A drug to treat inflammation plays a surprising role reducing the level of infection caused by an opportunistic bug that is deadly for AIDS and cancer patients and others with weakened immune systems.
The drug, sulfasalazine, spurs the body to get rid of the fungal evaders by enhancing the body's ability to chew them up instead of leaving the debris to litter the lungs, where it would continue to provoke an onslaught of harmful inflammation.
Besides opening a new avenue for research on Pneumocystis pneumonia or PCP, caused by the fungus Pneumocystis jirovecii, the work with mice also offers the possibility of manipulating immune cells called macrophages to improve treatment of infections.
The findings by scientists at the University of Rochester Medical Center were published August 19 in the journal PLoS Pathogens.
During a bout with Pneumocystis, the lungs become a battlefield, where the body pits an array of impressive forces against marauding microbes. But even when the body gets the upper hand, the damage is tremendous. Immune cells like neutrophils and macrophages can flood the lungs, literally suffocating the patient. And when the debris from dead microbes fills the lungs, more and more immune cells are called in to clean up the area, making matters worse. It becomes harder and harder to breathe.
"Many people assume that once the microbe is dead, patients usually start to feel better immediately. But with Pneumocystis, patients do not always undergo a rapid clinical improvement following antibiotic treatment. Even though the bug has been killed, the debris that is left in the lungs continues to promote inflammation," said corresponding author Terry Wright, Ph.D., an infectious disease specialist and associate professor of Microbiology and Immunology and of Pediatrics.
Pneumocystis is a common bug that infects nearly everyone at some point; the authors say that
|Contact: Tom Rickey|
University of Rochester Medical Center