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Ciliostasis and loss of cilia induced by Mycoplasma hyopneumoniae in porcine tracheal organ cultures.

机译:猪气管器官培养物中猪肺炎支原体引起的纤毛停滞和纤毛丢失。

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摘要

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.
机译:将体内和体外生长的猪肺炎支原体微生物接种到新生仔猪气管器官培养物中,以提供该微生物与纤毛呼吸道上皮相互作用的模型。体内生长的猪肺炎支原体和体外生长的低传代培养物诱导气管环的纤毛停滞和纤毛丢失。即使由猪肺炎支原体引起的纤毛停滞和纤毛损失广泛,气管环上皮中钙调蛋白或脱氢酶的水平也没有改变。诱导上皮损伤的能力随着生物体的体外传代而降低。尝试通过补充猪肺提取物的支原体培养基来诱导高传代培养物附着在纤毛上,引起纤毛停滞或引起纤毛损伤。通过使用猪免疫血清或通过使用0.1微米孔径的膜将纤毛与纤毛分离,可以避免由猪肺炎支原体在气管环中引起的上皮损害。在该模型中,猪肺炎支原体与纤毛上皮的附着或至少紧密缔合似乎是诱导纤毛稳定和纤毛丧失的必要条件。

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