Caroline Wathieu

University of Liège

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Alain Chariot

University of Liège

Benjamin G Dewals

University of Liège

Kateryna Shostak

University of Liège

Sylvia Tielens

University of Liège

Christophe Desmet

University of Liège

Maud Vandereyken

University of Dundee

Marion Rolot

University of Liège

Souad Rahmouni

University of Liège

Ivan Nemazanyy

Inserm

Maneesh Singh

Tata Memorial Hospital

Cooperative Institutions

University of Liège

Centre Hospitalier Universitaire de Liège

Walloon Excellence in Lifesciences and Biotechnology

Inserm

VIB-UGent Center for Inflammation Research

Vlaams Instituut voor Biotechnologie

Centre National de la Recherche Scientifique

University Hospital Cologne

Molecular Oncology (United States)

Medical Research Council

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NF-κB Signaling in Ex-Vivo Mouse Intestinal Organoids

Methods in molecular biology (2021)

Kateryna Shostak Caroline Wathieu Sylvia Tielens Alain Chariot

Organoid

Ex vivo

10.1007/978-1-0716-1669-7_17

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Citations (2)

IL-4 RECEPTOR SIGNALING REGULATES LUNG MACROPHAGES DURING HELMINTH COINFECTION RESULTING IN ENHANCED GAMMAHERPESVIRUS PERMISSIVENESS

The Journal of Immunology (2023)

Gerogios Petrellis Marion Rolot Amira Preure Caroline Wathieu Annette Dougal

Abstract Helminth infection conditions lung macrophages in the long term, but little is known about how helminths affect lung macrophage responses to respiratory viral coinfection. Experimental helminth infection of BALB/c and C57BL/6 mice revealed an increased type 2 airway inflammation in C57BL/6 mice that was associated with pronounced phenotypic changes in lung macrophages. These changes consist of a disappearance reaction of SiglecF+ alveolar macrophages (AlvMs) and a concomitant recruitment of monocyte-derived macrophages. Monocyte-derived macrophages replenish macrophages in the airways and lung, as shown with Ms4a3TdT reporter mice, and have a distinct profile to tissue resident macrophages. Competent IL-4Rα responsiveness or intra-tracheal instillation of recombinant IL-4 or IL-13 reproduced the contraction of AlvMs and recruitment of monocyte-derived macrophages, while anti-IL13 antibody treatment impaired the phenotypic changes post helminth infection. Helminth infection of C57BL/6 mice resulted in enhanced permissiveness to subsequent infection with murid gammaherpesvirus 4 (MuHV-4) during the acute stage of the infection in vivo with viral early tropism mainly restricted to AlvMs. AlvMs isolated from helminth-infected C57BL/6 mice appear more permissive ex vivo to MuHV-4. This enhanced permissiveness of AlvMs after helminth infection was dependent on direct IL-4Rα signalling. Thus macrophages-specific IL-4Ra signalling is required for the observed macrophage phenotypic changes and renders AlvMs more permissive to gammaherpesvirus infection. Supported by FNRS-ASP

Permissiveness

10.4049/jimmunol.210.supp.72.36

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Loss of Elp3 blocks intestinal tuft cell differentiation via an mTORC1-Atf4 axis

The EMBO Journal (2024)

Caroline Wathieu Arnaud Lavergne Xinyi Xu Marion Rolot Ivan Nemazanyy

Nippostrongylus brasiliensis

Intestinal epithelium

10.1038/s44318-024-00184-4

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Dual-Specificity Phosphatase 3 Deletion Protects Female, but Not Male, Mice from Endotoxemia-Induced and Polymicrobial-Induced Septic Shock

The Journal of Immunology (2017)

Maud Vandereyken Pratibha Singh Caroline Wathieu Sophie Jacques Tinatin Zurashvilli

Abstract Dual-specificity phosphatase 3 (DUSP3) is a small phosphatase with poorly known physiological functions and for which only a few substrates are known. Using knockout mice, we recently reported that DUSP3 deficiency confers resistance to endotoxin- and polymicrobial-induced septic shock. We showed that this protection was macrophage dependent. In this study, we further investigated the role of DUSP3 in sepsis tolerance and showed that the resistance is sex dependent. Using adoptive-transfer experiments and ovariectomized mice, we highlighted the role of female sex hormones in the phenotype. Indeed, in ovariectomized females and in male mice, the dominance of M2-like macrophages observed in DUSP3−/− female mice was reduced, suggesting a role for this cell subset in sepsis tolerance. At the molecular level, DUSP3 deletion was associated with estrogen-dependent decreased phosphorylation of ERK1/2 and Akt in peritoneal macrophages stimulated ex vivo by LPS. Our results demonstrate that estrogens may modulate M2-like responses during endotoxemia in a DUSP3-dependent manner.

Adoptive Cell Transfer

Knockout mouse

10.4049/jimmunol.1602092

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Citations (16)

Elp3‐mediated codon‐dependent translation promotes mTORC2 activation and regulates macrophage polarization

The EMBO Journal (2022)

Dawei Chen Ivan Nemazanyy Olivier Peulen Kateryna Shostak Xinyi Xu

Abstract Macrophage polarization is a process whereby macrophages acquire distinct effector states (M1 or M2) to carry out multiple and sometimes opposite functions. We show here that translational reprogramming occurs during macrophage polarization and that this relies on the Elongator complex subunit Elp3, an enzyme that modifies the wobble uridine base U34 in cytosolic tRNAs. Elp3 expression is downregulated by classical M1‐activating signals in myeloid cells, where it limits the production of pro‐inflammatory cytokines via FoxO1 phosphorylation, and attenuates experimental colitis in mice. In contrast, alternative M2‐activating signals upregulate Elp3 expression through a PI3K‐ and STAT6‐dependent signaling pathway. The metabolic reprogramming linked to M2 macrophage polarization relies on Elp3 and the translation of multiple candidates, including the mitochondrial ribosome large subunit proteins Mrpl3, Mrpl13, and Mrpl47. By promoting translation of its activator Ric8b in a codon‐dependent manner, Elp3 also regulates mTORC2 activation. Elp3 expression in myeloid cells further promotes Wnt‐driven tumor initiation in the intestine by maintaining a pool of tumor‐associated macrophages exhibiting M2 features. Collectively, our data establish a functional link between tRNA modifications, mTORC2 activation, and macrophage polarization.

Macrophage polarization

10.15252/embj.2021109353

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Citations (20)

Dusp3 deletion in mice promotes experimental lung tumour metastasis in a macrophage dependent manner

PLoS ONE (2017)

Maud Vandereyken Sophie Jacques Eva Van Overmeire Mathieu Amand Natacha Rocks

Vaccinia-H1 Related (VHR) dual-specificity phosphatase, or DUSP3, plays an important role in cell cycle regulation and its expression is altered in several human cancers. In mouse model, DUSP3 deletion prevents neo-angiogenesis and b-FGF-induced microvessel outgrowth. Considering the importance of angiogenesis in metastasis formation, our study aimed to investigate the role of DUSP3 in tumour cell dissemination. Using a Lewis Lung carcinoma (LLC) experimental metastasis model, we observed that DUSP3-/- mice developed larger lung metastases than littermate controls. DUSP3-/- bone marrow transfer to lethally irradiated DUSP3+/+ mice was sufficient to transfer the phenotype to DUSP3+/+ mice, indicating that hematopoietic cells compartment was involved in the increased tumour cell dissemination to lung tissues. Interestingly, we found a higher percentage of tumour-promoting Ly6Cint macrophages in DUSP3-/- LLC-bearing lung homogenates that was at least partially due to a better recruitment of these cells. This was confirmed by 1) the presence of higher number of the Ly6Bhi macrophages in DUSP3-/- lung homogenates and by 2) the better migration of DUSP3-/- bone marrow sorted monocytes, peritoneal macrophages and bone marrow derived macrophages (BMDMs), compared to DUSP3+/+ monocytes, macrophages and BMDMs, in response to LLC-conditioned medium. Our study demonstrates that DUSP3 phosphatase plays a key role in metastatic growth through a mechanism involving the recruitment of macrophages towards LLC-bearing lungs.

Lewis lung carcinoma

10.1371/journal.pone.0185786

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Citations (17)