References of "Louis, Edouard"
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See detailUntargeted serum metabolite profiling of colorectal cancer using GC-Orbitrap technology
Di Giovanni, Nicolas ULg; Cojocariu, C; Silcock, P et al

Poster (2017, June)

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See detailOLFM4, KNG1 and Sec24C identified by proteomics and immunohistochemistry as potential markers of early colorectal cancer stages
QUESADA-CALVO, Florence ULg; MASSOT, Charlotte ULg; Bertrand, Virginie ULg et al

in Clinical Proteomics (2017), 24(9),

Abstract Background: Despite recent advances in colorectal cancer (CRC) diagnosis and population screening programs, the identification of patients with preneoplastic lesions or with early CRC stages ... [more ▼]

Abstract Background: Despite recent advances in colorectal cancer (CRC) diagnosis and population screening programs, the identification of patients with preneoplastic lesions or with early CRC stages remains challenging and is important for reducing CRC incidence and increasing patient’s survival. Methods: We analysed 76 colorectal tissue samples originated from early CRC stages, normal or inflamed mucosa by label-free proteomics. The characterisation of three selected biomarker candidates was performed by immunohisto‑ chemistry on an independent set of precancerous and cancerous lesions harbouring increasing CRC stages. Results: Out of 5258 proteins identified, we obtained 561 proteins with a significant differential distribution among groups of patients and controls. KNG1, OLFM4 and Sec24C distributions were validated in tissues and showed differ‑ ent expression levels especially in the two early CRC stages compared to normal and preneoplastic tissues. Conclusion: We highlighted three proteins that require further investigations to better characterise their role in early CRC carcinogenesis and their potential as early CRC markers. [less ▲]

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See detailProteomic differential distribution of 53BP1 in serrated and conventional adenomas validated by histological characterisation
QUESADA-CALVO, Florence ULg; Merli, Angela-Maria ULg; MASSOT, Charlotte ULg et al

Poster (2017, February 10)

INTRODUCTION: Sessile serrated adenoma/polyp (SSA/p) is a precancerous lesion, mostly located in the right side of the colon (cecum, ascending and transverse colon). The difficulty is to visualize this ... [more ▼]

INTRODUCTION: Sessile serrated adenoma/polyp (SSA/p) is a precancerous lesion, mostly located in the right side of the colon (cecum, ascending and transverse colon). The difficulty is to visualize this lesion during colonoscopy because of its subtle appearance. MATERIAL AND METHOD: We compared proteomes of serrated polyps (SSA/p) and conventional adenomas using residual human formalin fixed paraffin embedded (FFPE) samples. FFPE-FASP method was applied on samples before label free proteomic analysis. Immunohistochemistry (IHC) characterisation of one candidate marker was performed for tissue validation on an independent set of samples including: conventional adenomas (low and high-grade dysplasia), serrated polyps (hyperplastic polyps, SSA/p and traditional serrated adenoma) and finally normal colon (taken at the margin of colorectal cancer (CRC) or of diverticular disease). RESULTS: Proteomics provided 765 proteins (out of 5992 proteins identified) significantly discriminating conventional adenomas from serrated lesions. We selected 53BP1 (Tumor suppressor p53-binding protein 1) among these for IHC validation, because of its tumor suppressor gene function and role as a mediator of DNA damage checkpoint. 53BP1 appeared significantly up-regulated in proteomes of low and high grade adenomas compared to these of normal tissue and SSA/p. 53BP1 IHC signal was located in the nucleus and the percentage of positive nucleus decreased in serrated polyps, especially in crypts and in the border epithelium, confirming part of the proteomic results. CONCLUSION: This study highlights potential marker proteins, including 53BP1 from which IHC signal was strongly decreased in some serrated polyps. The loss of 53BP1 has been associated with tumour progression and poor prognosis, while little is currently known about its involvement in precancerous CRC lesions. 53BP1 decrease of expression in the nucleus and therefore possible loss of function in some epithelial cells could reflect important changes occurring during dysplasia to neoplasia progression in serrated lesions. [less ▲]

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See detailIdentification of proteins discriminating inflammation induced dysplasia from simple inflammation in ulcerative colitis by laser capture microdissection and label free proteomics – a pilot study
Merli, Angela-Maria ULg; QUESADA-CALVO, Florence ULg; MASSOT, Charlotte ULg et al

Conference (2017, February 09)

Chronic colonic inflammation in ulcerative colitis (UC) may induce dysplasia, which can itself progress and transform into neoplasia. Diagnosis of dysplasia in UC remains difficult particularly when ... [more ▼]

Chronic colonic inflammation in ulcerative colitis (UC) may induce dysplasia, which can itself progress and transform into neoplasia. Diagnosis of dysplasia in UC remains difficult particularly when tissue inflammation is present. The aim of this retrospective pilot study was to highlight proteins specifically associated with inflammation induced dysplasia in UC. We performed a pilot experiment on 15 Formalin-Fixed, Paraffin-Embedded (FFPE) samples isolated from 5 cases of UC patients with a Polypoïd Pedunculated dysplasia (UC-PP). We compared the proteomes of the UC-PP, the inflammatory (UC-I) and the normal (UC-NL) tissues of each patient. We performed Laser Capture Microdissection (LCM) in order to collect only epithelial cells, avoiding inflammatory infiltrating ones. Label free proteomic analysis using a 2D-nanoUPLC coupled with a hybrid Quadrupole-Orbitrap was applied, as well as differential analysis on the paired samples. Immunohistochemistry (IHC) characterisation of one of the selected proteins of interest was used for validation. Out of 985 quantified proteins, 7 were found significantly more abundant in UC-PP compared to UC-I tissues, with 6 being only detected in UC-PP using proteomics. One of these is Solute Carrier Family 12 member 2 (SLC12A2), also known as Na-K-2Cl co-transporter 1 (NKCC1), a protein involved in ionic balance, in T-cell migration promotion and in some features involved in cancer development like proliferation, migration or invasion. IHC results obtained were in correlation with proteomic results and showed that SLC12A2 was more abundant in UC-PP tissue than in UC-I and UC-NL tissues, with a signal clearly delimiting the dysplastic region from the surrounding inflammatory tissue. This pilot experiment shows a different proteomic profile in inflammation-associated dysplasia and simple inflammation. This should be replicated using other types of dysplasia in IBD. SLC12A2 could be a potential biomarker of inflammation-associated dysplasia. [less ▲]

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See detailIdentification of proteins discriminating inflammation induced dysplasia from simple inflammation in ulcerative colitis by laser capture microdissection and label free proteomics – a pilot study
Merli, Angela-Maria ULg; QUESADA-CALVO, Florence ULg; MASSOT, Charlotte ULg et al

Poster (2017, February 01)

Chronic colonic inflammation in ulcerative colitis (UC) may induce dysplasia, which can itself progress and transform into neoplasia. Diagnosis of dysplasia in UC remains difficult particularly when ... [more ▼]

Chronic colonic inflammation in ulcerative colitis (UC) may induce dysplasia, which can itself progress and transform into neoplasia. Diagnosis of dysplasia in UC remains difficult particularly when tissue inflammation is present. The aim of this retrospective pilot study was to highlight proteins specifically associated with inflammation induced dysplasia in UC. We performed a pilot experiment on 15 Formalin-Fixed, Paraffin-Embedded (FFPE) samples isolated from 5 cases of UC patients with a Polypoïd Pedunculated dysplasia (UC-PP). We compared the proteomes of the UC-PP, the inflammatory (UC-I) and the normal (UC-NL) tissues of each patient. We performed Laser Capture Microdissection (LCM) in order to collect only epithelial cells, avoiding inflammatory infiltrating ones. Label free proteomic analysis using a 2D-nanoUPLC coupled with a hybrid Quadrupole-Orbitrap was applied, as well as differential analysis on the paired samples. Immunohistochemistry (IHC) characterisation of one of the selected proteins of interest was used for validation. Out of 985 quantified proteins, 7 were found significantly more abundant in UC-PP compared to UC-I tissues, with 6 being only detected in UC-PP using proteomics. One of these is Solute Carrier Family 12 member 2 (SLC12A2), also known as Na-K-2Cl co-transporter 1 (NKCC1), a protein involved in ionic balance, in T-cell migration promotion and in some features involved in cancer development like proliferation, migration or invasion. IHC results obtained were in correlation with proteomic results and showed that SLC12A2 was more abundant in UC-PP tissue than in UC-I and UC-NL tissues, with a signal clearly delimiting the dysplastic region from the surrounding inflammatory tissue. This pilot experiment shows a different proteomic profile in inflammation-associated dysplasia and simple inflammation. This should be replicated using other types of dysplasia in IBD. SLC12A2 could be a potential biomarker of inflammation-associated dysplasia. [less ▲]

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See detailThe role of mesenchymal stem cells in the treatment of ulcerative colitis and Crohn's disease
GREGOIRE, Céline ULg; Louis, Edouard ULg; BRIQUET, Alexandra ULg et al

in The Biology and Therapeutic Application of Mesenchymal Cells (2017)

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See detailMesenchymal stromal cell therapy for inflmmatory bowel diseases
GREGOIRE, Céline ULg; LECHANTEUR, Chantal ULg; BRIQUET, Alexandra ULg et al

in Alimentary Pharmacology & Therapeutics (2017), 45

Background Inflammatory bowel diseases (IBD) are chronic relapsing diseases in which pro-inflammatory immune cells and cytokines induce intestinal tissue damage and disability. Mesenchymal stromal cells ... [more ▼]

Background Inflammatory bowel diseases (IBD) are chronic relapsing diseases in which pro-inflammatory immune cells and cytokines induce intestinal tissue damage and disability. Mesenchymal stromal cells (MSCs) exert powerful immunomodulatory effects and stimulate tissue repair. Aim To review the current data on mesenchymal stromal cell therapy in IBD. Method We searched PubMed and ‘ClinicalTrials.gov’ databases using the terms ‘mesenchymal stromal cells’, ‘mesenchymal stem cell transplantation’, ‘inflammatory bowel diseases’, ‘Crohn disease’ and ‘colitis, ulcerative’. Additional publications were identified from individual article reference lists. Results MSCs include inhibition of Th1/Th17 lymphocytes and recruitment of regulatory T lymphocytes, induction of antigen-presenting cells into a regulatorylike profile, and stimulation of epithelial cell differentiation and proliferation. More than 200 patients with refractory fistulas have been treated with local injections of MSCs, resulting in complete response in more than half, and in overall response in approximately two thirds of patients. In refractory luminal Crohn’s disease, 49 cases of systemic MSC infusions have been reported, while trials with autologous MSCs resulted in mitigated responses, studies using allogeneic MSCs were promising, with around 60% of patients experiencing a response and around 40% achieving clinical remission. Conclusions Mesenchymal stromal cells might represent a promising therapy for IBD, especially for Crohn’s disease. There remain many unsolved questions concerning the optimal origin and source of mesenchymal stromal cells, dosage and modalities of administration. Moreover, mesenchymal stromal cells still need to prove their effectiveness compared with conventional treatments in randomised controlled trials. [less ▲]

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See detailGC×GC-(HR)TOFMS in Cancer Research
Pesesse, Romain ULg; Stefanuto, Pierre-Hugues ULg; Bertrand, Virginie ULg et al

Conference (2016, May 30)

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See detailGlucocorticoid-induced leucine zipper (GILZ) is involved in glucocorticoid-induced and mineralocorticoid-induced leptin production by osteoarthritis synovial fibroblasts.
MALAISE, Olivier ULg; Relic, Biserka; Charlier, Edith ULg et al

in Arthritis Research & Therapy (2016), 18(1), 219

BACKGROUND: Glucocorticoid-induced leucine zipper (GILZ) is a mediator of the anti-inflammatory activities of glucocorticoids. However, GILZ deletion does not impair the anti-inflammatory activities of ... [more ▼]

BACKGROUND: Glucocorticoid-induced leucine zipper (GILZ) is a mediator of the anti-inflammatory activities of glucocorticoids. However, GILZ deletion does not impair the anti-inflammatory activities of exogenous glucocorticoids in mice arthritis models and GILZ could also mediate some glucocorticoid-related adverse events. Osteoarthritis (OA) is a metabolic disorder that is partly attributed to adipokines such as leptin, and we previously observed that glucocorticoids induced leptin secretion in OA synovial fibroblasts. The purpose of this study was to position GILZ in OA through its involvement in the anti-inflammatory activities of glucocorticoids and/or in the metabolic pathway of leptin induction. The influences of mineralocorticoids on GILZ and leptin expression were also investigated. METHODS: Human synovial fibroblasts were isolated from OA patients during knee replacement surgery. Then, the cells were treated with a glucocorticoid (prednisolone), a mineralocorticoid (aldosterone), a glucocorticoid receptor (GR) antagonist (mifepristone), a selective glucocorticoid receptor agonist (Compound A), mineralocorticoid receptor (MR) antagonists (eplerenone and spironolactone), TNF-alpha or transforming growth factor (TGF)-beta. Cells were transfected with shRNA lentiviruses for the silencing of GILZ and GR. The leptin, IL-6, IL-8 and matrix metalloproteinase (MMP)-1 levels were measured by ELISA. Leptin, the leptin receptor (Ob-R), GR and GILZ expression levels were analyzed by western blotting and/or RT-qPCR. RESULTS: (1) The glucocorticoid prednisolone and the mineralocorticoid aldosterone induced GILZ expression dose-dependently in OA synovial fibroblasts, through GR but not MR. Similar effects on leptin and Ob-R were observed: leptin secretion and Ob-R expression were also induced by prednisolone and aldosterone through GR; (2) GILZ silencing experiments demonstrated that GILZ was involved in the glucocorticoid-induced and mineralocorticoid-induced leptin secretion and Ob-R expression in OA synovial fibroblasts; and (3) GILZ inhibition did not alter the production of pro-inflammatory cytokines by OA synovial fibroblast or the anti-inflammatory properties of glucocorticoids. CONCLUSIONS: The absence of GILZ prevents corticoid-induced leptin and Ob-R expression without affecting the anti-inflammatory properties of glucocorticoids in OA synovial fibroblasts. Mineralocorticoids also induce leptin and Ob-R expression through GILZ. [less ▲]

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See detailLong-term evolution and predictive factors of mild inflammatory bowel disease.
REENAERS, Catherine ULg; Pirard, C.; VAN KEMSEKE, Catherine ULg et al

in Scandinavian Journal of Gastroenterology (2016), 51(6), 712-9

BACKGROUND: Crohn's disease (CD) and ulcerative colitis (UC) are potentially progressive diseases. Few data are available on the prevalence and the factors associated with mild inflammatory bowel diseases ... [more ▼]

BACKGROUND: Crohn's disease (CD) and ulcerative colitis (UC) are potentially progressive diseases. Few data are available on the prevalence and the factors associated with mild inflammatory bowel diseases (IBD). AIM: Our aim was to assess the natural history of mild CD and mild UC and to identify predictive factors of mild evolution over the long term. METHODS: Retrospective study of IBD patients registered in the database of the university hospital CHU of Liege, Belgium. Mild CD was defined as an inflammatory luminal disease (no stricture, abdominal or perianal fistulae) requiring no immunomodulator (IM), anti-TNF and no surgery. Mild UC was defined as no requirement for IM, anti-TNF and no colectomy. RESULTS: Four hundred and seventy-three CD and 189 UC were included (median follow-up: 13 and 11 years respectively). At 1 year, 147 patients had mild CD. At 5 years and the maximum follow-up, 56% and 13% patients still had mild CD, respectively. At 1 year, 142 patients had mild UC. At 5 years and the maximum follow-up, 72% and 44% still had a mild UC, respectively. Factors associated with long-term mild CD and UC were older age at diagnosis and absence of corticosteroids in the first year. In UC proctitis location was associated with mild UC. CONCLUSIONS: In this cohort, 90% of CD patients and 3/4 of UC with mild disease at 1 year lost their mild disease status over time. An old age at diagnosis was predictive of the persistence of a mild CD and UC. [less ▲]

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See detailAnti-TNF Monotherapy for Crohn's Disease: a 13-year Multicentre Experience.
Peyrin-Biroulet, Laurent; Salleron, Julia; Filippi, Jerome et al

in Journal of Crohn's and Colitis [=JCC] (2016), 10(5), 516-24

BACKGROUND: Anti-tumour necrosis factor [TNF] therapy in combination with thiopurine is the most effective strategy for Crohn's disease, but raises safety concerns. METHODS: In a retrospective multicentre ... [more ▼]

BACKGROUND: Anti-tumour necrosis factor [TNF] therapy in combination with thiopurine is the most effective strategy for Crohn's disease, but raises safety concerns. METHODS: In a retrospective multicentre study, we investigated long-term outcome of patients starting anti-TNF monotherapy for Crohn's disease and investigated whether introducing an immunomodulator in patients losing response to anti-TNF monotherapy is effective for resetting immunogenicity. RESULTS: A total of 350 adult patients with Crohn's disease received either infliximab [n = 178, 51%] or adalimumab [n = 172, 49%] monotherapy. Mean duration of follow-up was 42 months. An immunomodulator was initiated in 53 patients [15%]. At last follow-up, 73.1% [n = 38] were in clinical remission [one patient with missing data]. Multivariate analysis identified anti-TNF type [higher need for starting immunomodulator for infliximab than for adalimumab; p = 0.0058] and first- vs second-/third-/fourth-line anti-TNF therapy [p = 0.014] as predictors of immunomodulator initiation. Among the 18 patients with available data, introduction of an immunomodulator was able to restore infliximab trough level within the therapeutic range and to induce clinical remission in 10 patients [55%]. Cumulative probability of remaining on anti-TNF therapy was 57.9% at 5 years among the 297 patients not starting an immunomodulator during follow-up. CONCLUSION: An immunomodulator was initiated in 15% of patients with Crohn's disease starting anti-TNF monotherapy. Independent predictors of immunomodulator initiation were infliximab use and second-/third-/fourth-line anti-TNF therapy. Resetting immunogenicity with an immunomodulator was effective in half of patients in a sub-study. Persistence of anti-TNF treatment at 5 years was observed in half of the 297 patients not starting an immumodulator in a real-life setting. [less ▲]

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