PRIMING OF HUMAN POLYMORPHONUCLEAR NEUTROPHILIC LEUKOCYTES BY INSULIN-LIKE GROWTH-FACTOR-I - INCREASED PHAGOCYTIC CAPACITY, COMPLEMENT RECEPTOR EXPRESSION, DEGRANULATION, AND OXIDATIVE BURST
PRIMING OF HUMAN POLYMORPHONUCLEAR NEUTROPHILIC LEUKOCYTES BY INSULIN-LIKE GROWTH-FACTOR-I - INCREASED PHAGOCYTIC CAPACITY, COMPLEMENT RECEPTOR EXPRESSION, DEGRANULATION, AND OXIDATIVE BURST
复制标题
DOI：
10.1210/jc.80.6.1948
复制
发表时间：
1995-06-01
影响因子：
5.8
通讯作者：
AARSKOG, D
中科院分区：
文献类型：
--
作者：
BJERKNES, R;AARSKOG, D
胰岛素样生长因子I（IGF-I）是一种调节哺乳动物生长的GH依赖性肽，对于免疫系统的正常发育和功能似乎很重要。多形核中性粒细胞白细胞（PMNL）是宿主防御必不可少的终极分化的吞噬细胞，在本研究中，重组人IGF-I被证明是成熟人类PMNL的强大引物。 IGF-I增加了两种免疫球蛋白G-opsonized葡萄球菌和补体的白色念珠菌的PMNL吞噬作用。此外，生长因子增加了PMNL补体受体表达[补体受体I（CD35）和3（CD11b）]，并将细胞启动至更强的F-Met-Leu-Phe诱导的特异性和硫粒颗粒的脱粒化[标记：CD11B：CD11B ，CD35和CD67（特定颗粒）； CD63（Azurophilic颗粒）]。相比之下，IGF-I没有改变FC Gamma RI（CD64），FC Gamma RII ：（ CDW32）或FC Gamma RIII（CD16）的PMNL表面表达。暴露于IGF-I的PMNL增加了其F-met-Leu-Phe和佛罗杆菌肉豆蔻酸酯诱导的氧化爆发，如通过过氧化氢的产生评估，而IGF-I不影响PMNL肌动蛋白聚合。 TGF-I对PMNL的启动取决于时间和浓度，并且对IGF-I受体的单克隆抗体的饱和量使该肽对PMNL的启动进行了黑色。这些实验表明，IGF-I可以选择性地刺激成熟的PMNL功能，从而进一步证明免疫系统与内分泌系统之间的相互作用。
Insulin-like growth factor I (IGF-I) is a GH-dependent peptide regulating mammalian growth that seems to be of importance for the normal development and function of the immune system. Polymorphonuclear neutrophilic leukocytes (PMNLs) are terminally differentiated phagocytes essential for host defense, and in the present study, recombinant human IGF-I was shown to be a powerful primer of mature human PMNLs. IGF-I augmented the PMNL phagocytosis of both immunoglobulin G-opsonized Staphylococcus aureus and complement-opsonized Candida albicans. In addition, the growth factor increased PMNL complement receptor expression [complement receptors I (CD35) and 3 (CD11b)] and primed the cells to stronger f-met-leu-phe-induced degranulation of both specific and azurophilic granules [markers: CD11b, CD35 and CD67 (specific granules); CD63 (azurophilic granules)]. In contrast, IGF-I did not alter the PMNL surface expression of Fc gamma RI (CD64), Fc gamma RII: (CDw32), or Fc gamma RIII (CD16). PMNLs exposed to IGF-I increased their f-met-leu-phe and phorbol myristate acetate-induced oxidative burst, as evaluated by hydrogen peroxide production, whereas IGF-I did not influence PMNL actin polymerization. The priming of PMNLs by TGF-I was dependent on time and concentration, and saturating amounts of a monoclonal antibody to the IGF-I receptor blacked the priming of PMNLs by this peptide. These experiments demonstrate that IGF-I can selectively stimulate mature PMNL functions, providing further evidence for the interaction between the immune and the endocrine systems.