ArticleInternational journal of molecular sciences2022
Activation of Inflammatory Networks in the Lungs Caused by Chronic Cold Stress Is Moderately Attenuated by Glucose Supplementation.
Article in International journal of molecular sciences, 2022. 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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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
15 citing papers in PubMed, 37 citations in OpenAlex.
- Gut microbiota as key mediators of animal acclimation to temperature changes: mechanisms and interventions.Applied and environmental microbiology · 2026Review
- Seawater Immersion Hypothermia Triggers Cardiac Pyroptosis via the NF-κB/NLRP3 Inflammasome Axis: A Mechanistic Study in Rats.International journal of molecular sciences · 2026Article
- Distinct damage levels and transcriptional responses of lung in Hezuo pigs and Bama pigs during cold exposure.Animal bioscience · 2026Article
- The therapeutic effects of labetalol in chronic stress- and immuno-agonist-induced cough hypersensitivity and lung inflammation involve reducing interferon-γ-producing T lymphocytes.ERJ open research · 2026Article
- Chronic cold stress induced transcriptomic alterations in multi-metabolically active tissues of pigs.Communications biology · 2025Article
- Unlocking the Antioxidant Potential of Sea Cucumber Viscera: Pre-Treatment Modulates the Keap1-Nrf2 Pathway and Gut Microbiota to Attenuate Cold Stress-Induced Oxidative Damage.Antioxidants (Basel, Switzerland) · 2025Article
- Dietary Full-Fat Rice Bran or Glucose Regulates Bile Acid Circulation, Colonic Microbiota, and Short-Chain Fatty Acids in Pigs During Chronic Cold Stress.Animals : an open access journal from MDPI · 2025Article
- Review
- Analysis of Potential Genes, Acute Phase Proteins and Hormonal Profiles Associated with Methicillin-ResistantVeterinary sciences · 2025Article
- Developing an IPF Prognostic Model and Screening for Key Genes Based on Cold Exposure-Related Genes Using Bioinformatics Approaches.Biomedicines · 2025Article
- Mitochondrial fusion protein: a new therapeutic target for lung injury diseases.Frontiers in physiology · 2025Review
- Coevolution of specific gut microbiota of Min pig with host cold adaptation through enhanced vitamin B1 synthesis.Frontiers in microbiology · 2024Article
- Effects of fat source in calf starter on growth performance, blood fatty acid profiles, and inflammatory markers during cold season.Scientific reports · 2023Article
- Article
- Characteristics of glucose and lipid metabolism and the interaction between gut microbiota and colonic mucosal immunity in pigs during cold exposure.Journal of animal science and biotechnology · 2023Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Mammals that live in cold climates endure months of exposure to low temperature in the winter. The incidence of respiratory diseases has increased. The goal of this study was to investigate the effects of chronic cold stress on lung inflammatory networks, apoptosis, and mitochondrial function via Yorkshire pig models, as well as the ameliorative effect of glucose as energy supplements. Here, two trials were conducted (chronic cold stress and glucose supplementation). The results showed that chronic cold stress induced obvious inflammatory cell infiltration in the lungs and damaged the lung tissue structure. Compared with the Y-Con group, the expression of toll-like receptor 4 (TLR4), myeloid differentiation primary response 88 (MyD88), high mobility group box 1 (HMGB1), nucleotide-binding domain, and leucine-rich repeat protein 3 (NLRP3), IL-1β, IL-2, IL-6, and IFN-γ in the lungs of the Y-CS group was enhanced by chronic cold stress (p < 0.05). Moreover, chronic cold stress promoted the expression of the Bax and Mfn2 in lungs of Y-CS group (p < 0.05). Interestingly, dietary glucose supplementation significantly reduced inflammatory cell infiltration in the lungs. Moreover, glucose supplementation inhibited the expression of TLR4, MyD88, HMGB1, NLRP3, IL-1β, IL-2, IL-6, IFN-γ, and Bax during chronic cold stress. In conclusion, chronic cold stress promoted inflammatory networks, apoptosis, and mitochondrial fusion in the lungs. Dietary glucose supplementation inhibited the inflammatory network during chronic cold stress.
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Registered trials
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