Gut microbial signatures and their functions in Behcet's uveitis and Vogt-Koyanagi-Harada disease

Uveitis is an intraocular inflammatory disease which can lead to serious visual impairment worldwide [1]. Although clinical features vary significantly among different uveitis entities, several risk factors such as genetic, environmental, infectious and immunological factors have been shown to play an important role in their pathogenesis [2]. Recently evidence is emerging concerning the role of the gut microbiome in the pathogenesis of uveitis [3].

The gut microbiome plays an important role in modulating host immune homeostasis [4,5]. Dysbiosis of the gut microbiota has been found in a series of immune-mediated diseases including Ankylosing Spondylitis (AS), Rheumatoid Arthritis (RA), Crohn's disease (CD) and Ulcerative Colitis (UC) using metagenomic sequence (MGS) [[6], [7], [8]]. Studies dealing with the pathogenesis of these immune-mediated diseases have suggested that the gut microbiome contributes to immune disorders via production of homologous peptides, effector proteins and metabolites [[9], [10], [11]]. In our previous metagenomic studies, we also showed that gut microbiome composition was associated with Behcet's uveitis (BU) and Vogt-Koyanagi-Harada disease (VKH), which are common non-infectious uveitis entities [12,13]. BU is an autoinflammatory disease causing multisystemic inflammation in various organs including the eye (uveitis) and skin (lesions and ulcers) [14]. VKH is different from BU and is commonly considered as an autoimmune disease directed against melanocyte associated antigens and which is characterized by bilateral granulomatous panuveitis with systemic manifestations, such as tinnitus, vertigo and meningism [15]. Several studies identified similarities and differences concerning the pathogenetic mechanisms between BU, VKH and various immune-mediated diseases including AS, RA, CD and UC [[16], [17], [18], [19]]. However, few studies have focused on the differences of the gut microbiome composition between these diseases and this was therefore the subject of the study presented here. With a number of metagenomic datasets, publicly available in the NCBI sequence read archive (SRA) and the platform of MICrobiome HELminth INteractions database (MICHELINdb) [20], this allowed comparative analyses of the metagenomic studies on BU and VKH with other immune-mediated diseases. In this study, we integrated the sequencing data of five metagenomic studies and identified the gut microbial signatures in two separate uveitis entities (BU and VKH). Moreover, we identified gut microbial markers and the functional consequences for these two uveitis entities based on their specific microbial signatures.

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