Abstract
The purpose of this study was to determine whether administration of the microorganism Eubacterium rectale (E. rectale) could regulate dendritic cell (DC) activation and systemic inflammation in herpes simplex virus type 1-induced Behçet’s disease (BD). E. rectale, butyrate-producing bacteria, was administered to BD mice. Peripheral blood leukocytes (PBL) and lymph node cells were isolated and analyzed by flow cytometry. 16S rRNA metagenomic analysis was performed in the feces of mice to determine the differences in the composition of the microbial population between normal and BD mice. Serum cytokine levels were measured by enzyme-linked immunosorbent assay. The frequency of DC activation marker CD83 positive cells was significantly increased in PBL of BD mice. Frequencies of CD83+ cells were also significantly increased in patients with active BD. 16S rRNA metagenomic analysis revealed different gut microbiota composition between normal and BD mice. The administration of E. rectale to BD mice reduced the frequency of CD83+ cells and significantly increased the frequency of NK1.1+ cells with the improvement of symptoms. The co-administration of colchicine and E. rectale also significantly reduced the frequency of CD83+ cells. Differences in gut microbiota were observed between normal mice and BD mice, and the administration of E. rectale downregulated the frequency of CD83, which was associated with BD deterioration. These data indicate that E. rectale could be a new therapeutic adjuvant for BD management.
Highlights
The exact cause of Behçet’s disease (BD) is unknown [1, 2]
We investigated the microbiota associated with BD in the Herpes simplex virus (HSV)-1 induced BD mouse model and demonstrated that E. rectale regulated dendritic cell (DC) activation, leading to an improvement in BD
In active BD patients, oral ulcers were found in 8 patients (57.12%), genital ulcers in 2 patients (14.28%), arthritis in 12 patients (85.68%), gastrointestinal inflammation in 1 patient (7.14%), and nodular erythema in 4 patients (25.6%)
Summary
The exact cause of Behçet’s disease (BD) is unknown [1, 2]. BD is characterized by chronic systemic inflammation accompanied by oral aphthous ulcers, genital ulcers, skin lesions, ocular involvement, arthritis, and gastrointestinal and central nervous system involvement [1, 2]. Herpes simplex virus (HSV) is considered one of the causative factors of BD pathogenesis, and HSV viral DNA particles have been detected in the ocular fluids [3], peripheral blood [4], saliva [5], and skin lesions [6] of BD. BD has been reported to be associated with significant gut microbiota changes [6]. The microbiota has been described as contributing to immune system balance to maintain host homeostasis [8] and understanding the normal gut microbiota has made the therapeutic manipulation of the gut ecosystem a rational and realistic future prospect [9]. BD is a T-helper cell type 1 (Th1) polarized disease [11] and is a chronic inflammatory disease associated with significant gut microbiome changes [12]
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