Dr. Gibbs is a microbiologist, who is interested in the social behavior of the bacteria Proteus mirabilis, a leading cause of urinary tract infections.
Karine Gibbs, Ph.D.
Associate Professor of Molecular and Cellular Biology (Harvard University)
Dr. Gibbs is originally from Jamaica and grew up in Baltimore. She was an undergraduate at Harvard University, earned her Ph.D. at Stanford University, and completed postdoctoral training at the University of Washington. In 2012, she was named as a Packard Foundation Fellow. This award is given each year to 16 early-career researchers and provides $850,000 over five years.
The ability to distinguish self from non-self is critical in multi-cellular organisms like humans. This ability is what allows our immune system to recognize invading pathogens and fight off infection, and is also responsible for the problem of organ rejection after transplantation. However, it is more surprising to find it in a single-cell bacterium like P. mirabilis. However, it has been shown that as these bacteria move through space, they group together with neighbors of the same strain and avoid being neighbors with bacteria from other strains. It is as if the bacteria recognize others of the same strain as part of their own body and other strains as an infection. Dr. Gibbs sees this as a good opportunity to learn about how these bacteria can distinguish self and non-self.
This behavior has been shown in several species of bacteria, and in each case works as kind of a lock-and-key system: for instance, P. mirabilis have two proteins, idsD and idsE, that interact with each other and are slightly different between different strains. Each bacterium secretes idsD to its neighbors, which can only be neutralized by the complementary idsE.
Dr. Gibbs and her postdoc wanted to study this system in P. mirabilis because there was no obvious toxic effect of non-neutralized idsE. In a recent paper, they found that mismatched idsD and idsE caused 32 genes to be down-regulated (“turned down”), and that these genes were needed for growth and movement. They also caused 3 stress genes to be up-regulated (“turned up”) to deal with the mismatch - interestingly this had the side effect of causing increased antibiotic resistance. Finally, they found that these changes in gene expression did not occur while the bacteria were moving as a swarm. Instead, they occurred in the pauses between swarming events, which had the result of gradually leaving the non-self bacteria behind.