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Dysfunctional phagocytosis capacity, granulocyte recruitment and inflammatory factor secretion of Kupffer cells in diabetes mellitus reversed by Lidocaine

Authors Wang R, Sheng M, Shi F, Zhao Y, Zhao L, Wu J, Wu G, Song Q

Received 6 September 2018

Accepted for publication 17 October 2018

Published 26 November 2018 Volume 2018:11 Pages 827—834

DOI https://doi.org/10.2147/DMSO.S186695

Checked for plagiarism Yes

Review by Single-blind

Peer reviewers approved by Dr Colin Mak

Peer reviewer comments 3

Editor who approved publication: Dr Juei-Tang Cheng


Ruibin Wang,1 Minjia Sheng,2 Feng Shi,3 Yanjie Zhao,4 Lin Zhao,5 Jiangping Wu,4 Guangjiang Wu,6 Qingkun Song7–9

1Department of Emergency, Beijing Shijitan Hospital, Capital Medical University, Beijing 100038, China; 2Department of Gynaecology and Obstetrics, China-Japan Union Hospital of Jilin University, Changchun, Jilin 130033, China; 3Department of Pathology, Beijing Shijitan Hospital, Capital Medical University, Beijing 100038, China; 4Department of Medical Oncology, Beijing Shijitan Hospital, Capital Medical University, Beijing 100038, China; 5Department of Medical Records and Statistics, Xuanwu Hospital, Capital Medical University, Beijing 100045, China; 6Department of Infection Control, Beijing Shijitan Hospital, Capital Medical University, Beijing 100038, China; 7Department of Gynaecology and Obstetrics, Beijing Key Laboratory of Cancer Therapeutic Vaccine, Beijing 100038, China; 8Department of Evidence-based Medicine, Oncology School of Capital Medical University, Beijing 100038, China; 9Department of Science and Technology, Beijing Shijitan Hospital, Capital Medical University, Beijing 100038, China

Purpose: Kupffer cells (KCs) present dysfunctional immunity capacity among the diabetes mellitus patients. This study aims to investigate whether Lidocaine could reverse dysfunctions of KCs, in terms of phagocytosis, granulocyte recruitment and inflammatory mediator secretion.
Methods: db/db and C57BL/6 mice were employed to establish diabetic and nondiabetic models. Upon intravenous injection of Lidocaine, KCs were isolated and cultured ex vivo. The functions of phagocytosis, recruiting granulocytes and inflammatory mediator secretion in KCs were compared between Lidocaine-treated and untreated (control) groups.
Results: Comparing with nondiabetic mice, KCs in diabetic mice presented reduced phagocytosis, activated granulocyte recruitment, increased expression of intercellular cell adhesion molecule-1 (ICAM-1) and activated levels of inflammatory mediators. With Lidocaine injection, phagocytic functions of KCs in diabetic mice were improved significantly; in contrast, recruitment of granulocytes, expression of ICAM-1 and secretion of inflammatory mediators were reduced markedly. However, Lidocaine intervention did not alter KC functions in phagocytosis, granulocyte recruitment, ICAM-1 expression or inflammatory mediator secretion among nondiabetic mice.
Conclusion: Lidocaine reversed diabetes-related dysfunctions of KCs in terms of phagocytosis, granulocyte recruitment, ICAM-1 expression or inflammatory mediator secretion.

Keywords: macrophages, diabetes, phagocytosis, granulocyte recruitment, inflammatory mediator, Lidocaine
 

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