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CURRENT POSITION
KEY COLLABORATORS
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| Eduardo Groisman |
Salmonella gets around. The bacterium has been isolated in hosts ranging from chickens to cockroaches to elephants, not to mention humans. Outbreaks of salmonella poisoning in humans regularly make the news. In spite of the best efforts of public health officials to eradicate the bacteria, they have proved remarkably resilient.
Eduardo Groisman wants to know why: How, exactly, did salmonellae become such effective survivors and potent disease causers?
The thrill of discovery explains why Groisman, originally from Argentina, became a microbiologist and not an engineer, as his grandfather had urged him to be. The laws of physics don’t change, Groisman recalls his grandfather saying; but in medicine or other biological fields, “they’re always discovering new things. You always have to keep learning.”
Groisman’s work with salmonella began during a stint as a postdoctoral student at the Scripps Research Institute in La Jolla, Calif. After completing a degree in biochemistry at the University of Buenos Aires in Argentina, Groisman spent a year and a half working at a clinical microbiology lab there. But he yearned for something else.
“I was running this lab, doing more sort-of applied stuff, and it wasn’t appealing to me at all.” Despite assurances, opportunities to do basic research never materialized. So Groisman convinced his fiancé, who didn’t speak English and had no family in America, to come to California with him so he could work on a Ph.D.
Seventeen years later, Groisman is still in the States (at Washington University in St. Louis), married to his sweetheart, and doggedly on the trail of unraveling salmonella’s biochemical bag of tricks.
One line of research focuses on how salmonella survive inside macrophages, which are cells in the immune system that engulf invading bacteria and kill them by releasing poison from bubble-like structures called lysosomes. In 1989, Groisman’s colleague, Patty Fields, identified mutated strains of salmonella that did not survive inside macrophages, isolated them, and examined their genes. They eventually discovered that salmonella can “sense” that it is inside a cell because the level of the mineral magnesium drops. That change turns on genes in the bacteria that help it to survive and multiply inside the macrophage.
Microscopic view of Salmonella. © 2001 Dennis Kunkel Microscopy, Inc.
More recently, Groisman has been looking at how salmonella changes its external surface structure to fight off the action of antimicrobial peptides, an ancient form of defense against disease-causing agents (pathogens). Peptides are molecules similar to, but smaller than, proteins. Besides raising hope for new forms of antibacterial drugs, Groisman’s research also provides insight into the fundamental question of what makes a microorganism a pathogen.
“We know a lot [about Salmonella], but we still have a long way to go,'' he notes. “This organism has 4,300–4,500 genes. We probably still don’t know the function of at least half of them.” But the advantage is that finding out these functions is “doable.”
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