Proteomics-based functional studies reveal that galectin-3 plays a protective role in the pathogenesis of intestinal Behçet’s disease

Lee, Hyun Jung; Kim, Jae Hyun; Hong, Sujeong; Hwang, Inhwa; Park, Soo Jung; Kim, Tae Il; Yu, Je-Wook; Kim, Seung Won; Cheon, Jae Hee

doi:10.1038/s41598-019-48291-1

Cited by 8 publications

(7 citation statements)

References 54 publications

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“…Acetate is known to attenuate inflammasome activation ( 60 ). Increased inflammasome expression has been reported in BD patients with skin manifestations ( 61 ) and BD patients with intestinal problems ( 62 ). B. vulgatus attenuated atherosclerosis through Foxp3 upregulation and TNFα downregulation ( 63 ).…”

Section: Discussionmentioning

confidence: 99%

Eubacterium rectale Attenuates HSV-1 Induced Systemic Inflammation in Mice by Inhibiting CD83

et al. 2021

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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.

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Section: Discussionmentioning

confidence: 99%

Eubacterium rectale Attenuates HSV-1 Induced Systemic Inflammation in Mice by Inhibiting CD83

et al. 2021

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“…Galectin-3 is a 31-kDa chimeric lectin involved in the pathophysiological processes of a variety of cells (29,39). It has become a biomarker for cardiovascular diseases such as heart failure (41), aortic stenosis (15), and myocardial aging (26).…”

Section: Discussionmentioning

confidence: 99%

Macrophage galectin-3 enhances intimal translocation of vascular calcification in diabetes mellitus

Sun

Zhang

et al. 2020

American Journal of Physiology-Heart and Circulatory Physiology

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The clinical risks and prognosis of diabetic vascular intimal calcification (VIC) and medial calcification (VMC) are different. This study aims to investigate the mechanism of VIC/VMC translocation. Anterior tibial arteries were collected from patients with diabetic foot amputation. The patients were then divided into VIC and VMC groups. There were plaques in all anterior tibial arteries, while the enrichment of galectin-3 in arterial plaques in the VIC group was significantly higher than that in the VMC group. Furthermore, a macrophage/vascular smooth muscle cell (VSMC) coculture system was constructed. VSMC-derived extracellular vesicles (EVs) was labeled with fluorescent probe. After macrophages were pretreated with recombinant galectin-3 protein, the migration of VSMC-derived EVs and VSMC-derived calcification was more pronounced. And anti-galectin-3 antibody can inhibit this process of EVs and calcification translocation. Then, lentivirus (LV)-treated bone marrow cells (BMCs) were transplanted into apolipoprotein E-deficient (ApoE−/−) mice, and a diabetic atherosclerosis mouse model was constructed. After 15 wk of high-fat diet, ApoE−/− mice transplanted with LV-shgalectin-3 BMCs exhibited medial calcification and a concentrated distribution of EVs in the media. In conclusion, upregulation of galectin-3 in macrophages promotes the migration of VSMC-derived EVs to the intima and induces diabetic vascular intimal calcification. NEW & NOTEWORTHY The clinical risk and prognosis of vascular intimal and medial calcification are different. Macrophage galectin-3 regulates the migration of vascular smooth muscle cell-derived extracellular vesicles and mediates diabetic vascular intimal/medial calcification translocation. This study may provide insights into the early intervention in diabetic vascular calcification.

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“…There was no correlation between HSPA6 expression levels and oral ulcers, genital ulcers, or disease activity among Crohn’s disease patients. 65 Additionally, Lee et al 66 found increased HSP27 and decreased HSP60 protein expression levels in 17 BS patients compared to 17 healthy controls, using two-dimensional (2D) electrophoresis and MALDI-TOF/TOF MS methods.…”

Section: Heat Shock Proteins In Behçet Syndromementioning

confidence: 99%

Heat Shock Proteins in Behçet Syndrome

Aydın¹,

Hatemi²

2023

Balkan Med J

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Behçet syndrome (BS) is a systemic vasculitis of unknown etiology that affects the skin, mucosa, joints, eyes, central nervous system, gastrointestinal system, arteries, and veins. It is generally believed to have a complex genetic background where both innate and adaptive immune systems are activated through environmental factors, such as infections, and auto-antigens. Heat shock proteins (HSPs) are highly conserved and immunogenic endogenous proteins that are thought to play both an enhancing and regulating role in several autoimmune and inflammatory diseases, such as rheumatoid arthritis, juvenile idiopathic arthritis, and Type I diabetes. There is evidence supporting the role of various microorganisms in BS, which may be using a common pathway to trigger or activate BS through molecular mimicry. The significant homology between microbial and human HSPs suggests that HSPs could serve as a common trigger. This review summarizes the work on the role of HSPs in the pathogenesis of BS. However, it remains unknown whether the HSPs detected in BS lesions play a causative role, their presence is a result of the ongoing inflammation, or they have a protective role against inflammation, as suggested in some other diseases.

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Proteomics-based functional studies reveal that galectin-3 plays a protective role in the pathogenesis of intestinal Behçet’s disease

Cited by 8 publications

References 54 publications

Eubacterium rectale Attenuates HSV-1 Induced Systemic Inflammation in Mice by Inhibiting CD83

Eubacterium rectale Attenuates HSV-1 Induced Systemic Inflammation in Mice by Inhibiting CD83

Macrophage galectin-3 enhances intimal translocation of vascular calcification in diabetes mellitus

Heat Shock Proteins in Behçet Syndrome

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