دورية أكاديمية

Insulin Modulates Cytokine Release, Collagen and Mucus Secretion in Lung Remodeling of Allergic Diabetic Mice.

التفاصيل البيبلوغرافية
العنوان: Insulin Modulates Cytokine Release, Collagen and Mucus Secretion in Lung Remodeling of Allergic Diabetic Mice.
المؤلفون: Ferreira SS; Laboratory of Immunoendocrinology, Department of Clinical and Toxicological Analyses, Faculty of Pharmaceutical Sciences of University São Paulo (FCF/USP), São Paulo, Brazil., Nunes FPB; Laboratory of Immunoendocrinology, Department of Clinical and Toxicological Analyses, Faculty of Pharmaceutical Sciences of University São Paulo (FCF/USP), São Paulo, Brazil., Casagrande FB; Laboratory of Immunoendocrinology, Department of Clinical and Toxicological Analyses, Faculty of Pharmaceutical Sciences of University São Paulo (FCF/USP), São Paulo, Brazil., Martins JO; Laboratory of Immunoendocrinology, Department of Clinical and Toxicological Analyses, Faculty of Pharmaceutical Sciences of University São Paulo (FCF/USP), São Paulo, Brazil.
المصدر: Frontiers in immunology [Front Immunol] 2017 Jun 09; Vol. 8, pp. 633. Date of Electronic Publication: 2017 Jun 09 (Print Publication: 2017).
نوع المنشور: Journal Article
اللغة: English
بيانات الدورية: Publisher: Frontiers Research Foundation] Country of Publication: Switzerland NLM ID: 101560960 Publication Model: eCollection Cited Medium: Print ISSN: 1664-3224 (Print) Linking ISSN: 16643224 NLM ISO Abbreviation: Front Immunol Subsets: PubMed not MEDLINE
أسماء مطبوعة: Original Publication: [Lausanne : Frontiers Research Foundation]
مستخلص: Introduction: The role of insulin in lung remodeling in a model of asthma in healthy and diabetic mice was evaluated.
Material and Methods: Diabetic male BALB/c mice (alloxan, 50 mg/kg, intravenous) and controls were sensitized by subcutaneous (s.c.) injection of ovalbumin (OA, 20 µg) in aluminum hydroxide (Al(OH) 3 , 2 mg) 10 days after the alloxan injection and received the same dose 12 days later. Six days after the last sensitization, animals were nebulized with OA solution for 7 days. The first set of diabetic and control mice received 2 and 1 IU, respectively, of s.c. neutral protamine Hagedorn (NPH) insulin and were analyzed 8 h later. The second set of diabetic and control mice received 2 and 1 IU, respectively, of insulin 12 h before the OA challenge and half doses of insulin 2 h before each the seven OA challenges. Twenty-four hours after the last challenge, the following analyses were performed: (a) quantification of the cells in the bronchoalveolar lavage fluid (BALF), the white cell count, and blood glucose; (b) morphological analysis of lung tissues by hematoxylin and eosin staining; (c) quantification of collagen deposition in lung tissues and mucus by morphometric analysis of histological sections stained with Masson's trichrome and periodic acid-Schiff (PAS), respectively; and (d) quantification of the cytokine concentrations (IL-4, IL-5, and IL-13) in the BALF supernatant.
Results: Compared to controls, diabetic mice had significantly reduced inflammatory cells (81%) in the BALF, no eosinophils in the BALF and peripheral blood and reduced collagen deposition and mucus in the lungs. BALF concentrations of IL-4 (48%) and IL-5 (31%) decreased and IL-13 was absent. A single dose of insulin restored peripheral blood eosinophils and BALF mononuclear cells but not BALF eosinophils, collagen deposition, and mucus levels. However, multiple doses of insulin restored both total cells and eosinophils in the BALF and peripheral blood, BALF cytokines, and collagen deposition and mucus secretion into the lungs.
Conclusion: The results suggest that insulin modulates the production/release of cytokines, cell migration, deposition of collagen, and mucus secretion in lung remodeling of a mouse model of asthma.
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فهرسة مساهمة: Keywords: asthma; collagen; diabetes mellitus; eosinophils; insulin; lung; mucus; remodeling
تواريخ الأحداث: Date Created: 20170627 Latest Revision: 20240601
رمز التحديث: 20240601
مُعرف محوري في PubMed: PMC5465276
DOI: 10.3389/fimmu.2017.00633
PMID: 28649241
قاعدة البيانات: MEDLINE
الوصف
تدمد:1664-3224
DOI:10.3389/fimmu.2017.00633