Can Gut Microbiota Affect Dry Eye Syndrome?

Abstract

Using metagenomics, continuing evidence has elicited how intestinal microbiota trigger distant autoimmunity. Sjögren’s syndrome (SS) is an autoimmune disease that affects the ocular surface, with frequently unmet therapeutic needs requiring new interventions for dry eye management. Current studies also suggest the possible relation of autoimmune dry eye with gut microbiota. Herein, we review the current knowledge of how the gut microbiota interact with the immune system in homeostasis as well as its influence on rheumatic and ocular autoimmune diseases, and compare their characteristics with SS. Both rodent and human studies regarding gut microbiota in SS and environmental dry eye are explored, and the effects of prebiotics and probiotics on dry eye are discussed. Recent clinical studies have commonly observed a correlation between gut dysbiosis and clinical manifestations of SS, while environmental dry eye portrays characteristics in between normal and autoimmune. Moreover, a decrease in both the Firmicutes/Bacteroidetes ratio and genus Faecalibacterium have most commonly been observed in SS subjects. The presumable pathways forming the “gut dysbiosis–ocular surface–lacrimal gland axis” are introduced. This review may provide perspectives into the link between the gut microbiome and dry eye, enhance our understanding of the pathogenesis in autoimmune dry eye, and be useful in the development of future interventions.

Age-Dependent Distinct Distributions of Dendritic Cells in Autoimmune Dry Eye Murine Model

“…Given that gut dysbiosis has a significant impact on the maturation and differentiation of B cells [59], an increase in mesenteric nodal MHC-II hi B cells may be gut-related. Considering that recent studies have shown that intestinal dysbiosis is related to autoimmune dry eyes [26][27][28], the increase in lacrimal glandial MHC-II hi B cells observed in the present study may correspond to changes in the gut. In primary Sjögren's syndrome, CD27 + memory B cells, marginal zone B cells, plasmablasts, and plasma cells are the key subsets of B cells [47].…”

“…However, a study on the DC distributions in the cornea or LG associated with an autoimmune dry eye models is currently under-investigated. Although existing studies provide some evidence for the role of intestinal dysbiosis in autoimmune dry eyes [26][27][28], there are no pertinent studies on DED directly linking changes in DCs with the ocular-gut axis. Therefore, we investigated whether the distribution of DC subsets is distinct in aged NOD.B10.H2 b (NOD) mice that mimic Sjögren's syndrome-like changes when compared to the distribution in aged C57BL/6 (B6) mice [26].…”

Association between aging-dependent gut microbiome dysbiosis and dry eye severity in C57BL/6 male mouse model: a pilot study

“…A suggested pathophysiology of gut dysbiosis associated with dry eye disease may involve modulating effector T cells directly or via either dendritic cell activation or disturbing gut-derived metabolites [ 19 ]. In this study, we found that microbial taxa associated with dysbiosis change with age, and that these microbial taxa were associated with dry eye severity signs.…”

“…Moreover, recent studies have demonstrated that alterations in gut microbiota may lead to several ocular diseases including autoimmune uveitis, age related macular degeneration, and dry eye associated with Sjögren’s syndrome [ 15 – 18 ]. A recent review also indicates that gut microbiota may interact with the eye [ 19 ].…”

“…The gut microbiota changes with aging and this aging-related microbiota alteration is associated with inflammaging and chronic geriatric diseases [ 20 ]. Given that the gut dysbiosis is associated with dry eye disease [ 19 ], aging-related microbiome dysbiosis may also contribute to aging-related dry eye disease. Therefore, in this pilot study, we aimed to investigate (1) whether aging-related dysbiosis is present in C57BL/6 (B6) male mice and (2) which taxa that altered with aging may be associated with the severity of dry eye.…”