Journal News

New lipid class may shed light on causes of dental disease

Gelareh (Abulwerdi)  Vinueza
Dec. 29, 2020

Myriad microbial species live in the mouth, and an imbalance in their relative numbers can lead to dental disease. In chronic adult periodontitis, a destructive inflammatory disease, researchers have found Porphyromonas gingivalis, of the Bacteroidetes phylum, in increased numbers between the tooth and gum.

myupchar.com/Wikimedia commons
This illustration compares a healthy tooth with one from a patient with periodontitis, a disease caused by the bacterium Porphyromonas gingivalis.

Gingivitis precedes development of periodontitis, which occurs when the inflammatory lesion of gingivitis becomes destructive, resulting in bone loss and detachment. Researchers believe virulence factors of P. gingivalis contribute to this progression. These factors include lipopolysaccharide that may promote bone resorption, expression of hairlike fimbriae that may help bacteria attach to epithelial cells between tooth and gum, and proteolytic enzymes that may promote tissue degradation. These factors could work together to promote destruction of tissue surrounding a diseased tooth.

Frank Nichols, a professor at the University of Connecticut School of Dental Medicine, described one of the possible mechanisms for delivering bacterial lipids to gingival tissues: “P. gingivalis can attach to the epithelium through its cell surface adhesion molecules, including fimbriae on the bacteria’s outer surface, and in so doing, it may deliver its cell wall lipids to epithelial cells through a process of lateral diffusion.”

In a new study in the Journal of Lipid Research, Nichols and colleagues describe isolating a new lipid class from lab-grown P. gingivalis using high-performance liquid chromatography, or HPLC, and mass spectrometry. “We noticed a small late-emerging lipid peak that eluted well after other lipid classes of P. gingivalis total lipids,” Nichols said.

The new lipid peak contained a group of related lipid species, with the most abundant having a negative ion mass of m/z 1256. The team had identified a new class of P. gingivalis lipid products — Lipid 1256. They later found that this lipid is elevated in diseased tissues and plaque samples from around teeth with periodontitis.

The Lipid 1256 class appears to be produced through a lipid synthetic pathway involving addition of amino acid or fatty acid components to the base glycine lipid structure, Lipid 342, with the final step being addition of diacylated phosphoglycerol to the serine dipeptide lipid class Lipid 654.

The researchers found that a neutralizing antibody blocked activation of human embryonic kidney cells transfected with human Toll-like receptor 2, or TLR2, demonstrating that Lipid 1256 engages TLR2. They also found that Lipid 1256 is a strong ligand for TLR2 when compared to the other serine/glycine lipid classes. Lipid 1256 stimulates release of two cytokines, IL-1β and TNF-α, from peripheral blood monocytes, both known to increase bone resorptive processes.

“Bacteria of the phylum Bacteroidetes are represented in large numbers in the gastrointestinal tract,” Nichols said, “so we wondered if Lipid 1256 is prevalent in those organisms.” They found that two common GI Bacteroidetes organisms produce Lipid 1256, suggesting they might affect chronic inflammatory disease of the GI tract by exposing the GI wall to these lipids.

Recovery of Lipid 1256 in the mouth and intestine means that both sources could contribute to diseases such as rheumatoid arthritis or atherosclerosis. Other researchers have found that these diseases may involve engagement of TLR2, which could occur if either the bacterial lipid or the bacteria enters the bloodstream. Future research evaluating the recovery of Lipid 1256 in human tissue samples may implicate lipids of the Bacteroidetes phylum in systemic diseases with a TLR2-dependent chronic inflammatory response.

 

Enjoy reading ASBMB Today?

Become a member to receive the print edition monthly and the digital edition weekly.

Learn more
Gelareh (Abulwerdi)  Vinueza

Gelareh (Abulwerdi) Vinueza graduated with her Ph.D. from the molecular medicine program at the University of Maryland, Baltimore. She is currently a policy fellow at the Food and Drug Administration. She has been an ASBMB volunteer writer since 2018 and is passionate about science communication and science policy. Outside of work, she enjoys photography, hiking and cooking.

Get the latest from ASBMB Today

Enter your email address, and we’ll send you a weekly email with recent articles, interviews and more.

Latest in Science

Science highlights or most popular articles

A simple method to determine phase preference of proteins on live cell membranes
Journal News

A simple method to determine phase preference of proteins on live cell membranes

May 22, 2022

“The phase preference of molecules used to be difficult and time-consuming to establish. This new method, detected by chance, provides results in at most 15 minutes on live cells,” Thorsten Wohland said.

Study of Alzheimer’s marker prompts warning about serine supplements
News

Study of Alzheimer’s marker prompts warning about serine supplements

May 20, 2022

They have been advertised to improve memory and cognitive function.

Why is the 100-year-old BCG vaccine so broadly protective in newborns?
News

Why is the 100-year-old BCG vaccine so broadly protective in newborns?

May 19, 2022

Study finds changes in metabolite and lipid profiles, providing clues for designing future vaccines for newborns.

How genome organization influences cell fate
News

How genome organization influences cell fate

May 17, 2022

UC Riverside-led study identifies how blood stem cells maintain their fate.

Corals and sea anemones turn sunscreen into toxins
News

Corals and sea anemones turn sunscreen into toxins

May 14, 2022

Understanding how could help save coral reefs.

The body’s response to allergic asthma also helps protect against COVID-19
News

The body’s response to allergic asthma also helps protect against COVID-19

May 14, 2022

It all comes down to an immune system protein known as interleukin-13