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  1. Article ; Online: Emerging therapeutic targets in systemic sclerosis.

    O'Reilly, Steven

    Journal of molecular medicine (Berlin, Germany)

    2024  Volume 102, Issue 4, Page(s) 465–478

    Abstract: Systemic sclerosis is an autoimmune connective tissue disease which is characterised by vascular perturbations, inflammation, and fibrosis. Although huge progress recently into the underlying molecular pathways that are perturbed in the disease, ... ...

    Abstract Systemic sclerosis is an autoimmune connective tissue disease which is characterised by vascular perturbations, inflammation, and fibrosis. Although huge progress recently into the underlying molecular pathways that are perturbed in the disease, currently no therapy exists that targets the fibrosis element of the disease and consequently there is a huge unmet medical need. Emerging studies reveal new dimensions of complexity, and multiple aberrant pathways have been uncovered that have shed light on disturbed signalling in the disease, primarily in inflammatory pathways that can be targeted with repurposed drugs. Pre-clinical animal models using these inhibitors have yielded proof of concept for targeting these signalling systems and progressing to clinical trials. This review will examine the recent evidence of new perturbed pathways in SSc and how these can be targeted with new or repurposed drugs to target a currently intractable disease.
    MeSH term(s) Animals ; Scleroderma, Systemic/drug therapy ; Scleroderma, Systemic/metabolism ; Fibrosis ; Autoimmune Diseases ; Signal Transduction
    Language English
    Publishing date 2024-02-22
    Publishing country Germany
    Document type Journal Article ; Review
    ZDB-ID 1223802-8
    ISSN 1432-1440 ; 0946-2716
    ISSN (online) 1432-1440
    ISSN 0946-2716
    DOI 10.1007/s00109-024-02424-w
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  2. Article ; Online: S100A4 a classical DAMP as a therapeutic target in fibrosis.

    O'Reilly, Steven

    Matrix biology : journal of the International Society for Matrix Biology

    2024  Volume 127, Page(s) 1–7

    Abstract: Fibrosis regardless of aetiology is characterised by persistently activated myofibroblasts that are contractile and secrete excessive amounts of extracellular matrix molecules that leads to loss of organ function. Damage-Associated Molecular Patterns ( ... ...

    Abstract Fibrosis regardless of aetiology is characterised by persistently activated myofibroblasts that are contractile and secrete excessive amounts of extracellular matrix molecules that leads to loss of organ function. Damage-Associated Molecular Patterns (DAMPs) are endogenous host-derived molecules that are released from cells dying or under stress that can be triggered by a variety of insults, either chemical or physical, leading to an inflammatory response. Among these DAMPs is S100A4, part of the S100 family of calcium binding proteins that participate in a variety of cellular processes. S100A4 was first described in context of cancer as a pro-metastatic factor. It is now appreciated that aside from its role in cancer promotion, S100A4 is intimately involved in tissue fibrosis. The extracellular form of S100A4 exerts its effects through multiple receptors including Toll-Like Receptor 4 and RAGE to evoke signalling cascades involving downstream mediators facilitating extracellular matrix deposition and myofibroblast generation and can play a role in persistent activation of myofibroblasts. S100A4 may be best understood as an amplifier of inflammatory and fibrotic processes. S100A4 appears critical in systemic sclerosis pathogenesis and blocking the extracellular form of S100A4 in vivo in various animal models of disease mitigates fibrosis and may even reverse established disease. This review appraises S100A4's position as a DAMP and its role in fibrotic conditions and highlight therapeutically targeting this protein to halt fibrosis, suggesting that it is a tractable target.
    MeSH term(s) Animals ; Fibrosis ; Myofibroblasts ; Neoplasms ; Scleroderma, Systemic ; Signal Transduction ; Humans
    Language English
    Publishing date 2024-01-12
    Publishing country Netherlands
    Document type Journal Article ; Review
    ZDB-ID 1183793-7
    ISSN 1569-1802 ; 0945-053X
    ISSN (online) 1569-1802
    ISSN 0945-053X
    DOI 10.1016/j.matbio.2024.01.002
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  3. Article ; Online: Senescence in diffuse systemic sclerosis is elevated and may play a role in fibrosis.

    O'Reilly, Steven

    Clinical and experimental immunology

    2023  

    Language English
    Publishing date 2023-07-17
    Publishing country England
    Document type Journal Article
    ZDB-ID 218531-3
    ISSN 1365-2249 ; 0009-9104 ; 0964-2536
    ISSN (online) 1365-2249
    ISSN 0009-9104 ; 0964-2536
    DOI 10.1093/cei/uxad077
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  4. Article ; Online: At the crossroads of inflammation and fibrosis: epiregulin.

    O'Reilly, Steven

    Annals of the rheumatic diseases

    2023  Volume 82, Issue 6, Page(s) 740–741

    MeSH term(s) Humans ; Epiregulin ; Fibroblasts ; Fibrosis ; Inflammation/pathology ; Intercellular Signaling Peptides and Proteins ; Scleroderma, Systemic/pathology ; Skin/pathology
    Chemical Substances Epiregulin ; Intercellular Signaling Peptides and Proteins
    Language English
    Publishing date 2023-02-07
    Publishing country England
    Document type Journal Article ; Comment
    ZDB-ID 7090-7
    ISSN 1468-2060 ; 0003-4967
    ISSN (online) 1468-2060
    ISSN 0003-4967
    DOI 10.1136/ard-2023-223851
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  5. Article ; Online: Interleukin-11 and its eminent role in tissue fibrosis: a possible therapeutic target.

    O'Reilly, Steven

    Clinical and experimental immunology

    2023  Volume 214, Issue 2, Page(s) 154–161

    Abstract: Interleukin-11 is a cytokine from the IL-6 family of cytokines that includes IL-6 and oncostatin-M. Initially described for its role in platelet generation, it is now appreciated that this cytokine has multiple functions. Recently it has been found that ... ...

    Abstract Interleukin-11 is a cytokine from the IL-6 family of cytokines that includes IL-6 and oncostatin-M. Initially described for its role in platelet generation, it is now appreciated that this cytokine has multiple functions. Recently it has been found that IL-11 is critical in fibrosis in multiple different organ systems and systemically as in the autoimmune disease systemic sclerosis. Animal models of fibrosis have determined that animals with IL-11 receptor deletions have retarded fibrosis and that in wild-type animals IL-11 is found at the organ of fibrosis. Recent evidence suggests that IL-11 may be a master regulator of fibrosis regardless of end target organ. With the development of neutralizing antibodies targeting the cytokine in pre-clinical models this could be a possible therapeutic, in a disease in which no specific therapies exist. This review appraises the evidence of the role of IL-11 in tissue fibrosis, its signalling properties, and therapeutic targeting. The review ends with an appraisal of indications for which IL-11 modulation is targeted.
    MeSH term(s) Animals ; Interleukin-11 ; Interleukin-6 ; Fibrosis ; Cytokines ; Signal Transduction ; Interleukin-33
    Chemical Substances Interleukin-11 ; Interleukin-6 ; Cytokines ; Interleukin-33
    Language English
    Publishing date 2023-09-16
    Publishing country England
    Document type Review ; Journal Article
    ZDB-ID 218531-3
    ISSN 1365-2249 ; 0009-9104 ; 0964-2536
    ISSN (online) 1365-2249
    ISSN 0009-9104 ; 0964-2536
    DOI 10.1093/cei/uxad108
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  6. Article ; Online: Toll-like receptor triggering in systemic sclerosis: time to target.

    O'Reilly, Steven

    Rheumatology (Oxford, England)

    2022  Volume 62, Issue SI, Page(s) SI12–SI19

    Abstract: SSc is an autoimmune disease that has features of vascular abnormalities, inflammation and skin and lung fibrosis. Toll-like receptors (TLRs) are sentinel receptors that serve to recognize pathogens or internal danger signals leading to downstream ... ...

    Abstract SSc is an autoimmune disease that has features of vascular abnormalities, inflammation and skin and lung fibrosis. Toll-like receptors (TLRs) are sentinel receptors that serve to recognize pathogens or internal danger signals leading to downstream signalling pathways that ultimately lead to inflammation and modification of adaptive immunity. Inflammation and fibrosis appear intricately connected in this disease and TLR ligation on fibroblasts can directly activate these cells to produce copious amounts of collagen, a hallmark of disease. The presence of damage-associated molecular patterns in association with fibrosis has been highlighted. Given their prominent role in disease, this review discusses the evidence of their expression and role in disease pathogenesis and possible therapeutic intervention to mitigate fibrosis.
    MeSH term(s) Humans ; Toll-Like Receptors ; Scleroderma, Systemic ; Signal Transduction ; Fibrosis ; Inflammation
    Chemical Substances Toll-Like Receptors
    Language English
    Publishing date 2022-07-18
    Publishing country England
    Document type Review ; Journal Article
    ZDB-ID 1464822-2
    ISSN 1462-0332 ; 1462-0324
    ISSN (online) 1462-0332
    ISSN 1462-0324
    DOI 10.1093/rheumatology/keac421
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    Zs.MO 497: Show issues

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  7. Article ; Online: Interleukin-36α is elevated in diffuse systemic sclerosis and may potentiate fibrosis.

    O'Reilly, Steven

    Cytokine

    2022  Volume 156, Page(s) 155921

    Abstract: Systemic sclerosis (SSc) is an autoimmune prototypical connective tissues disease that results in alterations in vasculature, inflammation and fibrosis of the skin. Interleukin-1 family cytokines has been implicated in the disease including IL-1. IL-36α ... ...

    Abstract Systemic sclerosis (SSc) is an autoimmune prototypical connective tissues disease that results in alterations in vasculature, inflammation and fibrosis of the skin. Interleukin-1 family cytokines has been implicated in the disease including IL-1. IL-36α is an IL-1 family member that is clearly implicated in psoriatic skin disease but its role in systemic sclerosis disease is not clear. The aim of this work is to evaluate the levels and role of IL-36α in systemic sclerosis. Early diffuse SSc patients sera was isolated along with healthy controls and IL-36 levels quantified by ELISA. In vitro analysis was also undertaken with primary dermal fibroblasts with recombinant IL-36α and keratinocyte cells were also incubated with IL-36α. Cytokines were measured by ELISA. Serum IL-36 was significantly elevated compared to healthy controls. Elevated neutrophil elastase was also elevated in the matched sera. IL-36 was not directly pro-fibrotic in dermal fibroblasts but did induce pro-inflammatory cytokines that were dependant on the MAPK pathway for their release. IL-36α also led to release of CCL20 and CCL2 in keratinocytes which may potentiate fibrosis. IL-36α is elevated in SSc serum and whilst not directly pro-fibrotic it may through keratinocytes, potentiate fibrosis through keratinocyte-immune fibroblast cross-talk.
    MeSH term(s) Cytokines/metabolism ; Fibroblasts/metabolism ; Fibrosis ; Humans ; Interleukin-1/blood ; Interleukin-1/metabolism ; Interleukins/metabolism ; Scleroderma, Diffuse/metabolism ; Scleroderma, Diffuse/pathology ; Scleroderma, Systemic/metabolism ; Skin/metabolism
    Chemical Substances Cytokines ; IL36A protein, human ; Interleukin-1 ; Interleukins
    Language English
    Publishing date 2022-06-03
    Publishing country England
    Document type Journal Article
    ZDB-ID 1018055-2
    ISSN 1096-0023 ; 1043-4666
    ISSN (online) 1096-0023
    ISSN 1043-4666
    DOI 10.1016/j.cyto.2022.155921
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    Zs.A 2840: Show issues Location:
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  8. Article ; Online: Elevated interleukin-11 in systemic sclerosis and role in disease pathogenesis.

    Steadman, Thomas / O'Reilly, Steven

    The Journal of dermatology

    2023  Volume 50, Issue 10, Page(s) 1255–1261

    Abstract: Systemic sclerosis (SSc) is an autoimmune connective tissue disease in which there is elevated inflammation, aberrant cytokine expression, and subsequent fibrosis. Interleukin-11 (IL-11) is a recently described profibrotic cytokine that can mediate ... ...

    Abstract Systemic sclerosis (SSc) is an autoimmune connective tissue disease in which there is elevated inflammation, aberrant cytokine expression, and subsequent fibrosis. Interleukin-11 (IL-11) is a recently described profibrotic cytokine that can mediate fibrosis in the heart, lungs, and skin and is upregulated by transforming Growth Factor-β (TGF-β1). The objective of this study was to quantify the serum levels of IL-11 in early diffuse SSc patients. Also, if IL-11 could regulate the alarmin IL-33 in dermal fibroblasts was quantified. Early diffuse SSc patient sera was isolated and IL-11 was quantified by specific commercial ELISA compared to healthy control (n = 17). Healthy dermal fibroblasts were cultured in vitro and then serum starved and incubated with or without recombinant IL-11. At specific early and late time points the supernatant was quantified for the alarmin IL-33 by specific ELISA. In early diffuse SSc patients it was demonstrated that they have elevated IL-11 in their sera. In a subgroup of SSc patients with interstitial lung disease (ILD) this elevation was particularly pronounced compared to those devoid of fibrotic lung disease. In vitro incubation of healthy dermal fibroblasts led to a significant induction of IL-33 cytokine release into the cell media. IL-11 is a profibrotic cytokine that is elevated in early diffuse SSc and is particularly elevated in those with ILD. This suggests that IL-11 could be a possible biomarker of ILD in SSc. It was also found that IL-11 led to release of the cytokine alarmin IL-33 in fibroblasts at earlier time points but not late time points, suggesting early stimulation elicits an inflammatory response in the local microenvironment but prolonged stimulation leads to fibrosis.
    MeSH term(s) Humans ; Interleukin-11/metabolism ; Interleukin-33/metabolism ; Alarmins/metabolism ; Scleroderma, Systemic ; Fibrosis ; Scleroderma, Diffuse/pathology ; Cytokines/metabolism ; Lung Diseases, Interstitial/pathology ; Fibroblasts/pathology ; Skin/pathology
    Chemical Substances Interleukin-11 ; Interleukin-33 ; Alarmins ; Cytokines
    Language English
    Publishing date 2023-06-08
    Publishing country England
    Document type Journal Article
    ZDB-ID 800103-0
    ISSN 1346-8138 ; 0385-2407
    ISSN (online) 1346-8138
    ISSN 0385-2407
    DOI 10.1111/1346-8138.16854
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  9. Article ; Online: Keeping time on liver fibrosis.

    O'Reilly, Steven

    Acta pharmacologica Sinica

    2021  Volume 43, Issue 5, Page(s) 1215–1216

    MeSH term(s) Humans ; Liver/pathology ; Liver Cirrhosis/pathology
    Language English
    Publishing date 2021-08-11
    Publishing country United States
    Document type Journal Article
    ZDB-ID 1360774-1
    ISSN 1745-7254 ; 0253-9756 ; 1671-4083
    ISSN (online) 1745-7254
    ISSN 0253-9756 ; 1671-4083
    DOI 10.1038/s41401-021-00716-2
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  10. Article ; Online: Serum amyloid A as a universal biomarker in lung disease.

    O'Reilly, Steven

    Internal medicine journal

    2021  Volume 51, Issue 7, Page(s) 1195–1196

    MeSH term(s) Biomarkers ; Humans ; Lung Diseases/diagnosis ; Serum Amyloid A Protein
    Chemical Substances Biomarkers ; Serum Amyloid A Protein
    Language English
    Publishing date 2021-07-19
    Publishing country Australia
    Document type Letter ; Comment
    ZDB-ID 2045436-3
    ISSN 1445-5994 ; 1444-0903
    ISSN (online) 1445-5994
    ISSN 1444-0903
    DOI 10.1111/imj.15324
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