In order to understand how chlamydia causes disease, researchers at Thomas Jefferson University investigate how it creates a protective niche inside an infected cell, where it is free to grow and replicate exponentially.

In this context, Fabienne Paumet, PhD, Associate Professor in the department of Microbiology and Immunology and colleagues looked at the process that allows Chlamydia to build this protective compartment called an inclusion, and siphon off the host cell’s resources to generate more bacteria.

The researchers found that a single bacterial protein called CT813 was able to hijack two different types of cytoskeleton scaffolding elements from their host cell. This event enables the inclusion to grow and attract the Golgi to the inclusion, which provides nutrients that Chlamydia needs to survive. Dr. Paumet found that the bacterial protein CT813 was able to execute this feat by manipulating a normal cellular protein called ADP–ribosylation factor, or ARF. Prior to this paper, no one had known that ARF had these functions in the cell.

“We owe much of our understanding of normal cellular functions to viruses and bacteria,” says Dr. Paumet. “Likewise, not only does this research gives us a better understanding of how Chlamydia survives inside human cells, we’ve also gained a better understanding about how our cells control the cytoskeletal proteins that change a cell’s shape or help it move.”