Skip to main content
. Author manuscript; available in PMC: 2010 Jun 29.
Published in final edited form as: Microbes Infect. 2007 Jun 9;9(11):1285–1290. doi: 10.1016/j.micinf.2007.05.020

Fig. 4.

Fig. 4

Representative photomicrographs of lung sections of C57BL/6 mice infected with M. tuberculosis H37Rv wild-type, mce1 mutant and complemented strains. At 12 weeks, more extensive lesions were present in the mce1 mutant group compared to wild-type and complemented groups (hematoxylin/eosin stain; magnification ×20, bar = 300 μm) (A, B, C). At 21 weeks, >90% of the lung parenchyma were affected in mice infected with the mce1 mutant, compared to 50–60% for mice infected with the wild type or complemented mutant (hematoxylin/eosin stain; magnification ×20, bar = 300 μm) (D, E, F). At different magnification (×100, bar = 60 μm) (G, H, I), lesions showed nodular pattern with lymphocyte cuffing around airways or lymphocytes densely packed in clusters in the wild type and complemented groups (asterisks), while in the mce1 mutant group lymphocytes are more dispersed in the parenchyma intermingled with the foamy macrophage population (arrows). Just before death, no difference in the number of bacilli was observed, and they were evenly distributed inside macrophages, in all groups (solid arrows) (Ziehl-Neelsen method; magnification ×1000, bar = 6 μm) (J, K, L).