Curli Could Be Making You Sick

Temple University scientists make breakthrough in lupus research

wanda writes about lupus

On July 6, 2015, scientist at Temple University issued a press release about the research they have been conducting with regards to lupus.

This research, headed by Çagla Tükel and Stefania Gallucci, found that biofilm – or bacterial communities in the body – may be what is provoking the onset of lupus.

“Basically biofilms are these bacterial communities,” says Tükel, an assistant professor of microbiology and immunology at TUSM. “And when these communities are formed, they are very resistant to treatment. And actually what we found is happening with these biofilms is there is this protein called an amyloid protein. We think there could be a link between biofilm associated diseases and amyloid associated diseases.”

There is a specific protein of interest, an amyloid called curli. Tükel says curli is currently being treated with antibodies.

“We are thinking maybe the flares in lupus could be associated with the spikes in the curli antibodies and maybe this could be a biomarker for the disease,” Tükel says. “Another thing is the mechanism – how acceleration of lupus is caused in a patient.”

“Our study is suggesting that underlying infections may actually trigger the disease,” says Galluci, the associate chair of microbiology and immunology and an associate professor in microbiology and immunology at TUSM. “It’s important to go and study ways to better diagnose these underlying infections and treat them.”

Their next step will be to begin looking at patients using this information.

The research at TUSM was supported by the National Institutes of Health, the National Institutes of Allergy and Infectious Diseases, the Fox Chase Cancer Center-Temple University Nodal grant, the Lupus Research Institute Innovation Research Grant, the Lupus Foundation’s Goldie Simon Preceptorship Award and the National Institute of Arthritis and Musculoskeletal Skin Diseases.


From the life and mind of Lupus Patient Wanda M. Argersinger

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