Chlamydia trachomatis is an obligate intracellular bacterium responsible for one 
of the most common sexually transmitted diseases. In epithelial cells, C. 
trachomatis resides in a modified membrane-bound vacuole known as an inclusion, 
which is isolated from the endocytic pathway. However, the maturation process of 
C. trachomatis within immune cells, such as macrophages, has not been studied 
extensively. Here, we demonstrated that RAW macrophages effectively suppressed 
C. trachomatis growth and prevented Golgi stack disruption, a hallmark defect in 
epithelial cells after C. trachomatis infection. Next, we systematically 
examined association between C. trachomatis and various endocytic pathway 
markers. Spinning disk confocal time-lapse studies revealed significant and 
rapid association between C. trachomatis with Rab7 and LAMP1, markers of late 
endosomes and lysosomes. Moreover, pretreatment with an inhibitor of lysosome 
acidification led to significant increases in C. trachomatis growth in 
macrophages. At later stages of infection, C. trachomatis associated with the 
autophagy marker LC3. TEM analysis confirmed that a significant portion of C. 
trachomatis resided within double-membrane-bound compartments, characteristic of 
autophagosomes. Together, these results suggest that macrophages can suppress C. 
trachomatis growth by targeting it rapidly to lysosomes; moreover, autophagy is 
activated at later stages of infection and targets significant numbers of the 
invading bacteria, which may enhance subsequent chlamydial antigen presentation.