Does the Microbiome Cause B27-related Acute Anterior Uveitis?

Abstract

The microbiome is strongly implicated in a broad spectrum of immune-mediated diseases. Data support the concept that HLA molecules shape the microbiome. We provide hypotheses to reconcile how HLA B27 might affect the microbiome and in turn predispose to acute anterior uveitis. These theories include bacterial translocation, antigenic mimicry, and dysbiosis leading to alterations in regulatory and effector T cell subsets.

Implicating Dysbiosis of the Gut Fungal Microbiome in Uveitis, an Inflammatory Disease of the Eye

“…Earlier studies had indicated dysbiosis in the gut bacterial microbiome of rats and mice with auto-immune UVT. [5][6][7] Our own study also confirmed gut bacterial microbiome dysbiosis in human beings with auto-immune and idiopathic UVT. 4 Two papers 6,7 indicated that HLA B27 affects the microbiome and in turn predisposes to UVT.…”

“…[5][6][7] Our own study also confirmed gut bacterial microbiome dysbiosis in human beings with auto-immune and idiopathic UVT. 4 Two papers 6,7 indicated that HLA B27 affects the microbiome and in turn predisposes to UVT. Systemic inflammatory diseases like asthma, diabetes, rheumatoid arthritis, ulcerative colitis, Crohn's disease, etc., have also been implicated in bacterial Interaction networks of the bacterial and fungal genera in gut microbiomes of HC and UVT patients.…”

“…[2][3][4] Studies in mice models also suggested a role for the gut microbiome in the pathophysiology of UVT and indicated that altering the bacterial composition would attenuate the disease. [5][6][7] The most probable mechanism by which gut microbiome influences disease pathology is through the interaction with host immune system. 8,9 Studies showing association of gut fungal microbiome with diseases are less compared to bacterial microbiomes, which may be attributed to the several challenges that are faced in characterizing fungal communities right from extraction of genomic DNA to molecular identification, the latter mainly due to the presence of high sequence length variability in fungal sequences (ITS1 and ITS2) and due to the incomplete availability of fungal reference sequence databases.…”

Epidemiology and pathogenesis of uveitis: A review

“…The study on experimental autoimmune uveitis (EAU) by Rosenbaum et al in mice models has shown that oral antibiotics modulate the severity of EAU by increasing lymphocytes in the gut and extra-intestinal tissues and by decreasing effectors T cells and cytokines. 12 The study suggests that protective and uveitogenic bacteria exist and some antibiotics may be able to alter the microbiota away from the uveal tissue. Whereas, other antibiotics may promote potentially uvetiogenic bacteria.…”

A Possible Role of Intestinal Microbiota in the Pathogenesis of Ankylosing Spondylitis

“…These pathogen-specific antibodies not only react with microbes but also bind to host self-antigens, which will subsequently result in inflammation and tissue damage. Molecular mimicry or cross-reactivity hypothesis is another mechanism which could trigger AS [96], while molecular mimicry is the major mechanism of rheumatic fever [97]. …”