<HashMap><database>biostudies-arrayexpress</database><scores/><additional><submitter>SOURA CHAKRABORTY</submitter><organism>Mus musculus</organism><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/E-MTAB-17666</full_dataset_link><description>Bulk RNA sequencing was performed on lung tissue from control and immune cell-specific Cyp11a1 conditional knockout (Cyp11a1fl/fl;Vav1Cre) mice following lipopolysaccharide (LPS)-induced acute lung injury. The experiment was designed to characterise genome-wide transcriptional changes associated with Cyp11a1 deficiency in immune cells during inflammation and its resolution. We collected lung samples at defined time points after LPS treatment and performed paired-end RNA sequencing. We compared transcriptomic profiles between genotypes and across time points to identify changes in inflammatory, immune-response, and tissue-repair pathways.</description><repository>biostudies-arrayexpress</repository><sample_protocol>Library Construction - cDNA libraries were constructed from high-quality total RNA for paired-end RNA sequencing by Novogene.</sample_protocol><sample_protocol>Growth Protocol - Mice were maintained under specific pathogen-free conditions with a 12-hour light/dark cycle. Mice aged 8–16 weeks were used for experiments.</sample_protocol><sample_protocol>Sample Collection - Lung tissues were collected from control and immune cell-specific Cyp11a1 conditional knockout (Cyp11a1fl/fl;Vav1Cre) mice following LPS-induced acute lung injury at the indicated experimental time points. Lung tissue was collected for bulk RNA sequencing.</sample_protocol><sample_protocol>Nucleic Acid Extraction - Total RNA was extracted from lung tissue using the RNeasy Mini Kit (QIAGEN) according to the manufacturer's instructions. High-quality total RNA was used for RNA sequencing.</sample_protocol><sample_protocol>Sequencing - cDNA libraries were sequenced using an Illumina NovaSeq X Plus Series platform with paired-end  (PE150) sequencing, generating an average of approximately 50 million reads per library.</sample_protocol><sample_protocol>Sample Treatment - Mice were anesthetized with isoflurane and administered 50 µL of lipopolysaccharide (LPS) from Escherichia coli O111:B4 (Sigma-Aldrich) in sterile PBS via the intranasal route. Mice were sacrificed at the indicated time points following LPS administration.</sample_protocol><figure_sub>Organization</figure_sub><figure_sub>MINSEQE Score</figure_sub><figure_sub>Assays and Data</figure_sub><figure_sub>MAGE-TAB Files</figure_sub><omics_type>Unknown</omics_type><omics_type>Transcriptomics</omics_type><omics_type>Genomics</omics_type><omics_type>Proteomics</omics_type><instrument_platform>Illumina NovaSeq X</instrument_platform><instrument_platform>RNeasy Mini Kit (QIAGEN)</instrument_platform><instrument_platform>Illumina NovaSeq X Plus</instrument_platform><pubmed_abstract>Effective resolution of inflammation following acute lung infection or injury is critical for restoring immune and tissue homeostasis to ensure functional recovery. Prolonged or unresolved inflammation can impair lung repair, promote fibrosis, and contribute to pulmonary dysfunction. While systemic steroid signalling is known to modulate general immune responses, the specific role of immune cell-mediated steroidogenesis in regulating lung inflammation and repair remains unknown. Here, we show that immune cell  de novo steroidogenesis is essential for resolving inflammation and promoting recovery in a murine model of acute lung injury. During the resolution phase, steroid-synthesizing immune cells, predominantly basophils, are enriched in the lung. Mice with immune cell-specific ablation of  de novo steroidogenesis exhibit exacerbated lung injury, impaired resolution of inflammation, and defective tissue repair. These findings reveal a previously unrecognized immunoregulatory function of immune cell-derived steroids and identify immune cell steroidogenesis as a potential therapeutic target for promoting resolution and recovery in inflammatory lung diseases.</pubmed_abstract><study_type>RNA-seq of coding RNA</study_type><species>Mus musculus</species><pubmed_title>Immune cell de novo steroidogenesis regulates inflammation resolution and recovery in acute lung injury</pubmed_title><pubmed_authors>Hosni A.M. Hussein, Sanu Korumadathil Shaji, Clara Veiga-Villauriz, Soura Chakraborty, Jhuma Pramanik, Fatma Abo Zakaib Ali, Jing Yuan, Esam Khanfar, Ntombizodwa Makuyana, Youssif M. Ali, Qiuchen Zhao, Daniel Hebenstreit, Bidesh Mahata</pubmed_authors><pubmed_authors>SOURA CHAKRABORTY</pubmed_authors></additional><is_claimable>false</is_claimable><name>Immune cell-specific Cyp11a1 deletion impairs inflammation resolution following LPS-induced acute lung injury in mice</name><description>Bulk RNA sequencing was performed on lung tissue from control and immune cell-specific Cyp11a1 conditional knockout (Cyp11a1fl/fl;Vav1Cre) mice following lipopolysaccharide (LPS)-induced acute lung injury. The experiment was designed to characterise genome-wide transcriptional changes associated with Cyp11a1 deficiency in immune cells during inflammation and its resolution. We collected lung samples at defined time points after LPS treatment and performed paired-end RNA sequencing. We compared transcriptomic profiles between genotypes and across time points to identify changes in inflammatory, immune-response, and tissue-repair pathways.</description><dates><release>2026-09-15T00:00:00Z</release><modification>2026-09-22T11:02:24.47Z</modification><creation>2026-09-22T11:02:06.913Z</creation></dates><accession>E-MTAB-17666</accession><cross_references><ENA>ERP206734</ENA><EFO>EFO_0002944</EFO><EFO>EFO_0004170</EFO><EFO>EFO_0003789</EFO><EFO>EFO_0005518</EFO><EFO>EFO_0003738</EFO><EFO>EFO_0004184</EFO><EFO>EFO_0003969</EFO><doi>10.1101/2025.08.29.673039</doi></cross_references></HashMap>