ArticleMolecular medicine (Cambridge, Mass.)2012
Gene expression profiles in alveolar macrophages induced by lipopolysaccharide in humans.
Article in Molecular medicine (Cambridge, Mass.), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 1 of them a synthesis that pooled it.
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Who cites it
36 citing papers in PubMed, 1 synthesis or guideline pooled it, 47 citations in OpenAlex.
- Gene Expression Analysis to Assess the Relevance of Rodent Models to Human Lung Injury.American journal of respiratory cell and molecular biology · 2017Pooled it
- Dexamethasone inhibits endotoxin-induced coagulopathy in human lungs.Journal of thrombosis and haemostasis : JTH · 2016Trial
- Mature-StageInternational journal of molecular sciences · 2026Article
- Integrative transcriptomic analysis reveals cross-species conserved core genes and pathways in alveolar macrophages during ALI/ARDS.BMC pulmonary medicine · 2025Article
- CMTM7 inhibits TLR4 signaling pathway via promoting Rab5 activation and alleviates acute liver injury.Cellular and molecular life sciences : CMLS · 2025Article
- Lipid metabolism-related genes are involved in the formation of macrophage extracellular traps in allergic airway inflammation.Genes and immunity · 2025Article
- Uncovering metabolic pathways in human alveolar macrophages in response to lipopolysaccharide.Clinical and experimental immunology · 2025Article
- IKZF1 exacerbates the inflammatory response by epigenetically modulating mitochondrial function following acute peritonitis.Frontiers in immunology · 2025Article
- Dissecting metabolic landscape of alveolar macrophage.Scientific reports · 2024Article
- Absence of c-Maf and IL-10 enables Type I IFN enhancement of innate responses to low-dose LPS in alveolar macrophages.bioRxiv : the preprint server for biology · 2024Article
- GCH1 reduces LPS-induced alveolar macrophage polarization and inflammation by inhibition of ferroptosis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023Article
- The Gene Signature of Activated M-CSF-Primed Human Monocyte-Derived Macrophages Is IL-10-Dependent.Journal of innate immunity · 2022Article
- Article
- Structure of the full-length human Pannexin1 channel and insights into its role in pyroptosis.Cell discovery · 2021Article
- P23 Acts as Functional RBP in the Macrophage Inflammation Response.Frontiers in molecular biosciences · 2021Article
- Article
- Tim‑3 regulates the ability of macrophages to counter lipopolysaccharide‑induced pulmonary epithelial barrier dysfunction via the PI3K/Akt pathway in epithelial cells.Molecular medicine reports · 2020Article
- MAFB and MAF Transcription Factors as Macrophage Checkpoints for COVID-19 Severity.Frontiers in immunology · 2020Article
- Computational Approach to Identifying Universal Macrophage Biomarkers.Frontiers in physiology · 2020Article
- RNF144B inhibits LPS-induced inflammatory responses via binding TBK1.Journal of leukocyte biology · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Lipopolysaccharide (LPS) is ubiquitous in the environment. Inhalation of LPS has been implicated in the pathogenesis and/or severity of several lung diseases, including pneumonia, chronic obstructive pulmonary disease and asthma. Alveolar macrophages are the main resident leukocytes exposed to inhaled antigens. To obtain insight into which innate immune pathways become activated within human alveolar macrophages upon exposure to LPS in vivo, we conducted a study in eight healthy humans, in which we instilled sterile saline into a lung segment by bronchoscope, followed by instillation of LPS into the contralateral lung. Six hours later, a bilateral bronchoalveolar lavage was performed and whole-genome transcriptional profiling was done on purified alveolar macrophages, comparing cells exposed to saline or LPS from the same individuals. LPS induced differential expression of 2,932 genes in alveolar macrophages; 1,520 genes were upregulated, whereas 1,440 genes were downregulated. A total of 26 biological functions were overrepresented in LPS-exposed macrophages; 44 canonical pathways affected by LPS were identified, among which the genes associated with the role of pattern recognition receptors in recognition of bacteria and viruses represented the top pathway. Other pathways included cellular immune response, signaling by tumor necrosis factor (receptor) family members, cytokine signaling and glucocorticoid receptor signaling. These results reveal for the first time a large number of functional pathways influenced by the biologically relevant challenge provided by LPS administered into the airways. These data can assist in identifying novel targets for therapeutic intervention in pulmonary diseases associated with LPS exposure, including pneumonia, asthma and chronic obstructive pulmonary disease.
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Registered trials
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