Dataset's files
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| GSE296392_merged_gene_counts.txt.gz | Txt |
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Similar Datasets
Project description:Chronic obstructive pulmonary disease (CODP) including emphysema affects approximately 400 million individuals worldwide. Therapies to treat COPD remain limited and fail to prevent disease progression. Alveolar macrophages (AMs) reside in the alveoli of the lung and are ideally positioned to encounter inhaled particles and pathogens. Despite exposure to these stimuli, AMs exhibit specialized phenotypes that restrict inflammation to prevent alveolar damage. Here we demonstrate that AMs express high levels of the surface bound enzyme carbonic anhydrase 4 (Car4). Deletion of Car4 on AMs results in increased susceptibility to emphysematous pathology and therapeutic treatment with Car4 is sufficient to prevent emphysema-like disease. Consistent with our murine studies, reduced levels of Carbonic anhydrase 4 (CAIV) distinguishes COPD patients with emphysema from those without emphysema. Mechanistically, murine and human Car4 directly inhibit elastase that promotes destruction of alveolar walls. Collectively, these studies reveal an underappreciated function for Car4 in preventing lung pathology.
2026-03-23 | GSE298037 | GEO
Project description:Purpose: The goal of this study is to investigate the alteration of gene expression pattern of alveolar macrophages by allergen challenge in human asthmatics. Method: By using subsegmental bronchial provocation with allergen (SBP-AG) protocol, we obtained BAL fluids, before and 48 hours after allergen challenge in the subjects enrolled in the protocol. Alveolar macrophages were purified from the BAL fluids and total RNA was isolated. Next-generation sequencing data were generated by using the Illumina system. Results: Using an optimized data analysis workflow, we mapped about 75 million sequence reads per sample to the human genome and identified 29,691 transcripts in the macrophage mRNAs. Among them, the change in the expression profiles of 37 transcripts were statistically significant. Conclusions: It has been well accepted that Th2 cytokine enriched environment transforms the phenotype of macrophages into alternatively activated form. However, the details of a genome-wide gene expression profiles of macrophages were not well investigated. Using RNA-seq technology, we provided comprehensive data of macrophage gene expression profiles in allergic lung inflammation. Our data could offer a framework to study biologic functions of alternatively activated macrophage in chronic inflammatory diseases. mRNA profiles of alveolar macrophages obtained from asthmatics, before and after allergen challenge.
2015-04-01 | E-GEOD-65039 | biostudies-arrayexpress
Project description:Community-acquired pneumonia is a widespread disease with significant morbidity and mortality. Alveolar macrophages are tissue-resident lung cells that play a crucial role in innate immunity against bacteria causing pneumonia. We hypothesized that alveolar macrophages display adaptive characteristics after resolution of bacterial pneumonia. We studied mice one to six months after self-limiting lung infection due to Streptococcus pneumoniae, the most common cause of bacterial pneumonia. Among the myeloid cells recovered from the lung, only alveolar macrophages showed long-term modifications of their surface marker phenotype. The remodeling of alveolar macrophages was: (i) long-lasting (still observed 6 months post infection), (ii) regionally localized (only observed in the affected lobe after lobar pneumonia), and (iii) associated with a macrophage-dependent enhanced lung protection to another pneumococcal serotype. Metabolomic and transcriptomic profiling revealed that alveolar macrophages of mice which recovered from pneumonia had new baseline activities and altered responses to infection. Thus, the enhanced lung protection after mild and self-limiting respiratory infection includes a profound remodeling of alveolar macrophages that is long-lasting, compartmentalized, and manifest across surface receptors, metabolites, and both resting and stimulated transcriptomes. We used microarrays to detail the global program of gene expression for mouse alveolar macrophages sorted from lungs that were naïve or infected more than a month previously, at rest and during an acute (4-hour) infection.
2020-04-17 | GSE133975 | GEO
Project description:Within the human lung, interplay between alveolar epithelial cells and resident macrophages shape lung development and function in both health and disease. To study these processes, we devised a strategy for co-culturing hPSC-derived alveolar epithelial organoids and induced macrophages to form functional environment, which we name alveolar assembloids (AlvAssemb). By scRNAseq and functional analysis of AlvAssemb, we identified alveolar type 2-like cells that produced GM-CSF, a response associated with tissue adaptation of macrophages, and that resident alveolar macrophage-like cells secreted interleukin-1β and interleukin-6, a core immune response function, and expressed genes required for surfactant metabolism. Remarkably, in response to alveolar epithelial injury, we found that macrophage-like cells within AlvAssemb efficiently eliminated damaged cells and absorbed oxidized lipids. Moreover, in response to lipopolysaccharide exposure and Mycobacterium tuberculosis infection, we found that core features of the human respiratory defense response were replicated in AlvAssemb. These findings support that AlvAssemb could serve as a valuable platform to investigate human lung development and pathology.
2024-09-30 | GSE269733 | GEO
Project description:The proteasome is a central regulatory hub for intracellular signaling by degrading numerous signaling mediators. Immunoproteasomes are specialized types of proteasomes known to be involved in shaping adaptive immune responses, but their role for innate immune signaling is elusive. Here, we analyzed immunoproteasome function for polarization of alveolar macrophages which are highly specialized tissue macrophages of the alveolar surface of the lung. Classical activation (M1 polarization) of primary alveolar macrophages by LPS/IFNγ transcriptionally induced all three immunoproteasome subunits LMP2, LMP7, and MECL-1. In contrast, IL-4 triggered alternative (M2) activation was accompanied by posttranscriptional upregulation of LMP2 and LMP7. Accordingly, immunoproteasome activity increased in M1 cells, and to some extent under M2 conditions. Analyzing the polarization capability from LMP7 deficient mice revealed no effect on the LPS/IFNγ triggered M1 profile, but uncovered a distorted M2 profile for IL-4 stimulated LMP7-/- alveolar macrophages as characterized by increased M2 marker gene expression and CCL17 cytokine release. This shift in immunoproteasome-dependent M2 polarization was accompanied by amplified AKT/STAT6 activation and IRF4 expression in LMP7-/- alveolar macrophages. IL-13 stimulation of LMP7 deficient cells induced a similar M2 skewed profile and IL4Rα protein expression was generally elevated in LMP7-/- alveolar macrophages, indicating that amplified IL4R signaling in immunoproteasome defective cells may contribute to augmented M2 polarization. Importantly, treatment with an LMP7-specific proteasome inhibitor recapitulated the findings of genetic LMP7 inactivation. Our results thus suggest a novel role of immunoproteasome function for regulating innate immune function of macrophages by limiting IL4R expression and signaling. Expression data of M0 and M2 macrophages derived from Lmp7 k.o. and control animals
2016-06-29 | E-GEOD-72000 | biostudies-arrayexpress
Project description:To investigate the effects of RACK1 myeloid deletion on the growth and development of alveolar macrophages in mice, we sorted alveolar macrophages from RACK1 myeloid deletion mice and control mice for transcriptome sequencing
2025-05-27 | GSE238089 | GEO
Project description:In this study, we determined the miRNA expression profile of bovine alveolar macrophages, using next-generation sequencing strategy. On an Illumina HiSeq 2000 machine, we sequenced 8 miRNA libraries, prepared from small RNA fractions of alveolar macrophages isolated from 8 different healthy animals (Bos taurus). From the data, the potential novel miRNAs were predicted, and the expression levels of the known miRNAs were determined. We report that 80 known bovine miRNAs are expressed in bovine alveolar macrophages with >100 reads per million. The most highly expressed miRNA was bta-miR-21, followed by bta-miR-27a. Additionally, one putatively novel bovine miRNA was identified. To our knowledge, this is the first RNA-seq study to profile miRNA expression in bovine alveolar macrophages and provides an important reference dataset for investigating the regulatory roles miRNAs play in this important immune cell type. Examination of bovine alveolar macrophage miRNA profiles, using RNA-seq. Alveolar macrophages were isolated from lung lavages from 8 animals. Small RNA fractions were prepared from the cells using the Qiagen RNeasy Plus mini kit, and miRNA sequencing libraries were prepared using the Epicentre Scriptminer multiplex kit. The sequencing was performed on an Illumina HiSeq 2000 machine.
2013-09-09 | E-GEOD-41138 | biostudies-arrayexpress
Project description:Purpose: The goal of this study is to investigate the alteration of gene expression pattern of alveolar macrophages by allergen challenge in human asthmatics. Method: By using subsegmental bronchial provocation with allergen (SBP-AG) protocol, we obtained BAL fluids, before and 48 hours after allergen challenge in the subjects enrolled in the protocol. Alveolar macrophages were purified from the BAL fluids and total RNA was isolated. Next-generation sequencing data were generated by using the Illumina system. Results: Using an optimized data analysis workflow, we mapped about 75 million sequence reads per sample to the human genome and identified 29,691 transcripts in the macrophage mRNAs. Among them, the change in the expression profiles of 37 transcripts were statistically significant. Conclusions: It has been well accepted that Th2 cytokine enriched environment transforms the phenotype of macrophages into alternatively activated form. However, the details of a genome-wide gene expression profiles of macrophages were not well investigated. Using RNA-seq technology, we provided comprehensive data of macrophage gene expression profiles in allergic lung inflammation. Our data could offer a framework to study biologic functions of alternatively activated macrophage in chronic inflammatory diseases.
2015-04-01 | GSE65039 | GEO
Project description:This series represents isolated alveolar macrophages from human subjects. Keywords: parallel sample
2005-10-04 | GSE2125 | GEO
Project description:In Nannochloropsis oceanica IMET1, transcript knockdown of a cytosolic carbonic anhydrase (CA2; g2018) specifically inhibited by HC resulted in ~45%, ~30% and ~40% elevation of photosynthetic oxygen evolution rate, growth rate and biomass accumulation rate under high CO2 (5% ), respectively. This CA2-knockdown mutant is demonated as M2. To probe mechanistic links underlying the mutant (M2; RNAi-knockdown line of carbonic anhydrase (CA2)) phenotypes, temporal transcriptomic profiles are compared between RNAi-knockdown line of carbonic anhydrase (CA2) and WT, at 12 h and 24h under high CO2 (5%).
2020-10-28 | GSE115445 | GEO