Increasing evidence — much of it discovered and actively being explored by Hopkins scientists — suggests that chronic inflammation may be an important instigator of prostate cancer. One source of chronic inflammation in the prostate is sexually transmitted infections (STIs, more commonly known as STDs).

Could having a sexually transmitted
infection make a man more
susceptible to prostate cancer?

And this begs the question — at least to epidemiologist Elizabeth A. Platz, Sc.D., one of the pioneers in this area of research, and colleagues including Jonathan M. Zenilman, M.D., Angelo M. De Marzo, M.D., Ph.D., and postdoctoral fellow Siobhan Sutcliffe, Ph.D: Could having a sexually transmitted infection make a man more susceptible to developing prostate cancer?

Before the scientists could answer this question, they had to narrow down the playing field. Which, of the more than 30 known sexually transmitted infections, should they study? First, they looked for an infection known to cause extensive inflammation in the prostate. They also looked for a silent one—one that causes no symptoms, that stays below the radar, in effect. A quiet infection, they reasoned, "would be less likely to be treated and cured, and thus might persist in the man's genitourinary tract." One infection that fit both criteria was trichomonosis, a sexually transmitted infection caused by the protozoan, Trichomonas vaginalis. "About 20 years ago, a pathologist named William A. Gardner Jr. noted that T. vaginalis was capable of infecting the prostate and causing a strong inflammatory immune response," explains Platz. "And yet, despite this interesting finding, essentially no work was done on the possible role that T. vaginalis might play in the development of prostate cancer."

To investigate this, the scientists selected 691 men with prostate cancer and 691 men without prostate cancer from participants in a large, Harvard-based project called the Health Professionals Follow-up Study. The lead role in the investigation was taken by Sutcliffe. Working with microbiologist John F. Alderete, Ph.D., who developed an assay to detect antibodies against T. vaginalis and tested the men's samples, they found that about 11 percent of men had antibodies against T. vaginalis. And significantly, "men who had these antibodies were about 40 percent more likely to develop prostate cancer than men who did not have these antibodies," says Sutcliffe.

Even more exciting — in research that continues work by Platz and others investigating the use of nonsteroidal anti-inflammatory agents as a preventive measure against prostate cancer— "We then separated men into those who did and did not regularly use aspirin," Platz says. Aspirin reduces inflammation. And in this study, among men who regularly used aspirin, those who had antibodies against this infection had the same risk of prostate cancer as men who had not been exposed to it. "But, among men who did not regularly use aspirin, those who had antibodies against T. vaginalis were twice as likely to develop prostate cancer." Sutcliffe, Platz and colleagues are quick to point out that these results are preliminary, and that much further study is needed. Even so, the Hopkins researchers are excited by these findings and now are looking to see whether young men in the U.S. military with antibodies against T. vaginalis have higher blood levels of a marker of prostate inflammation and cell damage than those who don't have antibodies. "This may indicate that T. vaginalis infected the prostate and caused cell damage in these men,” says Platz.