Academic Bibliography
https://biblio.ugent.be/
Ghent University Academic Bibliography2000-01-01T00:00+00:001monthlyStreptococcal quorum sensing peptide CSP-7 contributes to muscle inflammation and wasting
https://biblio.ugent.be/publication/01HS0MJ9VJ980MAD6TCJ93V6GA
De Spiegeleer, AntonDescamps, AmélieWynendaele, EvelienNaumovski, PetarCrombez, LiesbethPlanas, MartaFeliu, LidiaKnappe, DanielMouly, VincentBigot, AnneBielza, RafaelHoffmann, RalfVan Den Noortgate, NeleElewaut, DirkDe Spiegeleer, Bart2024Muscle wasting diseases, such as cancer cachexia and age-associated sarcopenia, have a profound and detrimental impact on functional independence, quality of life, and survival. Our understanding of the underlying mechanisms is currently limited, which has significantly hindered the development of targeted therapies. In this study, we explored the possibility that the streptococcal quorum sensing peptide Competence Stimulating Peptide 7 (CSP-7) might be a previously unidentified contributor to clinical muscle wasting. We found that CSP-7 selectively triggers muscle cell inflammation in vitro, specifically the release of IL-6. Furthermore, we demonstrated that CSP-7 can traverse the gastrointestinal barrier in vitro and is present in the systemic circulation in humans in vivo. Importantly, CSP-7 was associated with a muscle wasting phenotype in mice in vivo. Overall, our findings provide new mechanistic insights into the pathophysiology of muscle inflammation and wasting.application/pdfhttps://biblio.ugent.be/publication/01HS0MJ9VJ980MAD6TCJ93V6GAhttp://hdl.handle.net/1854/LU-01HS0MJ9VJ980MAD6TCJ93V6GAhttp://doi.org/10.1016/j.bbadis.2024.167094https://biblio.ugent.be/publication/01HS0MJ9VJ980MAD6TCJ93V6GA/file/01HS0MMJ9G6CYTVSZ0C8WBYTKRengNo license (in copyright)info:eu-repo/semantics/restrictedAccessBIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASEISSN: 0925-4439ISSN: 1879-260XMedicine and Health SciencesMuscle wastingCSP-7Competence stimulating peptideQuorum sensing peptideMicrobiotaSarcopeniaLC-MSHuman plasmaPeptidecachexiaStreptococcal quorum sensing peptide CSP-7 contributes to muscle inflammation and wastingjournalArticleinfo:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionRANKL blockade for erosive hand osteoarthritis : a randomized placebo-controlled phase 2a trial
https://biblio.ugent.be/publication/01HPRSKRFP1HX7K3DWJ9A3RXV6
Wittoek, RuthVerbruggen, GustVanhaverbeke, TineColman, RoosElewaut, Dirk2024Erosive hand osteoarthritis (OA) is a prevalent and disabling disease with limited treatment options. Here we present the results of a monocentric, placebo-controlled, double-blind, randomized phase 2a clinical trial with denosumab, a receptor activator of nuclear factor-kappa B ligand inhibitor, evaluating the effects on structure modification in erosive hand OA. Patients were randomized to 48 weeks treatment with denosumab 60 mg every 3 months (n = 51, 41 females) or placebo (n = 49, 37 females). The primary (radiographic) endpoint was the change in the total Ghent University Scoring System (GUSS) at week 24, where positive changes correspond to remodeling and negative changes to erosive progression. Secondary endpoints were the change in the GUSS at week 48 and the number of new erosive joints at week 48 by the anatomical phase scoring system. Baseline mean GUSS (standard deviation) of target joints was 155.9 (69.3) in the denosumab group and 158.7 (46.8) in the placebo group. The primary endpoint was met with an estimated difference between groups of 8.9 (95% confidence interval (CI) 1.0 to 16.9; P = 0.024) at week 24. This effect was confirmed at week 48 (baseline adjusted GUSS (standard error of the mean) denosumab and placebo were 163.5 (2.9) and 149.2 (3.9), respectively; with an estimated difference between groups of 14.3 (95% CI 4.6 to 24.0; P = 0.003)). At patient level, more new erosive joints were developed in the placebo group compared with denosumab at week 48 (odds ratio 0.24 (95% CI 0.08 to 0.72); P = 0.009). More adverse events occurred in the placebo group (125 events in 44 patients (90%)) compared with the denosumab group (97 events in 41 patients (80%)). These results demonstrate that denosumab has structure modifying effects in erosive hand OA by inducing remodeling and preventing new erosive joints. EU Clinical Trials Register identifier 2015-003223-53.
Denosumab, a receptor activator of nuclear factor-kappa B ligand inhibitor, previously developed for osteoporosis, was shown to be effective at inducing structural modification in patients with erosive hand osteoarthritis after 24 weeks.application/pdfhttps://biblio.ugent.be/publication/01HPRSKRFP1HX7K3DWJ9A3RXV6http://hdl.handle.net/1854/LU-01HPRSKRFP1HX7K3DWJ9A3RXV6http://doi.org/10.1038/s41591-024-02822-0https://biblio.ugent.be/publication/01HPRSKRFP1HX7K3DWJ9A3RXV6/file/01HPRSTFN0PQH0T0NPJDGQ8P04engSpringer Science and Business Media LLCCreative Commons Attribution 4.0 International Public License (CC-BY 4.0)info:eu-repo/semantics/openAccessNATURE MEDICINEISSN: 1078-8956ISSN: 1546-170XMedicine and Health SciencesRheumatologyErosive hand osteoarthritisDenosumabRANKL blockade for erosive hand osteoarthritis : a randomized placebo-controlled phase 2a trialjournalArticleinfo:eu-repo/semantics/articleinfo:eu-repo/semantics/acceptedVersionTregs protect against invariant NKT cell-mediated autoimmune colitis and hepatitis
https://biblio.ugent.be/publication/01HKD1W20NXZQGX96SX7YCMD71
Venken, KoenDecruy, Tine Sparwasser, TimElewaut, Dirk2024Immunomodulatory T cells play a pivotal role in protection against (auto)immune-mediated diseases that open perspectives for therapeutic modulation. However, how immune regulatory networks operate in vivo is less understood. To this end, we focused on FOXP3+CD4+CD25+ regulatory T cells (Tregs) and invariant natural killer T (iNKT) cells, two lymphocyte populations that independently regulate adaptive and innate immune responses. In vitro, a functional interplay between Tregs and iNKT cells has been described, but whether Tregs modulate the function and phenotype of iNKT cell subsets in vivo and whether this controls iNKT-mediated autoimmunity is unclear. Taking advantage of the conditional depletion of Tregs, we examined the in vivo interplay between iNKT and Treg cells in steady state and in preclinical models of liver and gut autoimmunity. Under non-inflamed conditions, Treg depletion enhanced glycolipid-mediated iNKT cell responses, with a general impact on Type 1, 2 and 17 iNKT subsets. Moreover, in vivo iNKT activation in the absence of Tregs suppressed the induction of iNKT anergy, consistent with a reduction in programmed cell death receptor 1 (PD-1) expression. Importantly, we unveiled a clear role for an in vivo Treg-iNKT crosstalk both in concanavalin A-induced acute hepatitis and oxazolone-induced colitis. Here, the absence of Tregs led to a markedly enhanced liver and gut pathology, which was not observed in iNKT-deficient mice. Taken together, these results provide evidence for a functional interplay between regulatory T cell subsets critical in controlling the onset of autoimmune disease.application/pdfhttps://biblio.ugent.be/publication/01HKD1W20NXZQGX96SX7YCMD71http://hdl.handle.net/1854/LU-01HKD1W20NXZQGX96SX7YCMD71http://doi.org/10.1111/imm.13718https://biblio.ugent.be/publication/01HKD1W20NXZQGX96SX7YCMD71/file/01HKD22GT68VRCM7VWRT1ZMHTGengNo license (in copyright)info:eu-repo/semantics/restrictedAccessIMMUNOLOGYISSN: 0019-2805ISSN: 1365-2567Biology and Life SciencesMedicine and Health SciencesTregsinnate-like T cellsimmunoregulationhepatitiscolitisautoimmunityTregs protect against invariant NKT cell-mediated autoimmune colitis and hepatitisjournalArticleinfo:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersion