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Review
. 2021 Oct 25;16(4):631-643.
doi: 10.18502/jovr.v16i4.9754. eCollection 2021 Oct-Dec.

Atopobiosis and Dysbiosis in Ocular Diseases: Is Fecal Microbiota Transplant and Probiotics a Promising Solution?

Affiliations
Review

Atopobiosis and Dysbiosis in Ocular Diseases: Is Fecal Microbiota Transplant and Probiotics a Promising Solution?

Triana Hardianti Gunardi et al. J Ophthalmic Vis Res. .

Abstract

Purpose: To highlight the role of atopobiosis and dysbiosis in the pathomechanism of autoimmune uveitis, therefore supporting fecal microbiota transplant (FMT) and probiotics as potential targeted-treatment for uveitis.

Methods: This review synthesized literatures upon the relation between gut microbiota, autoimmune uveitis, FMT, and probiotics, published from January 2001 to March 2021 and indexed in PubMed, Google Scholar, CrossRef.

Results: The basis of the gut-eye axis revolves around occurrences of molecular mimicry, increase in pro-inflammatory cytokines, gut epithelial barrier disruption, and translocation of microbes to distant sites. In patients with autoimmune uveitis, an increase of gut Fusobacterium and Enterobacterium were found. With current knowledge of aforementioned mechanisms, studies modifying the gut microbiome and restoring the physiologic gut barrier has been the main focus for pathomechanism-based therapy. In mice models, FMT and probiotics targeting repopulation of gut microbiota has shown significant improvement in clinical manifestations of uveitis. Consequently, a better understanding in the homeostasis of gut microbiome along with their role in the gut-eye axis is needed to develop practical targeted treatment.

Conclusion: Current preliminary studies are promising in establishing a causative gut-eye axis relationship and the possibility of conducting FMT and probiotics as targeted treatment to mitigate autoimmune uveitis, to shorten disease duration, and to prevent further complications.

Keywords: Autoimmune; Dysbiosis; Gut–Eye Axis; Uveitis; Atopobiosis.

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Conflict of interest statement

There are no conflicts of interest.

Figures

Figure 1
Figure 1
Flowchart for study selection process.
Figure 2
Figure 2
Illustrated pathogenesis of atopobiosis and dysbiosis in relation to uveitis. (1) Microbe recognition. (2) Bypass via tight junction. (3) Transcytosis via M-cells. (4) Phagocytosis by DCs and APCs. (5a) Microbes or bacteria enter the mesenteric lymph node. (6a) Bacteria enter the systemic circulation. (7a) Translocation of bacteria to ocular endothelial site. (5b) DCs, T cells, B cells enter the mesenteric lymph nodes. (6b) These cells may undergo cascades and enter the systemic circulation. (7b) Activated retina specific T-cells surpass the blood–retinal barrier causing inflammation. TLR, toll-like receptor; DC, dendritic cell; APC, antigen presenting cell; Th17, T helper

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