ArticlePloS one2013
Toll-like receptor 4 mediates acute lung injury induced by high mobility group box-1.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 73 citations in OpenAlex.
- Human resistin promotes neutrophil proinflammatory activation and neutrophil extracellular trap formation and increases severity of acute lung injury.Journal of immunology (Baltimore, Md. : 1950) · 2014Trial
- Electroacupuncture pretreatment alleviates myocardial ischemia/reperfusion-induced lung injury by inhibiting the expression of HMGB1/RAGE in male rats.Physiological reports · 2026Article
- Tumor-Bearing Status Accelerates Bleomycin-Induced Pulmonary Inflammation via Endothelial Activation.Thoracic cancer · 2026Article
- CDDO-imidazolide ameliorates sepsis-induced ARDS by enhancing mitophagy via the Nrf2 pathway to prohibit alveolar macrophage pyroptosis and HMGB1 release.Acta biochimica et biophysica Sinica · 2025Article
- Article
- Regulated Cell Death of Alveolar Macrophages in Acute Lung Inflammation: Current Knowledge and Perspectives.Journal of inflammation research · 2024Review
- Predictive role of circulatory levels of high-mobility group box 1 for radiation pneumonitis in patients with non-small cell lung cancer treated with definitive thoracic radiotherapy.International journal of clinical oncology · 2022Article
- Immunomonitoring of Monocyte and Neutrophil Function in Critically Ill Patients: From Sepsis and/or Trauma to COVID-19.Journal of clinical medicine · 2021Review
- Anti-inflammatory effects of microRNA-223 on sepsis-induced lung injury in rats by targeting the Toll-like receptor signaling pathway.Experimental and therapeutic medicine · 2021Article
- Predictive role of circulatory HMGB1 in postoperative acute exacerbation of interstitial lung disease in lung cancer patients.Scientific reports · 2021Article
- Beneficial effect of Indigo Naturalis on acute lung injury induced by influenza A virus.Chinese medicine · 2020Article
- GSK3 modulation in acute lung injury, myocarditis and polycystic kidney disease-related aneurysm.Biochimica et biophysica acta. Molecular cell research · 2020Review
- Article
- HMGB1 participates in LPS‑induced acute lung injury by activating the AIM2 inflammasome in macrophages and inducing polarization of M1 macrophages via TLR2, TLR4, and RAGE/NF‑κB signaling pathways.International journal of molecular medicine · 2020Article
- Cardiopulmonary Bypass Induces Acute Lung Injury via the High-Mobility Group Box 1/Toll-Like Receptor 4 Pathway.Disease markers · 2020Article
- Editorial: Multitasking Biomolecules in Human Pathologies: Known Players on Their Unexpected Journeys.Frontiers in medicine · 2020Article
- Compound amino acid combined with high-dose vitamin B6 attenuate traumatic coagulopathy via inhibiting inflammation by HMGB1/TLR4/NF-κB pathway.Journal of inflammation (London, England) · 2020Article
- Alcohol-dependent pulmonary inflammation: A role for HMGB-1.Alcohol (Fayetteville, N.Y.) · 2019Article
- Electroacupuncture Pretreatment Attenuates Acute Lung Injury Through α7 Nicotinic Acetylcholine Receptor-Mediated Inhibition of HMGB1 Release in Rats After Cardiopulmonary Bypass.Shock (Augusta, Ga.) · 2018Article
- NLRP3/ASC-mediated alveolar macrophage pyroptosis enhances HMGB1 secretion in acute lung injury induced by cardiopulmonary bypass.Laboratory investigation; a journal of technical methods and pathology · 2018Article
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAcute lung injury (ALI) is considered to be the major cause of respiratory failure in critically ill patients. Clinical studies have found that in patients with sepsis and after hemorrhage, the elevated level of high mobility group box-1(HMGB-1) in their circulation is highly associated with ALI, but the underlying mechanism remains unclear. Extracellular HMGB-1 has cytokine-like properties and can bind to Toll-like Receptor-4 (TLR4), which was reported to play an important role in the pathogenesis of ALI. The aim of this study was to determine whether HMGB-1 directly contributes to ALI and whether TLR4 signaling pathway is involved in this process.
methodsRecombinant human HMGB-1 (rhHMGB-1) was used to induce ALI in male Sprague-Dawley rats. Lung specimens were collected 2 h after HMGB-1 treatment. The levels of TNF-α, IL-1β, TLR4 protein, and TLR4 mRNA in lungs as well as pathological changes of lung tissue were assessed. In cell studies, the alveolar macrophage cell line, NR8383, was collected 24 h after rhHMGB-1 treatment and the levels of TNF-α and IL-1β in cultured medium as well as TLR4 protein and mRNA levels in the cell were examined. TLR4-shRNA-lentivirus was used to inhibit TLR4 expression, and a neutralizing anti-HMGB1 antibody was used to neutralize rhHMGB-1 both in vitro and in vivo.
resultsFeatures of lung injury and significant elevation of IL-1β and TNF-α levels were found in lungs of rhHMGB-1-treated animals. Cultured NR8383 cells were activated by rhHMGB-1 treatment and resulted in the release of IL-1β and TNF-α. TLR4 expression was greatly up-regulated by rhHMGB-1. Inhibition of TLR4 or neutralization of HMGB1 with a specific antibody also attenuated the inflammatory response induced by HMGB-1 both in vivo and in vitro.
conclusionHMGB-1 can activate alveolar macrophages to produce proinflammatory cytokines and induce ALI through a mechanism that relies on TLR-4.
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