Systemic sclerosis following COVID-19 infection with recurrent corticosteroid-induced scleroderma renal crisis

Carroll, Mitchell B.; Nagarajah, Vanitha; Campbell, Sian E.

doi:10.1136/bcr-2022-253735

Cited by 7 publications

(3 citation statements)

References 22 publications

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“…Our results indicate that genetically reduced expression of SH2B3 may lower the threshold of activation of CD8+ T cells in response to cytokines, for example IL-15 [33]. Consequently, CD8 T cells that are both more abundant and more sensitive to cytokine cues may provide protection against hypothesised infectious triggers of connective tissue disease, such as COVID19 [34,35]. Similarly, we identified a CD8 T cell csQTL colocalized with lower RDH14 expression, that encodes a retinol dehydrogenase, and that is also associated with an increased risk of mumps, a paediatric viral infection (Supplementary Figure 14D-F).…”

Section: Resultsmentioning

confidence: 99%

Milo2.0 unlocks population genetic analyses of cell state abundance using a count-based mixed model

Alice,

Marioni,

Morgan

2023

Preprint

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Cell type proportions vary between individuals and are heritable, as demonstrated by statistical genetic analysis of flow cytometry data [1,2]. Higher-resolution cell states can be identified by single-cell RNA-sequencing, the scalability of which now makes it applicable to population-scale cohorts. However, the integration of statistical genetic analysis of cell states using cohort-scale single-cell data requires appropriate algorithms to account for and model the genetic relationships and complex batch-processing inherent to these studies. We describe Milo2.0, which enables the discovery of cell state quantitative trait loci (csQTL), scaling to millions of cells across hundreds of individuals. We identify > 500 csQTLs across peripheral blood immune states and investigate their relationship with the genetic regulation of gene expression. Moreover, we colocalise immune csQTLs with human traits and identify links between immune regulators, cell state abundance and immune-mediated disease.

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Section: Resultsmentioning

confidence: 99%

Milo2.0 unlocks population genetic analyses of cell state abundance using a count-based mixed model

Alice,

Marioni,

Morgan

2023

Preprint

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“…lead to multi-organ dysfunction and autoimmunity 8 . Many autoimmune diseases that manifest in post-COVID-19 patients are systemic lupus erythematosus (SLE), polyarteritis nodosa, inflammatory myopathy, Graves disease, rheumatoid arthritis, immune thrombocytopenic purpura, vasculitis, and Guillain-Barre syndrome (GBS) 11 . Accurate data on new-onset SSc post-COVID-19 is unavailable, making our case a rare scenario.…”

Section: Clinical Discussionmentioning

confidence: 99%

Systemic sclerosis (Positive Anti-Ro 52 and Anti-Centromere antibodies) in a patient after COVID-19 infection: a rare case report

Oli,

Poudel,

et al. 2024

Annals of Medicine &Amp; Surgery

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Introduction and Importance: The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the source of COVID-19, a respiratory disease. It typically manifests as restricted pulmonary symptoms, but autoimmune dysfunction might occasionally show up. A COVID-19 infection may cause a multi-system connective tissue disease known as systemic sclerosis (SSc). In patients who recovered from COVID-19, autoimmunity may have multiple underlying causes. Case Presentation: We report the case of a 68-year-old female who, one month after contracting COVID-19, complained of dyspnea and muscle exhaustion. The patient was treated for post-COVID syndrome. She developed symptoms of chronic dyspnea, pale fingers, pursed lips, trouble chewing and swallowing, and muscle weakness after seven weeks. A chest HRCT (High-Resolution Computerised Tomography) scan suggested interstitial lung disease. Clinical characteristics and an autoantibody profile containing anti-Ro 52 and anti-centromere antibodies pointed towards systemic sclerosis. She was treated with azathioprine and prednisolone at a reduced dosage, and she is now stable with monthly follow-ups. Clinical Discussion: COVID-19 might induce cytokine storms and immunological dysregulation, ultimately culminating in autoimmune manifestations. Several autoantibodies are observed in autoimmune illnesses in post-COVID-19 infection patients. Our situation is distinct because systemic sclerosis following a COVID-19 infection is not commonly seen as an autoimmune illness. Conclusion: The number of patients with rare autoimmune diseases, like systemic sclerosis, following COVID-19 has been rising. Therefore, we should consider the possibility of autoimmune disease when looking into a patient who presents strangely or has developed new symptoms after COVID and should contact the patient’s management immediately.

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“…This cytokine storm can affect survival by modulating immune cell functions such as those of macrophages and lymphocytes [32,33]. Moreover, this in ammatory environment, coupled with intracellular adhesion molecule dysfunction, can increase vascular permeability, facilitating the migration of immune cells into the extracellular matrix [34,35]. Consequently, the activation of macrophages and CD4 T cells stimulates broblasts, leading to their proliferation and the synthesis of collagen and matrix metalloproteinases, which result in brosis and potentially internal organ dysfunction [36,37].…”

Section: Discussionmentioning

confidence: 99%

SARS-CoV-2 Spike Protein Accelerates Systemic Sclerosis by Increasing Inflammatory Cytokines, Th17 Cells, and Fibrosis

Jeong

Park

Woo

et al. 2023

Preprint

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Background Coronavirus disease 2019 (COVID-19) induces a dysfunctional immune response, inflammation, autoantibody production, and coagulopathy, which are symptoms that bear resemblance to those of autoimmune diseases, including systemic sclerosis (SSc). Methods While there is a single case report suggesting an association between COVID-19 and SSc, the effects of COVID-19 on SSc are not yet fully understood. Human embryonic kidney 293 (HEK293) cells were transfected with the SARS-CoV-2 spike protein gene, both in the absence and presence of TGF-β. The expression levels of fibrosis-related proteins were measured via Western blotting. A bleomycin (BLM)-induced SSc mouse model was employed, wherein mice were injected with the gene encoding the SARS-CoV-2 spike protein and the ACE2 receptor. The levels of fibrosis, autoantibodies, thrombotic factors, and inflammatory cytokines in tissues and serum were analyzed. Results In vitro, the expression levels of fibrosis marker proteins were elevated in the spike protein group compared to the control group. In vivo, the skin thickness of SSc mice increased following exposure to the SARS-CoV-2 spike protein. Furthermore, the levels of autoantibodies and thrombotic factors, such as anti-phospholipid antibodies (APLA), were significantly increased in the presence of the protein. Flow cytometry analysis revealed increased expression of the proinflammatory cytokine IL-17 in the skin, lungs, spleen, and blood. Moreover, tissue fibrosis and levels of inflammatory cytokines in skin and lung tissues were markedly escalated in SSc mice subjected to the protein. Conclusion COVID-19 may accelerate the development and progression of SSc by intensifying fibrosis through the upregulation of inflammation, autoantibody production, and thrombosis.

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Systemic sclerosis following COVID-19 infection with recurrent corticosteroid-induced scleroderma renal crisis

Cited by 7 publications

References 22 publications

Milo2.0 unlocks population genetic analyses of cell state abundance using a count-based mixed model

Milo2.0 unlocks population genetic analyses of cell state abundance using a count-based mixed model

Systemic sclerosis (Positive Anti-Ro 52 and Anti-Centromere antibodies) in a patient after COVID-19 infection: a rare case report

SARS-CoV-2 Spike Protein Accelerates Systemic Sclerosis by Increasing Inflammatory Cytokines, Th17 Cells, and Fibrosis

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