EXPRESSION OF PEROXIDASE-ACTIVITY IN RAT TRACHEAL EPITHELIAL-CELLS ASSOCIATED WITH MYCOPLASMA-PULMONIS
EXPRESSION OF PEROXIDASE-ACTIVITY IN RAT TRACHEAL EPITHELIAL-CELLS ASSOCIATED WITH MYCOPLASMA-PULMONIS
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DOI：
10.1152/ajplung.1992.262.1.l92
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发表时间：
1992-01-01
影响因子：
--
通讯作者：
HIRAI, KI
中科院分区：
文献类型：
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作者：
KINBARA, M;UEDA, T;HIRAI, KI
内源性过氧化物酶活性尚未定位于特定病原体（SPF）大鼠的气管粘膜上皮细胞。 SPF大鼠自然感染肺支原体后，过氧化物酶活性定位于气管纤毛或粘液分泌细胞的内质网、核被膜和高尔基体。 部分分泌细胞偶见过氧化物酶阳性分泌颗粒。 在1 wk M.发现肺吸虫附着于这些上皮细胞，然后在2wk时这些上皮细胞显示阳性过氧化物酶活性。 血清抗M. 5 wk时肺组织染色阳性。 这些结果表明，毒力支原体感染和相互作用与气管上皮细胞触发从头表达的过氧化物酶活性，这似乎发挥了作用，粘膜抗菌防御机制。
Endogenous peroxidase activity has not been localized in the tracheal mucosal epithelial cells of specific pathogen-free (SPF) rats. After natural infection with Mycoplasma pulmonis in SPF rats, peroxidase activity became localized to the endoplasmic reticulum, nuclear envelope, and Golgi apparatus of tracheal ciliated or mucous secretory cells. Some secretory cells occasionally had peroxidase-positive secretory granules. At 1 wk M. pulmonis was found to attach to these epithelial cells, which then showed positive peroxidase activity at 2 wk. Serum antibody titers against M. pulmonis were positive at 5 wk. These results suggest that virulent mycoplasma infection and interaction with the tracheal epithelial cells trigger the de novo expression of peroxidase activity, which seems to play a role in mucosal antimicrobial defense mechanisms.