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缺乏三种髓系集落刺激因子(粒细胞集落刺激因子、粒细胞-巨噬细胞集落刺激因子和巨噬细胞集落刺激因子)的小鼠仍能产生巨噬细胞和粒细胞,并在无菌性腹膜炎模型中引发炎症反应。

Mice lacking three myeloid colony-stimulating factors (G-CSF, GM-CSF, and M-CSF) still produce macrophages and granulocytes and mount an inflammatory response in a sterile model of peritonitis.

作者信息

Hibbs Margaret L, Quilici Cathy, Kountouri Nicole, Seymour John F, Armes Jane E, Burgess Antony W, Dunn Ashley R

机构信息

Signal Transduction Laboratory, Ludwig Institute for Cancer Research, Melbourne Tumour Biology Branch, Royal Melbourne Hospital, Victoria, and Department of Medicine, University of Melbourne, Parkville, Australia.

出版信息

J Immunol. 2007 May 15;178(10):6435-43. doi: 10.4049/jimmunol.178.10.6435.

Abstract

To assess the combined role of G-CSF, GM-CSF, and M-CSF in myeloid cell production, mice deficient in all three myeloid CSFs were generated (G-/-GM-/-M-/- mice). G-/-GM-/-M-/- mice share characteristics found in mice lacking individual cytokines: they are toothless and osteopetrotic and furthermore acquire alveolar proteinosis that is more severe than that found in either GM-/- or G-/-GM-/- mice. G-/-GM-/-M-/- mice have a significantly reduced lifespan, which is prolonged by antibiotic administration, suggesting compromised ability to control bacterial infection. G-/-GM-/-M-/- mice have circulating neutrophils and monocytes, albeit at significantly reduced numbers compared with wild-type mice, but surprisingly, have more circulating monocytes than M-/- mice and more circulating neutrophils than G-/-GM-/- mice. Due to severe osteopetrosis, G-/-GM-/-M-/- mice show diminished numbers of myeloid cells, myeloid progenitors, and B lymphocytes in the bone marrow, but have significantly enhanced compensatory splenic hemopoiesis. Although G-/-GM-/-M-/- mice have a profound deficiency of myeloid cells in the resting peritoneal cavity, the animals mount a moderate cellular response in a model of sterile peritonitis. These data establish that in the absence of G-CSF, GM-CSF, and M-CSF, additional growth factor(s) can stimulate myelopoiesis and acute inflammatory responses.

摘要

为了评估粒细胞集落刺激因子(G-CSF)、粒细胞-巨噬细胞集落刺激因子(GM-CSF)和巨噬细胞集落刺激因子(M-CSF)在髓系细胞生成中的联合作用,构建了三种髓系集落刺激因子均缺失的小鼠(G-/-GM-/-M-/-小鼠)。G-/-GM-/-M-/-小鼠具有缺乏单个细胞因子的小鼠所具有的特征:它们无牙且患骨质石化症,此外还会患上比GM-/-或G-/-GM-/-小鼠更严重的肺泡蛋白沉积症。G-/-GM-/-M-/-小鼠的寿命显著缩短,抗生素给药可延长其寿命,这表明其控制细菌感染的能力受损。G-/-GM-/-M-/-小鼠有循环中的中性粒细胞和单核细胞,尽管与野生型小鼠相比数量显著减少,但令人惊讶的是,其循环单核细胞比M-/-小鼠更多,循环中性粒细胞比G-/-GM-/-小鼠更多。由于严重的骨质石化症,G-/-GM-/-M-/-小鼠骨髓中的髓系细胞、髓系祖细胞和B淋巴细胞数量减少,但脾脏代偿性造血显著增强。尽管G-/-GM-/-M-/-小鼠在静息腹膜腔中髓系细胞严重缺乏,但在无菌性腹膜炎模型中,这些动物会产生适度的细胞反应。这些数据表明,在缺乏G-CSF、GM-CSF和M-CSF的情况下,其他生长因子可以刺激髓系造血和急性炎症反应。

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