Mouth-to-gut bacterial shift seen in autoimmune disease

Gut microbiome disturbances are well documented in connective tissue diseases such as systemic lupus erythematosus and primary Sjögren's syndrome, but the mouth has largely been studied separately. Animal work has suggested something more interesting: pathobionts relocating from the oral cavity to the intestine, producing coordinated disruption across two mucosal surfaces rather than one. Whether that pattern appears consistently in human patients was unknown. This review set out to synthesise the oral and gut microbiome literature in these two diseases and look specifically for opposing abundance patterns across the two sites that would be compatible with such relocation.

The authors systematically searched PubMed from inception to November 2024 for observational studies comparing adult patients with lupus or primary Sjögren's syndrome against healthy controls and reporting oral and/or gut microbiome data. Interventional studies, case reports, reviews and non-human studies were excluded. Study quality was assessed with the Newcastle-Ottawa Scale, and microbial names were harmonised to current NCBI taxonomy before being synthesised descriptively; no meta-analysis was attempted. Thirty-three studies were included, comprising 1,385 patients and 2,131 healthy controls, and the analysis focused on recurrent taxa showing opposite directions of change in the mouth versus the intestine.

Intestinal Shannon and Simpson alpha-diversity were frequently reduced in patients, while oral diversity was preserved or even increased — the two sites did not move together. Recurrent opposing abundance patterns emerged for specific taxa: most consistently Streptococcus and Actinomycetota in lupus, and Pseudomonadota in Sjögren's syndrome, each showing decreased relative abundance in the mouth alongside increased abundance in the intestine. Not everything followed that pattern; Veillonella and Veillonellaceae were enriched in parallel at both sites. The authors conclude that both diseases involve coordinated dysregulation of the oral and gut microbiomes, while stating plainly that causal inference is limited because the data are largely cross-sectional and based on relative abundances.

This is the first systematic attempt to check whether the oral-gut relocation seen in animal models leaves a detectable fingerprint in human autoimmune disease, and the directional consistency of the taxa is suggestive. It reframes microbiome research in connective tissue disease as a two-site problem rather than a gut problem. The central limitation is inherent to relative abundance data: a taxon can appear to fall in one compartment simply because others rise. Longitudinal sampling, absolute quantification and strain-level tracking would be needed to show that the same organisms are actually moving, and whether any of this precedes or follows disease onset is unresolved.

The useful concept to take away is the oral-gut axis: what lives in your mouth is not sealed off from what lives in your intestine, and researchers increasingly study the two together. In lupus and Sjögren's syndrome, the microbial picture appears coordinated across both sites rather than confined to the gut. This is pattern-spotting across observational studies, so it does not establish that oral bacteria drive autoimmune disease, nor that changing oral hygiene alters disease course. It is a reason to watch this research area, not a basis for any intervention.