RNA sequencing of chronic graft versus host disease skin lesions defines shared and unique inflammatory pathways characterizing lichen planus and morphea
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE157538 | GEO | 2022/01/11
REPOSITORIES: GEO
Similar Datasets
Project description:Cutaneous involvement of chronic graft-versus-host disease (cGVHD) has a wide range of manifestations including a lichenoid form with a currently assumed mixed Th1/Th17 signature and a sclerotic form with Th1 signature. Despite substantial heterogeneity of innate and adaptive immune cells recruited to the skin and of the different clinical manifestations, treatment depends mainly on the severity of the skin involvement and relies on systemic, high-dose glucocorticoids alone or in combination with a calcineurin inhibitor. We performed the first study using RNA sequencing to profile and compare the transcriptome of lichen planus cGVHD (n = 8), morphea cGVHD (n = 5), and healthy controls (n = 6). Our findings revealed shared and unique inflammatory pathways to each cGVHD subtype that are both pathogenic and targetable. In particular, the deregulation of IFN signaling pathway was strongly associated with cutaneous cGVHD, whereas the triggering receptor expressed on myeloid cells 1 pathway was found to be specific of lichen planus and likely contributes to its pathogenesis. The results were confirmed at a protein level by performing immunohistochemistry staining and at a transcriptomic level using real-time quantitative polymerase chain reaction.
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Project description:RNA sequencing of chronic graft versus host disease skin lesions defines shared and unique inflammatory pathways characterizing lichen planus and morphea
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Project description:Lichen planus (LP) is a T cell-mediated disease affecting the stratified squamous epithelia of the skin and/or mucus membrane. Histologically, the disease is characterized by a lichenoid inflammatory infiltrate and vacuolar degeneration of the basal layer of the epidermis. LP has three major subtypes: Cutaneous, mucosal and appendageal LP. Rarely, it may affect the nails in the absence of skin and/or mucosal changes. LP may also be induced by several drugs, typically anti-hypertensive medication or be associated with infections, particularly viral hepatitis. The diagnosis is based on the clinical presentation and characteristic histological findings. Although the disease is often self-limiting, the intractable pruritus and painful mucosal erosions result in significant morbidity. The current first-line treatment are topical and/or systemic corticosteroids. In addition, immunosuppressants may be used as corticosteroid-sparing agents. These, however are often not sufficient to control disease. Janus kinase inhibitors and biologics (anti-IL-12/23, anti-IL17) have emerged as novel future treatment options. Thus, one may expect a dramatic change of the treatment landscape of LP in the near future.
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Project description:Using a quantitative proteomics approach, we compared pooled plasma samples from 35 patients with cGVHD obtained at a median of 103 days post-HCT and 18 patients without cGVHD obtained at matched timepoints to identify biomarkers for cGVHD.
2016-05-27 | PXD002762 | Pride
Project description:Oral lichen planus (OLP) and oral lichenoid lesions (OLL) are clinically and histologically similar lesions but their treatment planning and prognosis are different. The review of the literature indicates numerous criteria to distinguish these two lesions; however there is a lot of inconsistency. Thus, the aim of this study was to determine the correlation of histopathology and clinical OLP and OLL diagnosis and to clarify which histopathologic criteria could best distinguish these two diagnoses. A retrospective study showed that clinically diagnosed 92 OLPs and 14 OLLs have been confirmed histopathologically in 52.2% and 42.9% of cases, respectively. In addition, histopathology showed statistically significant more eosinophils (P<0.0005), plasma cells (P<0.0005), and granulocytes (P<0.05) in OLL than OLP. To establish histopathological diagnosis of OLP and OLL it should be mandatory to define the type of cells in mononuclear infiltrate, which can be associated more accurately with clinical feature and patient history. Therefore, currently accepted diagnostic criteria for OLP and OLL should be modified and validated on a larger number of patients taking into account particular distinguishing histopathological features.
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Project description:The pathogenesis of oral lichen planus (OLP) remains unclear, and microbial dysbiosis has been proposed to play a role in the pathogenesis of OLP. Oral mucosal swabs from 77 OLP patients and 76 healthy subjects were collected. The bacterial community among the OLP lesion, the adjacent normal mucosal, and the oral mucosal surface in healthy people were analyzed by 16S sequencing. The factor of gender and age that may affect the flora distribution of OLP patients were explored. Results indicate no significant difference in microbiota between OLP and the adjacent group. Compared with the healthy group, Neisseria, Haemophilus, Fusobacterium, Porphyromonas, Rothia, Actinomyces, and Capnocytophaga significantly increased in the OLP group. Actinomyces increased in male OLP patients, and the other six bacteria increased in female OLP patients. In female OLP patients, Lautropia and Dialister were positively correlated with age. While in male OLP patients, Moraxella, Porphyromonas, and Fusobacterium were positively correlated with age. Functional enrichment analysis suggested that abnormal energy metabolism related to ATP synthases, abnormal transport and metabolism of glycans, amino acids, and vitamins, and disorders of the local immune microenvironment might exist in OLP lesion.
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Project description:Lichen planus (LP) is a chronic, debilitating, inflammatory disease of the skin and mucous membranes that affects 1-2% of Americans. Its molecular pathogenesis remains poorly understood, and there are no FDA-approved treatments. We performed single cell RNA sequencing on blood and affected and unaffected skin from 7 LP patients. LP affected skin exhibited a robust immune infiltrate primarily composed of CD8 T-cells. These cells were specifically recruited by cytokines secreted by both superficial and dermal layers of skin. Basal keratinocytes and fibroblasts secrete CXCL9 and CXCL10, and fibroblasts secrete CCL19. Molecular analysis of LP skin and blood samples increased our understanding of disease pathogenesis and identified CCL19 as a new therapeutic target for treatment.
2024-10-03 | GSE254542 | GEO
Project description:Oral lichen planus (OLP) is a chronic T cell-mediated inflammatory disease of unknown etiology. We previously proposed that the intracellular bacteria detected in OLP lesions are important triggering factors for T cell infiltration. This study aimed to identify OLP-associated bacterial species through the characterization of intratissue bacterial communities of OLP lesions. Seven pairs of bacterial communities collected from the mucosal surface and biopsied tissues of OLP lesions were analyzed by high-throughput sequencing of the 16S rRNA gene. The intratissue bacterial communities were characterized by decreased alpha diversity but increased beta diversity compared with those on the mucosal surface. While the relative abundance of most taxa was decreased within the tissues, that of Escherichia coli was significantly increased. Four E. coli strains were isolated from additional OLP biopsies and verified as K12 strains by whole-genome sequencing. The distribution of E. coli in sections of control (n = 12) and OLP (n = 22) tissues was examined by in situ hybridization. E. coli was detected in most OLP tissues, suggesting its potential role in the pathogenesis of OLP. The oral E. coli strains isolated from OLP tissues will be useful to investigate their role as triggering factors for T cell infiltration.
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Project description:Oral lichen planus (OLP) is a common chronic inflammatory disease of the oral mucosa. The prevalence rate of OLP in adults is 0.5%-2%. The etiology and pathogenesis of OLP are still unclear. The pathogenesis of OLP may be related to the genetic polymorphism of some genes. Currently, the gene families, including tumor necrosis factor, interferon, interleukin, enzyme, and receptor, have been extensively studied. This work reviews related studies on gene polymorphism of OLP.
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Project description:Lichen planus is a chronic disease affecting the skin, appendages, and mucous membranes. A cutaneous lichen planus is a rare disease occurring in less than 1% of the general population, while oral illness is up to five times more prevalent; still, both forms equally impair the patient's quality of life. The etiology of lichen planus is not entirely understood. Yet, immune-mediated mechanisms have been recognized since environmental factors such as hepatitis virus infection, mechanical trauma, psychological stress, or microbiome changes can trigger the disease in genetically susceptible individuals. According to current understanding, lichen planus immunopathogenesis is caused by cell-mediated cytotoxicity, particularly cytotoxic T lymphocytes, whose activity is further influenced by Th1 and IL-23/Th-17 axis. However, other immunocytes and inflammatory pathways complement these mechanisms. This paper presents a comprehensive insight into the actual knowledge about lichen planus, with the causal genetic and environmental factors being discussed, the immunopathogenesis described, and the principal effectors of its inflammatory circuits identified.
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