Goodrum K J, Guzman G S, Lindsey J R, Silberman M, Spitznagel J K
J Leukoc Biol. 1984 Aug;36(2):161-71. doi: 10.1002/jlb.36.2.161.
Elicited peritoneal macrophages from Sprague-Dawley rats conventionally bred and housed failed, as we have reported, to produce detectable elastolytic activity in culture. They did produce lysozyme and plasminogen activator. We now show that in contrast to these cells, macrophages from pathogen-free, barrier-sustained rats produced readily demonstrable elastolytic activity. Rats raised pathogen-free and subsequently housed conventionally for 2-4 wk appeared to lose the capacity to afford macrophages producing elastase. At the same time they acquired infections with several rat pathogens including Spironucleus muris, Kilham rat virus, sialodacryoadinitis virus, and mycoplasma pulmonis. The acquisition by the rats of one or more of these infections, conditions conducive to infection, or both factors may have suppressed their capacity to yield elastolytic activity.
正如我们所报道的,常规饲养和圈养的斯普拉格-道利大鼠诱导产生的腹膜巨噬细胞在培养中未能产生可检测到的弹性蛋白酶活性。它们确实产生了溶菌酶和纤溶酶原激活物。我们现在表明,与这些细胞不同,来自无病原体、屏障维持饲养的大鼠的巨噬细胞产生了易于证明的弹性蛋白酶活性。无病原体饲养随后常规饲养2 - 4周的大鼠似乎失去了提供产生弹性蛋白酶的巨噬细胞的能力。与此同时,它们感染了几种大鼠病原体,包括鼠螺旋体、基尔汉姆大鼠病毒、涎泪腺炎病毒和肺炎支原体。大鼠感染这些感染中的一种或多种、有利于感染的条件或这两个因素可能都抑制了它们产生弹性蛋白酶活性的能力。