Chlamydiae fight back, says Azenabor, His work shows that, as they are ingested, these two species of Chlamydia can manipulate the functions of protective cells like macrophages in creative ways.
One of the keys lies in the macrophages cell walls, which store cholesterol and usually tightly control it.
But when its infected with C. pneumoniae, the microbe traffics cholesterol from the macrophage cell membrane to its own, causing a change in the macrophage that makes it rigid and unable to move.
The bacterium also disturbs the macrophages production of toxins in a process that transforms them into signaling molecules, which support functions that keep the bacterium alive.
C. pneumoniae really wants to hijack the cell functions for its own use, like a parasite would, he says. The macrophage, though, wants to kill Chlamydia, but its killing ability has been converted to signaling.
This is the reason the infection becomes chronic, Azenabor says. Because of signaling, everything else in the human cell is still fine except for the altered toxins, so the bacteria can reproduce in a short time.
As the macrophages become immobile, they accumulate in the blood vessel walls, setting the stage for atherosclerosis.
Infection and pregnancy
Armed with new information about how C. pneumoniae sabotages the immune response, Azenabor, who had also been studying the effects of estrogen on macrophages, turned his attention to another Chlamydia-related puzzle.
How is Chlamydia trachomatis, the species that causes a sexually transmitted disease, involved in the occurrence of spontaneous abortions or miscarriages?
He was immediately drawn to the protective cells in the placenta during early pregnancy the trophoblasts.
Its not for nothing that trophoblasts are the early cells, says Azenabor. They prevent any kind of infectio
|Contact: Anthony Azenabor|
University of Wisconsin - Milwaukee