Evengård B, Sandstedt K, Bölske G, Feinstein R, Riesenfelt-Orn I, Smith C I
Department of Immunology, Microbiology, Pathology and Infectious Diseases, Karolinska Institute, Huddinge Hospital, Sweden.
Clin Exp Immunol. 1994 Dec;98(3):388-94. doi: 10.1111/j.1365-2249.1994.tb05502.x.
Mycoplasma pulmonis or Myc. pneumoniae were inoculated intranasally to C.B-17 scid/scid mice (severe combined immunodeficient (SCID) mice). Immunocompetent C.B-17 mice were inoculated as controls. During the observation period of 5 weeks the mice were killed and necropsied. Mycoplasma pulmonis was recovered from all of the inoculated mice, and dissemination to various tissues increased with time. SCID mice, unlike immunocompetent mice, did not show lung lesions but exhibited severe inflammatory changes of the joints. Mycoplasma pulmonis, however, was isolated both from the lungs and the articular lesions. In addition, SCID mice infected for more than 3 weeks suffered from a pronounced loss of weight and emaciation. In the experiment with Myc. pneumoniae the agent could be reisolated, but lesions were not found in any of the infected mice. Mycoplasma pulmonis infection in SCID mice may be useful as a model of arthritis in immunodeficient humans.
将肺炎支原体或肺炎支原体经鼻接种到C.B-17 scid/scid小鼠(严重联合免疫缺陷(SCID)小鼠)体内。将具有免疫活性的C.B-17小鼠作为对照进行接种。在5周的观察期内,将小鼠处死并进行尸检。从所有接种的小鼠中均分离出肺炎支原体,且随着时间推移,其在各组织中的播散有所增加。与具有免疫活性的小鼠不同,SCID小鼠未出现肺部病变,但出现了严重的关节炎症变化。然而,在肺部和关节病变处均分离出了肺炎支原体。此外,感染超过3周的SCID小鼠体重明显减轻且消瘦。在肺炎支原体实验中,该病原体可再次分离得到,但在任何感染小鼠中均未发现病变。SCID小鼠中的肺炎支原体感染可能作为免疫缺陷人类关节炎的模型。