Saunders B M, Cheers C
Microbiology Department, University of Melbourne, Parkville, Victoria, Australia.
Cell Immunol. 1996 Jul 10;171(1):48-54. doi: 10.1006/cimm.1996.0171.
Following intranasal infection of mice with Mycobacterium avium complex (MAC) organisms, bacterial growth plateaued at the fourth week postinfection and then remained relatively constant thereafter. Inflammatory cell numbers in the lungs increased 10-fold by 4 weeks postinfection, and lung cell cytotoxicity and the production of NO, H202, and 02- by lung cell cultures had all increased significantly by this time and remained elevated throughout the 15-week experimental study. Although these parameters are generally associated with increased bactericidal activity, there appeared to be a defect in phagocytosis by lung cells, so that bactericidal activity could not be demonstrated in either in vitro or in vivo experiments. This study suggests that following intranasal infection with MAC, inflammatory cells are activated, sufficient to prevent further bacterial growth in vivo but not sufficient to clear the infection. We suggest that the deficiency may lie in the phagocytic activity of the cells.
用鸟分枝杆菌复合群（MAC）菌株经鼻感染小鼠后，细菌生长在感染后第四周达到平台期，此后保持相对稳定。感染后4周，肺内炎性细胞数量增加了10倍，此时肺细胞毒性以及肺细胞培养物中NO、H2O2和O2-的产生均显著增加，并在整个15周的实验研究中一直保持升高。尽管这些参数通常与杀菌活性增加相关，但肺细胞吞噬作用似乎存在缺陷，因此在体外或体内实验中均未显示出杀菌活性。本研究表明，经鼻感染MAC后，炎性细胞被激活，足以在体内阻止细菌进一步生长，但不足以清除感染。我们认为缺陷可能在于细胞的吞噬活性。
