ArticleJournal of immunology (Baltimore, Md. : 1950)2012
Type I alveolar epithelial cells mount innate immune responses during pneumococcal pneumonia.
Article in Journal of immunology (Baltimore, Md. : 1950), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.
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Who cites it
63 citing papers in PubMed, 91 citations in OpenAlex.
- Exploring the Role ofACS infectious diseases · 2026Article
- Immunology of Sepsis.Clinics in chest medicine · 2026Review
- SomaticiScience · 2025Article
- Aging-Associated Molecular Changes in Human Alveolar Type I Cells.Journal of respiratory biology and translational medicine · 2024Article
- Lung repair and regeneration: Advanced models and insights into human disease.Cell stem cell · 2024Review
- Advances and Applications of Lung Organoids in the Research on Acute Respiratory Distress Syndrome (ARDS).Journal of clinical medicine · 2024Review
- Insights into the defensive roles of lncRNAs duringFrontiers in microbiology · 2024Review
- Altered circular RNA expressions in extracellular vesicles from bronchoalveolar lavage fluids in mice after bacterial infections.Frontiers in immunology · 2024Article
- Innate immune responses in pneumonia.Pneumonia (Nathan Qld.) · 2023Review
- Interaction between alveolar macrophages and epithelial cells duringFrontiers in cellular and infection microbiology · 2023Review
- Role of the cGAS/STING pathway in the control ofFrontiers in immunology · 2023Article
- The underappreciated role of resident epithelial cell populations in metastatic progression: contributions of the lung alveolar epithelium.American journal of physiology. Cell physiology · 2022Review
- New Insights into the Alveolar Epithelium as a Driver of Acute Respiratory Distress Syndrome.Biomolecules · 2022Review
- Minilungs from Human Embryonic Stem Cells to Study the Interaction of Streptococcus pneumoniae with the Respiratory Tract.Microbiology spectrum · 2022Article
- Review
- Teleost swim bladder, an ancient air-filled organ that elicits mucosal immune responses.Cell discovery · 2022Article
- Epithelial LIF signaling limits apoptosis and lung injury during bacterial pneumonia.American journal of physiology. Lung cellular and molecular physiology · 2022Article
- Article
- Regulatory mechanisms of neutrophil migration from the circulation to the airspace.Cellular and molecular life sciences : CMLS · 2021Review
- Microbial metabolism of L-tyrosine protects against allergic airway inflammation.Nature immunology · 2021Article
3 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
Pneumonia results from bacteria in the alveoli. The alveolar epithelium consists of type II cells, which secrete surfactant and associated proteins, and type I cells, which constitute 95% of the surface area and meet anatomic and structural needs. Other than constitutively expressed surfactant proteins, it is unknown whether alveolar epithelial cells have distinct roles in innate immunity. Because innate immunity gene induction depends on NF-κB RelA (also known as p65) during pneumonia, we generated a murine model of RelA mutated throughout the alveolar epithelium. In response to LPS, only 2 of 84 cytokine transcripts (CCL20 and CXCL5) were blunted in lungs of mutants, suggesting that a very limited subset of immune mediators is selectively elaborated by the alveolar epithelium. Lung CCL20 induction required epithelial RelA regardless of stimulus, whereas lung CXCL5 expression depended on RelA after instillation of LPS but not pneumococcus. RelA knockdown in vitro suggested that CXCL5 induction required RelA in type II cells but not type I cells. Sorted cell populations from mouse lungs revealed that CXCL5 was induced during pneumonia in type I cells, which did not require RelA. TLR2 and STING were also induced in type I cells, with RelA essential for TLR2 but not STING. To our knowledge, these data are the first direct demonstration that type I cells, which constitute the majority of the alveolar surface, mount innate immune responses during bacterial infection. These are also, to our knowledge, the first evidence for entirely RelA-independent pathways of innate immunity gene induction in any cell during pneumonia.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.