دورية أكاديمية

The influence of high glucose conditions on macrophages and its effect on the autophagy pathway.

التفاصيل البيبلوغرافية
العنوان: The influence of high glucose conditions on macrophages and its effect on the autophagy pathway.
المؤلفون: Sousa ESA; Laboratory of Immunoendocrinology, School of Pharmaceutical Sciences, Department of Clinical and Toxicological Analyses, University of São Paulo, São Paulo, Brazil., Queiroz LAD; Laboratory of Immunoendocrinology, School of Pharmaceutical Sciences, Department of Clinical and Toxicological Analyses, University of São Paulo, São Paulo, Brazil., Guimarães JPT; Laboratory of Immunoendocrinology, School of Pharmaceutical Sciences, Department of Clinical and Toxicological Analyses, University of São Paulo, São Paulo, Brazil., Pantoja KC; Laboratory of Immunoendocrinology, School of Pharmaceutical Sciences, Department of Clinical and Toxicological Analyses, University of São Paulo, São Paulo, Brazil., Barros RS; Laboratory of Immunoendocrinology, School of Pharmaceutical Sciences, Department of Clinical and Toxicological Analyses, University of São Paulo, São Paulo, Brazil., Epiphanio S; Laboratory of Malaria Cellular and Molecular Immunopathology, School of Pharmaceutical Sciences, Department of Clinical and Toxicological Analyses, University of São Paulo, São Paulo, Brazil., Martins JO; Laboratory of Immunoendocrinology, School of Pharmaceutical Sciences, Department of Clinical and Toxicological Analyses, University of São Paulo, São Paulo, Brazil.
المصدر: Frontiers in immunology [Front Immunol] 2023 Apr 12; Vol. 14, pp. 1130662. Date of Electronic Publication: 2023 Apr 12 (Print Publication: 2023).
نوع المنشور: Journal Article; Research Support, Non-U.S. Gov't
اللغة: English
بيانات الدورية: Publisher: Frontiers Research Foundation] Country of Publication: Switzerland NLM ID: 101560960 Publication Model: eCollection Cited Medium: Internet ISSN: 1664-3224 (Electronic) Linking ISSN: 16643224 NLM ISO Abbreviation: Front Immunol Subsets: MEDLINE
أسماء مطبوعة: Original Publication: [Lausanne : Frontiers Research Foundation]
مواضيع طبية MeSH: Tumor Necrosis Factor-alpha*/metabolism , Interleukin-6*/metabolism, Mice ; Animals ; Lipopolysaccharides/pharmacology ; Beclin-1/metabolism ; Nigericin/pharmacology ; Mice, Inbred C57BL ; Macrophages/metabolism ; Cytokines/metabolism ; Autophagy ; Glucose/metabolism
مستخلص: Introduction: Macrophages are central cells in mediating the inflammatory response.
Objective and Methods: We evaluated the effect of high glucose conditions on the inflammatory profile and the autophagy pathway in Bone-Marrow Derived Macrophages (BMDM) from diabetic (D-BMDM) (alloxan: 60mg/kg, i.v.) and non-diabetic (ND-BMDM) C57BL/6 mice. BMDM were cultured in medium with normal glucose (5.5 mM), or high glucose (25 mM) concentration and were primed with Nigericin (20µM) stimulated with LPS (100 ng/mL) at times of 30 minutes; 2; 4; 6 and 24 hours, with the measurement of IL-6, IL-1β and TNF-α cytokines.
Results: We have further identified changes in the secretion of pro-inflammatory cytokines IL-6, IL-1β and TNF-α, where BMDM showed increased secretion of these cytokines after LPS + Nigericin stimulation. In addition, changes were observed in the autophagy pathway, where the increase in the autophagic protein LC3b and Beclin-1 occurred by macrophages of non-diabetic animals in hyperglycemic medium, without LPS stimulation. D-BMDM showed a reduction on the expression of LC3b and Beclin-1, suggesting an impaired autophagic process in these cells.
Conclusion: The results suggest that hyperglycemia alters the inflammatory pathways in macrophages stimulated by LPS, playing an important role in the inflammatory response of diabetic individuals.
Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
(Copyright © 2023 Sousa, Queiroz, Guimarães, Pantoja, Barros, Epiphanio and Martins.)
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فهرسة مساهمة: Keywords: autophagy; diabetes mellitus; hyperglycemia; inflammation; macrophages
المشرفين على المادة: 0 (Tumor Necrosis Factor-alpha)
0 (Interleukin-6)
0 (Lipopolysaccharides)
0 (Beclin-1)
RRU6GY95IS (Nigericin)
0 (Cytokines)
IY9XDZ35W2 (Glucose)
تواريخ الأحداث: Date Created: 20230501 Date Completed: 20230502 Latest Revision: 20230502
رمز التحديث: 20230502
مُعرف محوري في PubMed: PMC10130370
DOI: 10.3389/fimmu.2023.1130662
PMID: 37122742
قاعدة البيانات: MEDLINE
الوصف
تدمد:1664-3224
DOI:10.3389/fimmu.2023.1130662