Gut microbes may influence many conditions, including autoimmune diseases. Now, a new study has found that Sjögren syndrome—an autoimmune condition that causes dry eyes and mouth—may be linked to broad gut microbiota disruptions.

The findings, published in Cell Reports Medicine, suggest that monitoring the gut microbiota could in the future help understand, diagnose, or manage Sjögren syndrome.

Previous studies focusing on this syndrome mostly focused on bacteria and often used lower-resolution sequencing. So, researchers led by Changming Chen at the Second Affiliated Hospital of Guizhou University of Traditional Chinese Medicine in Guiyang, China, set out to analyze stool samples from 206 people with Sjögren syndrome and 355 healthy individuals.

Microbial signature

People with Sjögren syndrome had more inflammatory bacteria such as Streptococcus, Veillonella, and Ligilactobacillus, whereas healthy individuals had more bacteria linked to gut health, including Faecalibacterium, Roseburia, and some Bacteroides species.

People with Sjögren syndrome also had more fungi such as Candida and Malassezia along with altered gut viruses.

Because bacteria, fungi, and viruses formed linked networks, machine-learning models trained using these microbial signatures could distinguish people with Sjögren syndrome from healthy individuals, the team found. 

Inflammatory responses 

The researchers also discovered that people with Sjögren syndrome had fewer protective metabolites such as butyrate and more inflammatory or toxic metabolites compared to healthy individuals.

Several bacteria enriched in people with Sjögren syndrome, as well as some Candida strains, were linked to harmful metabolites. In immune cells grown in a lab dish, some microbes associated with the syndrome triggered inflammatory responses.

Although the findings still need clinical validation, the authors say, “this multi-kingdom, multi-omic study provides a comprehensive resource for understanding gut microbiome alterations in [Sjögren syndrome], identifies robust diagnostic signatures, and offers mechanistic insights into host-microbe interactions that may inform future therapeutic strategies.”