DeBey M C, Ross R F
Veterinary Medical Research Institute, Iowa State University, Ames 50011.
Infect Immun. 1994 Dec;62(12):5312-8. doi: 10.1128/iai.62.12.5312-5318.1994.
In vivo- and in vitro-grown Mycoplasma hyopneumoniae organisms were inoculated onto newborn piglet tracheal organ cultures to provide a model for interaction of this organism with ciliated respiratory epithelium. Ciliostasis and loss of cilia in tracheal rings were induced by M. hyopneumoniae grown in vivo and with low-passage cultures when grown in vitro. Levels of calmodulin or dehydrogenase enzymes in tracheal ring epithelium were not altered even though ciliostasis and loss of cilia induced by M. hyopneumoniae were extensive. The capacity for inducing epithelial damage diminished with in vitro passage of the organism. Attempts to induce higher-passage cultures to attach to cilia, cause ciliostasis, or cause ciliary damage by supplementation of mycoplasmal medium with porcine lung extract failed. Epithelial damage induced by M. hyopneumoniae in tracheal rings was averted by using porcine immune serum or by separating the organisms from ciliated epithelium with a 0.1-microns-pore-size membrane. Attachment, or at least close association, of M. hyopneumoniae to ciliated epithelium appeared to be necessary to induce ciliostasis and loss of cilia in this model.
将体内和体外培养的猪肺炎支原体接种到新生仔猪气管器官培养物上，以提供该病原体与呼吸道纤毛上皮相互作用的模型。体内生长的猪肺炎支原体以及体外低代培养的猪肺炎支原体均可诱导气管环出现纤毛运动停滞和纤毛缺失。尽管猪肺炎支原体诱导的纤毛运动停滞和纤毛缺失广泛，但气管环上皮中的钙调蛋白或脱氢酶水平并未改变。随着该病原体体外传代，其诱导上皮损伤的能力减弱。通过在支原体培养基中添加猪肺提取物来诱导高代培养物附着于纤毛、引起纤毛运动停滞或造成纤毛损伤的尝试均告失败。使用猪免疫血清或用孔径为0.1微米的膜将病原体与纤毛上皮分离，可避免猪肺炎支原体在气管环中诱导上皮损伤。在该模型中，猪肺炎支原体附着于纤毛上皮，或至少与之紧密关联，似乎是诱导纤毛运动停滞和纤毛缺失所必需的。
