed_authors><pubmed_authors>Meyerholz DK</pubmed_authors><pubmed_authors>Perlman S</pubmed_authors><pubmed_authors>Ghimire S</pubmed_authors><pubmed_authors>Li K</pubmed_authors><pubmed_authors>Zheng J</pubmed_authors><pubmed_authors>McCray PB</pubmed_authors><pubmed_authors>Pezzulo AA</pubmed_authors><pubmed_authors>Gannon RM</pubmed_authors><pubmed_authors>Thurman AL</pubmed_authors><pubmed_authors>Wohlford-Lenane CL</pubmed_authors><pubmed_authors>Gong H</pubmed_authors></additional><is_claimable>false</is_claimable><name>IL-13 decreases susceptibility to airway epithelial SARS-CoV-2 infection but increases disease severity in vivo via eicosanoid signalling.</name><description>&lt;h4>Background&lt;/h4>Treatments available to prevent progression of virus-induced lung diseases, including coronavirus disease 2019 (COVID-19) are of limited benefit once respiratory failure occurs. The efficacy of approved and emerging cytokine signalling-modulating antibodies is variable and is affected by disease course and patient-specific inflammation patterns. Therefore, understanding the role of inflammation on the viral infectious cycle is critical for effective use of cytokine-modulating agents.&lt;h4>Methods&lt;/h4>The role of the type 2 cytokine IL-13 on SARS-CoV-2 binding/entry, replication, and host response was investigated in primary HAE cells in vitro and in a model of mouse-adapted SARS-CoV-2 infection in vivo using single-cell and bulk RNA-sequencing approaches. Additionally, the</description><dates><release>2025-01-01T00:00:00Z</release><publication>2025 Sep</publication><modification>2026-06-03T21:24:07.829Z</modification><creation>2026-05-01T03:11:10.936Z</creation></dates><accession>S-EPMC12466150</accession><cross_references><pubmed>40957220</pubmed><doi>10.1016/j.ebiom.2025.105920</doi></cross_references></HashMap>