Sjorgenův syndrom

Recent studies in patients with SS have demonstrated that the oral microbiome,[77] as well as the gut microbiome,[78] significantly differ from that in healthy individuals. Further, in SS patients, correlative evidence suggests a pathogenic influence of certain microbial species within the gut, ocular, and oral microbiota communities, which highlights the now termed gut-ocular-oral axis.[77] SS patients are also reported to have an increase abundance of Actinomyces and Lactobacillus in both stool and oral samples,[79] which implicated these taxa as potential pathobionts. This suggests the possibility that oral bacteria or their products may traverse buccal epithelial cells through local defects in the epithelial barrier. Furthermore, T cell epitope mimicry between SS antigen A (SSA) /Ro60 and various bacteria have been postulated as disease drivers.[80] In an independent cross-sectional study of human SS saliva, based on 16S rRNA amplimer sequencing taxonomic distribution in these communities were documented. These studies have identified four genera of bacteria, Bifidobacterium, Lactobacillus, Dialister and Leptotrichia as significantly different in abundance in SS patients compared to healthy controls.https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10729600/