Diabetes-induced alteration of F4/80+ macrophages: a study in mice with streptozotocin-induced diabetes for a long term.
Macrophages as an early stage of immune responses form a bridge between innate and acquired immunity and shape the adaptive immune response. The immunoregulatory functions of macrophages in hosts with a prolonged exposure to a diabetic milieu remain to be determined. The levels, phenotype, and immunity including antigen-presenting ability, phagocytosis and immunogenicity of F4/80+ splenic macrophages (SPMs), and peritoneal exudates macrophages (PEMs) were detected in age-matched control mice and mice with streptozotocin (STZ)-induced diabetes for 16 weeks. The numbers of F4/80+ SPMs and PEMs significantly decreased in STZ-induced diabetic mice, compared with age-matched non-diabetic mice (control) at 16 weeks after diabetes induction. Functional analysis showed that F4/80+ SPMs and PEMs in STZ-induced diabetic mice exhibit significantly lower immunogenicity and nonopsonic phagocytosis to allogeneic T cells than those of control mice both in vitro and in vivo. Coincidently, the antigen-presenting capacity of F4/80+ PEMs, but not F4/80+ SPMs, in mice with STZ-induced diabetes for 16 or more weeks is also significantly lower than that of control mice. Our results showed that total cell number and immune function of F4/80+ macrophages were significantly defective in mice with a prolonged exposure to a diabetic milieu, which may be a mechanism responsible for the increased macrophage-related complications in diabetic patients such as the high prevalence of infection and cardiovascular mortality.
Ma
Haixia
H
Transplantation Biology Research Division, State Key Laboratory of Biomembrane and Membrane Biotechnology, Institute of Zoology, Chinese Academy of Sciences, Datun Road, Chaoyang, Beijing 100101, China.
Liu
Guangwei
G
Ding
Wenjun
W
Wu
You
Y
Cai
Lu
L
Zhao
Yong
Y
D000818:Animals; D017951:Antigen Presentation; D000943:Antigens, Differentiation / Q000276:immunology*; D003921:Diabetes Mellitus, Experimental / Q000276:immunology*; D006801:Humans; D007371:Interferon-gamma / Q000276:immunology; D007376:Interleukin-2 / Q000276:immunology; D008264:Macrophages / Q000276:immunology*; D051379:Mice; D008807:Mice, Inbred BALB C; D008810:Mice, Inbred C57BL; D008822:Mice, Transgenic; D010587:Phagocytosis / Q000502:physiology; D013601:T-Lymphocytes / Q000276:immunology
D000943:Antigens, Differentiation; D007376:Interleukin-2; C036763:monocyte-macrophage differentiation antigen; D007371:Interferon-gamma