Group V Secretory Phospholipase A2 Modulates Phagosome Maturation and Regulates the Innate Immune Response against Candida albicans 1
Group V Secretory Phospholipase A2 Modulates Phagosome Maturation and Regulates the Innate Immune Response against Candida albicans 1
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V 组分泌性磷脂酶 A2 调节吞噬体成熟并调节针对白色念珠菌的先天免疫反应 1
作者：
B. Balestrieri;A. Maekawa;W. Xing;M. Gelb;H. Katz;J. Arm
磷脂酶A2（PLA 2）水解细胞膜磷脂的sn-2位置以释放脂肪酸和溶血磷脂。我们以前曾报道，V组分泌型PLA 2（sPLA 2）从高尔基体和回收内体的小鼠腹腔巨噬细胞新形成的吞噬体和调节酵母聚糖的吞噬作用，这表明在先天免疫中的作用。在这里，我们报告说，在缺乏V组sPLA 2的巨噬细胞，吞噬体成熟减少50-60%，在早期的时间点，而酵母聚糖的结合是不受损害的。V组sPLA 2调节吞噬作用的能力扩展到IgG和补体调理的绵羊红细胞的吞噬作用。此外，缺乏V组sPLA 2的巨噬细胞在吞噬、吞噬体成熟和杀死白色念珠菌方面有延迟。细胞因子的产生和类花生酸的产生并没有受到V组sPLA 2缺乏的影响。此外，在系统性念珠菌病模型中，缺乏V组sPLA 2的小鼠在感染后第7天肾脏、肝脏和脾脏中的真菌负荷增加，死亡率增加。因此，V组sPLA 2通过主要的吞噬受体调节吞噬作用，并有助于针对C.白念珠菌通过调节吞噬作用和通过可能依赖于吞噬溶酶体融合的机制杀死。
Phospholipase A2 (PLA2) hydrolyzes the sn-2 position of cell membrane phospholipids to release fatty acids and lysophospholipids. We have previously reported that group V secretory PLA2 (sPLA2) translocates from the Golgi and recycling endosomes of mouse peritoneal macrophages to newly formed phagosomes and regulates the phagocytosis of zymosan, suggesting a role in innate immunity. Here we report that in macrophages lacking group V sPLA2, phagosome maturation was reduced 50–60% at early time points while the binding of zymosan was unimpaired. The ability of group V sPLA2 to regulate phagocytosis extended to phagocytosis of IgG- and complement-opsonized sheep RBC. Moreover, macrophages lacking group V sPLA2 had delays in phagocytosis, phagosome maturation, and killing of Candida albicans. Cytokine production and eicosanoid generation were not impaired by the lack of group V sPLA2. Furthermore, in a model of systemic candidiasis, mice lacking group V sPLA2 had an increased fungal burden in the kidney, liver, and spleen at day 7 postinfection and increased mortality. Thus, group V sPLA2 regulates phagocytosis through major phagocytic receptors and contributes to the innate immune response against C. albicans by regulating phagocytosis and killing through a mechanism that is likely dependent on phagolysosome fusion.
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人类单核细胞上的β-葡聚糖可抑制受体：其与补体替代途径颗粒激活剂的吞噬细胞受体的同一性。
DOI：
--
发表时间：
1985
期刊：
Journal of immunology (Baltimore, Md. : 1950)
影响因子：
--
作者：
Czop,JK;Austen,KF
通讯作者：
Austen,KF
DOI：
10.1128/.61.2.170-192.1997
发表时间：
1997-06
期刊：
Microbiology and molecular biology reviews : MMBR
影响因子：
--
作者：
A. Vázquez-Torres;E. Balish
通讯作者：
A. Vázquez-Torres;E. Balish
影响因子：
15.9
作者：
Netea, Mihai G.;Gow, Neil A. R.;Kullberg, Bart Jan
通讯作者：
Kullberg, Bart Jan
影响因子：
2.2
作者：
Henry-Stanley, MJ;Garni, RM;Wells, CL
通讯作者：
Wells, CL