CCL1 released from M2b macrophages is essentially required for the maintenance of their properties
CCL1 released from M2b macrophages is essentially required for the maintenance of their properties
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DOI：
10.1189/jlb.0212107
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发表时间：
2012-10-01
影响因子：
5.5
通讯作者：
Suzuki, Fujio
中科院分区：
文献类型：
--
作者：
Asai, Akira;Nakamura, Kiwamu;Suzuki, Fujio
烧伤后10-30天的患者极易感染。M1M Phi(IL-10(-)IL-12(+)M Phi)是宿主抗MRSA感染的天然抗菌免疫中必不可少的细胞。然而，这些效应细胞不容易在携带M2bM Phi(IL-12(-)IL-10(+)CCL1(+)light(+)M Phi)的宿主中产生。M2bM Phi对M1M Phi的生成有抑制作用。本研究通过对M2bM phi活性的调节，提高了烧伤后10-30天小鼠对MRSA感染的抗菌力。未烧伤的小鼠在烧伤后10-30天接种M Phi制剂的小鼠对MRSA感染敏感，而未烧伤的小鼠接种来自CCL1反义ODN的M Phi制剂的未烧伤小鼠对感染具有抵抗力。从烧伤第15天小鼠分离的M2bM Phi在频繁更换培养基下培养3天后失去了M2bM Phi特性，而在添加rCCL1的相同培养条件下，其M2bM Phi特性保持不变。在培养中，经CCL1反义ODN处理的第15天烧伤小鼠的M Phi制剂不产生CCL1，并在热灭活MRSA刺激后转化为M1M Phi。此外，使用ODN治疗的第15天烧伤小鼠对MRSA感染具有抵抗力。这些结果表明，从M2bM Phi释放出来的CCL1是维持其性质所必需的。烧伤后10-30天小鼠对MRSA感染的易感性增加，可通过干预严重烧伤合并M2bM phi产生CCL1来控制。J.Leukoc。比奥尔。92：859-867；2012。
Patients with 10-30 days postburn injury are greatly susceptible to infections. M1M phi (IL-10(-)IL-12(+)M phi) are essential cells in host antibacterial innate immunity against MRSA infections. However, these effector cells are not easily generated in hosts who are carriers of M2bM phi (IL-12(-)IL-10(+)CCL1(+)LIGHT(+)M phi). M2bM phi are inhibitory on M1M phi generation. In this study, the antibacterial resistance of mice, 10-30 days postburn injury against MRSA infection, was improved by the modulation of M2bM phi activities. Unburned mice inoculated with M phi preparations from mice, 10-30 days after burn injury, were susceptible to MRSA infection, whereas unburned mice, inoculated with M phi preparations from the same mice that were previously treated with CCL1 antisense ODN, were resistant to the infection. M2bM phi, isolated from Day 15 burn mice, lost their M2bM phi properties 3 days after cultivation under frequent medium changes, whereas their M2bM phi properties remained in the same cultures supplemented with rCCL1. In cultures, M phi preparations from Day 15 burn mice treated with CCL1 antisense ODN did not produce CCL1 and did convert to M1M phi after heat-killed MRSA stimulation. Also, Day 15 burn mice treated with the ODN became resistant against MRSA infection. These results indicate that CCL1 released from M2bM phi is essentially required for the maintenance of their properties. The increased susceptibility of mice, 10-30 days after burn injury to MRSA infection, may be controlled through the intervention of CCL1 production by M2bM phi appearing in association with severe burn injuries. J. Leukoc. Biol. 92: 859-867; 2012.