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Pathological Alternations of Mediastinal Fat-Associated Lymphoid Cluster and Lung in a Streptozotocin-Induced Diabetic Mouse Model

Published online by Cambridge University Press:  21 December 2020

Yaser H.A. Elewa*
Affiliation:
Department of Histology and Cytology, Faculty of Veterinary Medicine, Zagazig University, Zagazig, Egypt Laboratory of Anatomy, Department of Basic Veterinary Sciences, Faculty of Veterinary Medicine, Hokkaido University, Kita18-Nishi 9, Kita-Ku, Sapporo, Hokkaido060-0818, Japan
Osamu Ichii
Affiliation:
Laboratory of Anatomy, Department of Basic Veterinary Sciences, Faculty of Veterinary Medicine, Hokkaido University, Kita18-Nishi 9, Kita-Ku, Sapporo, Hokkaido060-0818, Japan Laboratory of Agrobiomedical Science, Faculty of Agriculture, Hokkaido University, Sapporo, Japan
Teppei Nakamura
Affiliation:
Laboratory of Anatomy, Department of Basic Veterinary Sciences, Faculty of Veterinary Medicine, Hokkaido University, Kita18-Nishi 9, Kita-Ku, Sapporo, Hokkaido060-0818, Japan Department of Biological Safety Research, Chitose Laboratory, Japan Food Research Laboratories, Chitose, Japan
Yasuhiro Kon
Affiliation:
Laboratory of Anatomy, Department of Basic Veterinary Sciences, Faculty of Veterinary Medicine, Hokkaido University, Kita18-Nishi 9, Kita-Ku, Sapporo, Hokkaido060-0818, Japan
*
*Author for correspondence: Yaser Elewa, E-mail: y-elewa@vetmed.hokudai.ac.jp, yaserelewa@zu.edu.eg
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Abstract

Diabetes is a devastating global health problem and is considered a predisposing factor for lung injury progression. Furthermore, previous reports of the authors revealed the role of mediastinal fat-associated lymphoid clusters (MFALCs) in advancing respiratory diseases. However, no reports concerning the role of MFALCs on the development of lung injury in diabetes have been published. Therefore, this study aimed to examine the correlations between diabetes and the development of MFALCs and the progression of lung injury in a streptozotocin-induced diabetic mouse model. Furthermore, immunohistochemical analysis for immune cells (CD3+ T-lymphocytes, B220+ B-lymphocytes, Iba1+ macrophages, and Gr1+ granulocytes), vessels markers (CD31+ endothelial cells and LYVE-1+ lymphatic vessels “LVs”), and inflammatory markers (TNF-α and IL-5) was performed. In comparison to the control group, the diabetic group showed lung injury development with a significant increase in MFALC size, immune cells, LVs, and inflammatory marker, and a considerable decrease of CD31+ endothelial cells in both lung and MFALCs was observed. Furthermore, the blood glucose level showed significant positive correlations with MFALCs size, lung injury, immune cells, inflammatory markers, and LYVE-1+ LVs in lungs and MFALCs. Thus, we suggest that the development of MFALCs and LVs could contribute to lung injury progression in diabetic conditions.

Type
Biological Applications
Copyright
Copyright © The Author(s), 2020. Published by Cambridge University Press

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