NYC Healthcare News



Research marks new direction to treat Pneumocystis, inflammatory diseases

December 22, 2015

"We initially thought we had done something wrong, and so we repeated the experiment again and again. Then, when new technology was developed, we were able to document that the body cleared the infection more readily with sulfasalazine," added Wang.

Scientists have long known that the body's immune T cells are central to the body's response to fight off the infection. The Rochester team showed that the body's T cells spur macrophages to attack the fungus ?? to engulf its particles and chew them up in a process known as phagocytosis.

While scientists have long suspected that role for macrophages, the Rochester team relied on a new technology to gather the first direct evidence of macrophages engulfing fungal particles. The scientists worked closely with Timothy Bushnell, Ph.D., and others at Rochester's Flow Cytometry Resources Core, investigating new ways to use lasers to capture images of molecular events. Bushnell's team ultimately connected the team with scientists at Amnis. Together the group developed a new way to capture macrophage phagocytosis in single cells from mice infected with Pneumocystis. The technology enabled the team to capture more than 40,000 such events, compared to just a handful when using conventional microscopy.

The team showed that as macrophage activity increased, the animals' health improved and levels of fungus decreased. For example, 17 days after infection, mice treated with sulfasalazine had nine times as many macrophages that had engulfed fungal particles compared to mice that had not been treated with the compound.

"This marks a new direction in which to look for new therapies to treat Pneumocystis as well as other inflammatory diseases. Identifying modulators that can increase or decrease the action of our immune system in a precise manner is a growing area of research," said Wright. Recently researchers have come to realize that there are different kinds of macrophages, and Wright noted that the type whose activity is trigged by sulfasalazine does not contribute to inflammation.

SOURCE University of Rochester Medical Center