Role of M2b Macrophages in the Acceleration of Bacterial Translocation and Subsequent Sepsis in Mice Exposed to Whole Body [137Cs] Gamma-Irradiation
Role of M2b Macrophages in the Acceleration of Bacterial Translocation and Subsequent Sepsis in Mice Exposed to Whole Body [137Cs] Gamma-Irradiation
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DOI：
10.4049/jimmunol.1200350
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发表时间：
2012-07-01
影响因子：
4.4
通讯作者：
Suzuki, Fujio
中科院分区：
文献类型：
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作者：
Kobayashi, Makiko;Nakamura, Kiwamu;Suzuki, Fujio
研究了全身照射对粪肠球菌易位的抗菌宿主防御作用的影响。用5Gy[Cs-137]伽玛射线照射或不照射小鼠，用10(6)CFU/只小鼠口服感染粪肠球菌。感染后1~4d，照射组小鼠肠系膜淋巴结检出致病菌，而正常小鼠肠系膜淋巴结未检出粪肠球菌。所有受照射的小鼠在感染后5d内全部死亡，而感染该病原体的正常小鼠则无死亡。接种正常小鼠MLN巨噬细胞(M Phi)的受照小鼠表现出对感染的抵抗力，而接种受照小鼠MLNM Phi(I-MLNM Phi)的小鼠在感染后死亡。I-MLNM Phi被鉴定为IL-10(+)IL-12(-)CCL1(+)light(+)M Phi(M2bM Phi)，并显示出抑制M Phi从常驻M Phi到IL-10(-)IL-12(+)M Phi(M1M Phi)的作用。照射后10~35d，小鼠MLN内可见M_2bM_(Phi)。粪肠球菌抗原不能诱导M1Mphi，而正常小鼠MLNMPhi可在Ag刺激下转化为M1Mphi。经CCL1反义寡核苷酸处理后，照射小鼠MLN中M2bM Phi消失，粪肠球菌刺激后MLN产生M1MPhi。这些结果表明，在I-MLNM Phi群体中存在的M2bM Phi与伽玛射线照射小鼠对细菌易位和随后的脓毒症的抵抗力减弱有关。粪肠球菌易位和随后的败血症可以通过MLN中存在的M2bM Phi的干预在免疫上得到控制。免疫学杂志，2012,189：296-303。
The influence of whole-body gamma-irradiation on the antibacterial host defense against Enterococcus faecalis translocation was investigated. Mice irradiated with or without 5 Gy [Cs-137] gamma-rays were orally infected with 10(6) CFU/mouse E. faecalis. The pathogen was detected in the mesenteric lymph nodes (MLNs) of irradiated mice 1-4 d postinfection, whereas E. faecalis was not isolated from MLNs of normal mice. All irradiated mice died within 5 d of infection, whereas no mortality was shown in normal mice infected with the pathogen. Irradiated mice inoculated with normal mouse MLN macrophages (M phi) were shown to be resistant against the infection, although the same mice inoculated with irradiated mouse MLNM phi (I-MLNM phi) died postinfection. I-MLNM phi were identified as IL-10(+)IL-12(-)CCL1(+)LIGHT(+) M phi (M2bM phi) and were shown to be inhibitory on M phi conversion from resident M phi to IL-10(-)IL-12(+)M phi (M1M phi). M2bM phi were demonstrated in MLNs of mice 10-35 d after gamma-irradiation. M1M phi were not induced by E. faecalis Ag in cultures of I-MLNM phi, whereas normal mouse MLNM phi were converted to M1M phi in response to the Ag stimulation. After treatment with CCL1 antisense oligodeoxynucleotides, M2bM phi disappeared in MLNs of irradiated mice, and M1M phi were generated in MLNs of these mice following E. faecalis stimulation. These results indicate that M2bM phi presented in the I-MLNM phi populations were responsible for the impaired resistance of mice irradiated with gamma-rays to bacterial translocation and subsequent sepsis. E. faecalis translocation and subsequent sepsis may be controlled immunologically by the intervention of M2bM phi present in MLNs. The Journal of Immunology, 2012, 189: 296-303.