Altered Polarization, Morphology, and Impaired Innate Immunity Germane to Resident Peritoneal Macrophages in Mice with Long-Term Type 2 Diabetes

Type 2 diabetes (T2D) is associated with perturbed innate immunity. Macrophages, bridging innate immunity and metabolic disturbances, play important roles in controlling immune homeostasis. However, the effect of long-term diabetic milieu (DM) on the functions and phenotypes of macrophages is still...

Full description

Saved in:
Bibliographic Details
Published inJournal of biomedicine & biotechnology Vol. 2012; no. 2012; pp. 1 - 9
Main Authors Liu, Hui-Fang, Zhang, Hui-Jie, Hu, Qi-Xian, Liu, Xiao Yan, Wang, Zhi-Quan, Fan, Jia-Yan, Zhan, Ming, Chen, Feng-Ling
Format Journal Article
LanguageEnglish
Published Cairo, Egypt Hindawi Puplishing Corporation 2012
Online AccessGet full text

Cover

Loading…
More Information
Summary:Type 2 diabetes (T2D) is associated with perturbed innate immunity. Macrophages, bridging innate immunity and metabolic disturbances, play important roles in controlling immune homeostasis. However, the effect of long-term diabetic milieu (DM) on the functions and phenotypes of macrophages is still not clear. In this study, we used resident peritoneal macrophages (RPMs) from 5-month-old db/db mice to investigate the changes of macrophages. It was found that RPMs in db/db mice significantly reduced phagocytosis and adhesion capacity. After standardization with body weight, the number of F4/80+ RPMs markedly reduced in db/db mice, and, furthermore, the macrophages skewed to M2-polarizated macrophages. The results of morphology found that the RPMs shape of db/db mice was nearly round, but the RPMs shape of control mice was spindle-shaped and irregular. In this study, we found the cell numbers, morphology, and innate immunity functions of RPMs in 5-month-old type 2 diabetic mice (db/db mice) obtained by abdominal cavity lavage were significantly altered. Importantly, we also found the remarkably increased M2-RPMs in diabetic mice for the first time.
ISSN:1110-7243
1110-7251