Lipid Levels in Saliva May Serve as Non-invasive Biomarker in CF

Close link found to poor lung function, other complications: study

Steve Bryson, PhD avatar

by Steve Bryson, PhD |

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Lipid levels in human saliva were found to be significantly linked to complications related to cystic fibrosis (CF) — such as poor lung function — and may act as a biomarker for assessing disease activity, according to a new study.

These findings suggest that a non-invasive assessment of salivary lipids, the specific fat-like lipids in saliva, may help in guiding treatment for people with CF.

The researchers noted that larger studies are needed to examine the impact of diet and treatment on CF-related salivary lipids profiles.

The biomarker study, “Lipidomic alterations in human saliva from cystic fibrosis patients,” was published in the journal Scientific Reports.

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Investigating lipid levels in CF

In CF, inherited defects in CFTR, a protein that facilitates the movement of water and chloride ions across cell membranes, reduce the water content in the airways and digestive tract, leading to the buildup of thick mucus.

Emerging evidence suggests biological changes in CF also impact the metabolism of lipids — fat and fat-like molecules that participate in energy storage, cell membrane structure, and signaling.

These findings prompted researchers in Italy to examine the lipid profiles in the saliva of CF patients to determine their value in acting as non-invasive biomarkers that reflect disease activity and/or guide treatment.

The team recruited 70 adults with CF, median age 30, and 64 age-matched healthy volunteers as a control group. Participants were instructed not to eat or drink anything except water for at least two hours before saliva sample collection, which was carried out in the morning hours. Mass spectrometry was used to measure the levels of 523 salivary lipids.

Analysis revealed that the saliva of people with CF had significantly higher levels of the lipid classes called ceramides, hexosylceramides, triglycerides, and acylcarnitines compared with controls.

Across the 195 lipid levels that were significantly different, 175 (89.7%) were higher, and 20 were lower (10.2%). Levels of certain subclasses of phosphatidylcholine lipids and cholesterol esters could distinguish between CF and controls.

The researchers then examined the relationships between these lipid profiles and clinical CF characteristics to assess their value as biomarkers. Patients were divided into subgroups depending on the presence or absence of specific CF symptoms, including Pseudomonas Aeruginosa lung infection, pancreatic insufficiency, or CF-related liver disease or diabetes.

Lipids that distinguished patients with or without P. Aeruginosa infection included two types of phosphatidylcholines and two types of triglycerides. Similarly, two types of phosphatidylcholine lipids and one triglyceride were different between those with or without pancreatic insufficiency.

A cholesterol ester and a triglyceride discerned those with or without CF-related liver disease, while five triglycerides and one cholesterol ester distinguished patients with or without CF-related diabetes. Altogether, concentrations of 12 lipids were commonly altered in the saliva of CF patients across all comparisons.

The present study suggests that salivary lipid signatures are related to CF and to the severity and complications of the disease.

Finally, the team examined the relationships between lipid profiles and lung function, as assessed by FEV1, the amount of air that can force from the lungs in one second.

Statistical analysis found worse lung function in CF patients significantly correlated with elevated levels of two diacylglycerides, a phosphatidylcholine lipid, a cholesterol ester, and three so-called short-chain fatty acids (C2, C3, and C5).

“The present study suggests that salivary lipid signatures are related to CF and to the severity and complications of the disease,” the researchers wrote.

These data need to be confirmed in larger populations of participants investigating the impact of diet and treatment on CF lipid profiles, they noted. A key goal is to resolve “the argument that the lipid imbalances are due to CFTR dysfunction and not CF interventions,” the team concluded.

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