ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2023
Lactate produced by alveolar type II cells suppresses inflammatory alveolar macrophages in acute lung injury.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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The trial behind it
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Who cites it
24 citing papers in PubMed, 24 citations in OpenAlex.
- Apoptotic body-encapsulated nanoparticles regulate inflammation through macrophage polarization mediated by lactic acid.Annals of medicine · 2026Article
- SIRT7-mediated desuccinylation of FOXO4 suppresses ferroptosis to alleviate LPS-induced acute lung injury.Redox biology · 2026Article
- Epithelial-immune interface in asthma: Mechanistic insights driving novel therapeutic strategies.Seminars in immunopathology · 2026Review
- 6β-Acetoxysandaracopimaradien-1α,9α-diol Attenuates LPS-Induced Acute Lung Injury: Association with Alterations in Src, MAPK, and Akt/GSK-3β Signalling.International journal of molecular sciences · 2026Article
- Lactate regulation in high-altitude hypoxic adaptation attenuates LPS-Induced acute lung injury: links to glucose metabolism and anti-inflammatory therapeutic potential.Critical care (London, England) · 2026Article
- Muscle-lung crosstalk in COPD: how exercise training modulates protein metabolism and inflammation in experimental COPD models.Frontiers in immunology · 2026Review
- Innate immune circuits in acute lung injury: macrophage plasticity, ILC crosstalk, and tissue repair failure.Frontiers in immunology · 2026Review
- Lactate and Lactylation in Respiratory Diseases: from Molecular Mechanisms to Targeted Strategies.Lung · 2025Review
- HIF-1α: a bridge connecting sepsis and acute respiratory distress syndrome.European journal of medical research · 2025Review
- Review
- A prediction model for 30-day mortality in patients with ARDS admitted to the intensive care unit.European journal of medical research · 2025Article
- Phenylacetylglutamine produced from injury lung alveolar epithelial cells promotes the function of BMSCs by regulating NONRATT006276.2/Mapt pathway.Respiratory research · 2025Article
- Lactate, an Essential Metabolic Marker in the Diagnosis and Management of Pediatric Conditions.Diagnostics (Basel, Switzerland) · 2025Review
- Absence of c-Maf and IL-10 enables type I IFN enhancement of innate responses to LPS in alveolar macrophages.Journal of immunology (Baltimore, Md. : 1950) · 2025Article
- The relationship between genetic prediction of 486 blood metabolites and the risk of COPD: mendelian randomization study.Scientific reports · 2025Article
- Uncovering metabolic pathways in human alveolar macrophages in response to lipopolysaccharide.Clinical and experimental immunology · 2025Article
- Lactate attenuates PANoptosis and enhances ZBP-1 lactylation in macrophages in acute lung injury.Frontiers in immunology · 2025Article
- Unlocking the secrets of glucose metabolism reprogramming: the role in pulmonary diseases.Frontiers in pharmacology · 2025Review
- Decoding the HIF-1-driven metabolic-inflammatory-immune axis in sepsis-associated lung injury: a comprehensive overview.Frontiers in immunology · 2025Review
- Alveolar epithelial cells mitigate neutrophilic inflammation in lung injury through regulating mitochondrial fatty acid oxidation.Nature communications · 2024Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
Alveolar inflammation is a hallmark of acute lung injury (ALI), and its clinical correlate is acute respiratory distress syndrome-and it is as a result of interactions between alveolar type II cells (ATII) and alveolar macrophages (AM). In the setting of acute injury, the microenvironment of the intra-alveolar space is determined in part by metabolites and cytokines and is known to shape the AM phenotype. In response to ALI, increased glycolysis is observed in AT II cells, mediated by the transcription factor hypoxia-inducible factor (HIF) 1α, which has been shown to decrease inflammation. We hypothesized that in acute lung injury, lactate, the end product of glycolysis, produced by ATII cells shifts AMs toward an anti-inflammatory phenotype, thus mitigating ALI. We found that local intratracheal delivery of lactate improved ALI in two different mouse models. Lactate shifted cytokine expression of murine AMs toward increased IL-10, while decreasing IL-1 and IL-6 expression. Mice with ATII-specific deletion of Hif1a and mice treated with an inhibitor of lactate dehydrogenase displayed exacerbated ALI and increased inflammation with decreased levels of lactate in the bronchoalveolar lavage fluid; however, all those parameters improved with intratracheal lactate. When exposed to LPS (to recapitulate an inflammatory stimulus as it occurs in ALI), human primary AMs co-cultured with alveolar epithelial cells had reduced inflammatory responses. Taken together, these studies reveal an innate protective pathway, in which lactate produced by ATII cells shifts AMs toward an anti-inflammatory phenotype and dampens excessive inflammation in ALI.
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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.