ArticleInternational journal of molecular sciences2019
Pre-Treatment with Ten-Minute Carbon Dioxide Inhalation Prevents Lipopolysaccharide-Induced Lung Injury in Mice via Down-Regulation of Toll-Like Receptor 4 Expression.
Article in International journal of molecular sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 23 citations in OpenAlex.
- Molecular and Cellular Signaling Pathways of the Effects of Hypoxia and Hypercapnia on the Mechanisms of Neuroinflammation.International journal of molecular sciences · 2026Review
- Neuroplastic Effects Induced by Hypercapnic Hypoxia in Rat Focal Ischemic Stroke Are Driven via BDNF and VEGF Signaling.International journal of molecular sciences · 2025Article
- Midkine Deficiency Attenuates Lipopolysaccharide-Induced Pulmonary Inflammation.International journal of molecular sciences · 2025Article
- Carbon dioxide and MAPK signalling: towards therapy for inflammation.Cell communication and signaling : CCS · 2023Review
- Identification of macrophage-related genes in sepsis-induced ARDS using bioinformatics and machine learning.Scientific reports · 2023Article
- Intermittent Exposure of Hypercapnia Suppresses Allograft Rejection via Induction of Treg Differentiation and Inhibition of Neutrophil Accumulation.Biomedicines · 2022Article
- All‑trans retinoic acid promotes macrophage phagocytosis and decreases inflammation via inhibiting CD14/TLR4 in acute lung injury.Molecular medicine reports · 2021Article
- Carbon dioxide inhibits COVID-19-type proinflammatory responses through extracellular signal-regulated kinases 1 and 2, novel carbon dioxide sensors.Cellular and molecular life sciences : CMLS · 2021Article
- Trelagliptin Alleviates Lipopolysaccharide (LPS)-Induced Inflammation and Oxidative Stress in Acute Lung Injury Mice.Inflammation · 2021Article
- Carbon dioxide-dependent signal transduction in mammalian systems.Interface focus · 2021Review
- Hypercapnia in the critically ill: insights from the bench to the bedside.Interface focus · 2021Review
- Ischemia-reperfusion Injury in the Transplanted Lung: A Literature Review.Transplantation direct · 2021Review
- Iridin Prevented Against Lipopolysaccharide-Induced Inflammatory Responses of Macrophages via Inactivation of PKM2-Mediated Glycolytic Pathways.Journal of inflammation research · 2021Article
- Oxyberberine Prevented Lipopolysaccharide-Induced Acute Lung Injury through Inhibition of Mitophagy.Oxidative medicine and cellular longevity · 2021Article
- Humidified Warmed COFrontiers in medicine · 2020Article
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Authors and funding
9 authors at 4 institutions in 1 country.
Funding
Abstract
Various animal studies have shown beneficial effects of hypercapnia in lung injury. However, in patients with acute respiratory distress syndrome (ARDS), there is controversial information regarding the effect of hypercapnia on outcomes. The duration of carbon dioxide inhalation may be the key to the protective effect of hypercapnia. We investigated the effect of pre-treatment with inhaled carbon dioxide on lipopolysaccharide (LPS)-induced lung injury in mice. C57BL/6 mice were randomly divided into a control group or an LPS group. Each LPS group received intratracheal LPS (2 mg/kg); the LPS groups were exposed to hypercapnia (5% carbon dioxide) for 10 min or 60 min before LPS. Bronchoalveolar lavage fluid (BALF) and lung tissues were collected to evaluate the degree of lung injury. LPS significantly increased the ratio of lung weight to body weight; concentrations of BALF protein, tumor necrosis factor-α, and CXCL2; protein carbonyls; neutrophil infiltration; and lung injury score. LPS induced the degradation of the inhibitor of nuclear factor-κB-α (IκB-α) and nuclear translocation of NF-κB. LPS increased the surface protein expression of toll-like receptor 4 (TLR4). Pre-treatment with inhaled carbon dioxide for 10 min, but not for 60 min, inhibited LPS-induced pulmonary edema, inflammation, oxidative stress, lung injury, and TLR4 surface expression, and, accordingly, reduced NF-κB signaling. In summary, our data demonstrated that pre-treatment with 10-min carbon dioxide inhalation can ameliorate LPS-induced lung injury. The protective effect may be associated with down-regulation of the surface expression of TLR4 in the lungs.
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