Impaired phagocytosis in caveolin-1 deficient macrophages

被引:57
作者
Li, JW
Scherl, A
Medina, F
Frank, PG
Kitsis, RN
Tanowitz, HB
Sotgia, F
Lisanti, MP
机构
[1] Albert Einstein Coll Med, Dept Mol Pharmacol, Bronx, NY 10461 USA
[2] Albert Einstein Coll Med, Dept Med, Bronx, NY 10461 USA
[3] Albert Einstein Coll Med, Albert Einstein Canc Ctr, Bronx, NY 10461 USA
[4] Albert Einstein Coll Med, Dept Urol, Bronx, NY 10461 USA
[5] Albert Einstein Coll Med, Dept Cell Biol, Bronx, NY 10461 USA
[6] Albert Einstein Coll Med, Cardiovasc Res Ctr, Bronx, NY 10461 USA
[7] Albert Einstein Coll Med, Dept Pathol, Bronx, NY 10461 USA
[8] Univ Genoa, Muscular & Neurodegenerat Dis Unit, Genoa, Italy
[9] G Gaslini Pediat Inst, Genoa, Italy
关键词
caveolae; caveolin-1; macrophage; phagocytosis; innate immunity; autoimmune disease; apoptosis;
D O I
10.4161/cc.4.11.2117
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Caveolae are plasma membrane invaginations that function as important regulators of numerous cellular processes, including signal transduction, cholesterol trafficking, and endocytosis. Caveolin-1 (Cav-1) constitutes the main structural protein of caveolae membranes. Here, we report an in vivo increase in the number of apoptotic cells in the thymus and spleen of Cav-1 deficient mice, following whole-body gamma-irradiation. We demonstrate that this increase in apoptotic cells is not due to increased apoptosis in lymphocytes per se, which normally do not express Cav-1, but rather to the decreased phagocytic clearance of apoptotic cells by macrophages, which do express Cav-1. Utilizing in vitro phagocytosis assays of both apoptotic thymocytes and Escherichia coli K-12 BioParticles, we demonstrate that the loss of Cav-1 decreases the phagocytic ability of thioglycollate-elicited peritoneal macrophages. We suggest that impaired macrophage phagocytosis in Cav-1 knockout mice could have implications for altered innate immunity against pathogens, the regulation of inflammatory responses, and the development of autoimmune disease.
引用
收藏
页码:1599 / 1607
页数:9
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