ArticleShock (Augusta, Ga.)2013
CD11c+ alveolar macrophages are a source of IL-23 during lipopolysaccharide-induced acute lung injury.
Article in Shock (Augusta, Ga.), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 42 citations in OpenAlex.
- Proton-activated chloride channel 1 is essential for innate host defense against bacterial sepsis.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Weathering the Storm: How Age and Biologics Influence the COVID-19 Cytokine Surge.Pathogens (Basel, Switzerland) · 2025Review
- Tissue-plasminogen activator effects on the phenotype of splenic myeloid cells in acute inflammation.Journal of inflammation (London, England) · 2024Article
- The Role of IL-23 in the Pathogenesis and Therapy of Inflammatory Bowel Disease.International journal of molecular sciences · 2023Review
- Allergic airway inflammation induces upregulation of the expression of IL-23R by macrophages and not in CD3 + T cells and CD11cCell and tissue research · 2022Article
- Crossing the boundaries: IL-23 and its role in linking inflammation of the skin, gut and joints.Rheumatology (Oxford, England) · 2021Article
- Inflammatory Mediators and Gut Microbial Toxins Drive Colon Tumorigenesis by IL-23 Dependent Mechanism.Cancers · 2021Article
- Botanical formulation, TADIOS, alleviates lipopolysaccharide (LPS)-Induced acute lung injury in mice via modulation of the Nrf2-HO-1 signaling pathway.Journal of ethnopharmacology · 2021Article
- S1P Generation by Sphingosine Kinase-2 in Recruited Macrophages Resolves Lung Inflammation by Blocking STING Signaling in Alveolar Macrophages.Journal of cellular signaling · 2021Article
- Transcription factor NF-κB promotes acute lung injuryThe Journal of biological chemistry · 2020Article
- Vascular endothelial growth factor contributes to lung vascular hyperpermeability in sepsis-associated acute lung injury.Naunyn-Schmiedeberg's archives of pharmacology · 2020Article
- Impact of Bacterial Toxins in the Lungs.Toxins · 2020Review
- SPHK2-Generated S1P in CD11bCell reports · 2020Article
- A novel chalcone derivative exerts anti-inflammatory and anti-oxidant effects after acute lung injury.Aging · 2019Article
- T cell-directed IL-17 production by lung granular γδ T cells is coordinated by a novel IL-2 and IL-1β circuit.Mucosal immunology · 2018Article
- Elevated prostaglandin EMucosal immunology · 2018Article
- Geraniol alleviates LPS-induced acute lung injury in mice via inhibiting inflammation and apoptosis.Oncotarget · 2017Article
- Simvastatin Ameliorates PAK4 Inhibitor-Induced Gut and Lung Injury.BioMed research international · 2017Article
- Selective Biological Responses of Phagocytes and Lungs to Purified Histones.Journal of innate immunity · 2017Article
- Macrophage-epithelial interactions in pulmonary alveoli.Seminars in immunopathology · 2016Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
Acute lung injury (ALI) is a severe pulmonary disease causing high numbers of fatalities worldwide. Innate immune responses are an integral part of the pathophysiologic events during ALI. Interleukin 23 (IL-23) is a proinflammatory mediator known to direct the inflammatory responses in various settings of infection, autoimmunity, and cancer. Interleukin 23 has been associated with proliferation and effector functions in T(H)17 cells. Surprisingly, little is known about production of IL-23 during ALI. In this study, we found expression of mRNA for IL-23p19 to be 10-fold elevated in lung homogenates of C57BL/6 mice after lipopolysaccharide (LPS)-induced ALI. Likewise, concentrations of IL-23 significantly increased in bronchoalveolar lavage fluids. Experiments with IL-23-deficient mice showed that endogenous IL-23 was required for production of IL-17A during LPS-ALI. CD11c-diphtheria toxin receptor transgenic mice were used to selectively deplete CD11c cells, the data suggesting that IL-23 production is dependent at least in part on CD11c cells during ALI. No alterations of IL-23 levels were observed in Rag-1-deficient mice as compared with wild-type C57BL/6 mice following ALI. The mouse alveolar macrophage cell line, MH-S, as well as primary alveolar macrophages displayed abundant surface expression of CD11c. Activation of these macrophages by LPS resulted in release of IL-23 in vitro. Our findings identify CD11c macrophages in the lung are likely an important source of IL-23 during ALI, which may be helpful for better understanding of this disease.
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