Aspirin significantly decreases the nonopsonic phagocytosis and immunogenicity of macrophages in mice

被引：11

作者：

Javeed, Aqeel ^{[1
,2
]}

Hou, Yuzhu ^{[1
,2
]}

Duan, Kaizhong ^{[1
,2
]}

Zhang, Baojun ^{[1
,2
]}

Shen, Hong ^{[1
,2
,3
]}

Cao, Yuhong ^{[1
,2
]}

Zhao, Yong ^{[1
,2
]}

机构：

[1] Chinese Acad Sci, Inst Zool, State Key Lab Biomembrane & Membrane Biotechnol, Transplantat Biol Res Div, Beijing 100101, Peoples R China

[2] Chinese Acad Sci, China US Res Ctr Life Sci, Beijing 100101, Peoples R China

[3] China Agr Univ, Dept Anim Sci & Technol, Beijing 100094, Peoples R China

来源：

INFLAMMATION RESEARCH | 2011年 / 60卷 / 04期

关键词：

Aspirin; Macrophages; Phagocytosis; Immunogenicity; MIXED ALLOGENEIC CHIMERAS; REGULATORY T-CELLS; INDUCIBLE CYCLOOXYGENASE; RESIDENT MACROPHAGES; ANTIGEN PRESENTATION; SODIUM-SALICYLATE; DENDRITIC CELLS; RECOGNITION; TRANSPLANTATION; HETEROGENEITY;

D O I：

10.1007/s00011-010-0283-4

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

The effect of acetylsalicyclic acid (ASA) on the phagocytosis and immunogenicity of macrophages remains to be determined. BALB/c mice and peritoneal macrophages were used. BALB/c mice were treated with ASA (0, 6, or 60 mg/kg/day) intraperitoneally for 1 week. Flow cytometry and phagocytosis assay were employed. ASA significantly decreased cell numbers, nonopsonic phagocytosis, and immunogenicity as well as changing the phenotypes of peritoneal macrophages in vivo. After in vitro treatment with ASA, macrophages expressed low levels of MHC-II, CD80, and CD47 molecules, and showed significantly decreased phagocytosis. Importantly, ASA blocked the differentiation of macrophages from bone marrow cells in vitro as indicated by decreased macrophage cell numbers and phenotype alteration. The present study provides basic information on the direct effect of ASA on macrophages, supporting the potential application of ASA in patients with allo-grafts or autoimmune diseases.

引用

页码：389 / 398

页数：10

共 34 条

[1] Prostaglandin E2 inhibits alveolar macrophage phagocytosis through an E-prostanoid 2 receptor-mediated increase in intracellular cyclic AMP [J].