A5090058596- Immune Response and Inflammation
- Tuberculosis Research and Epidemiology
- Mycobacterium research and diagnosis
- IL-33, ST2, and ILC Pathways
- Asthma and respiratory diseases
- Signaling Pathways in Disease
- Inflammasome and immune disorders
- Immune Cell Function and Interaction
- Eosinophilic Esophagitis
- Interstitial Lung Diseases and Idiopathic Pulmonary Fibrosis
- Infectious Diseases and Tuberculosis
- Cytokine Signaling Pathways and Interactions
- Chronic Obstructive Pulmonary Disease (COPD) Research
- T-cell and B-cell Immunology
- Pediatric health and respiratory diseases
- interferon and immune responses
- Peptidase Inhibition and Analysis
- Immune cells in cancer
- Neonatal Respiratory Health Research
- Malaria Research and Control
- RNA Interference and Gene Delivery
- Neutrophil, Myeloperoxidase and Oxidative Mechanisms
- Inflammation biomarkers and pathways
- Renal Transplantation Outcomes and Treatments
- Monoclonal and Polyclonal Antibodies Research
Université d'Orléans
2016-2025
Centre National de la Recherche Scientifique
2016-2025
Immunologie et Neurogénétique Expérimentales et Moléculaires
2016-2025
Le Studium
2019-2022
University of Cape Town
2007-2016
Centre de Biophysique Moléculaire
2016
Matrix Research (United States)
2016
Boehringer Ingelheim (Germany)
2014
Bipar
2001-2011
Transgene (France)
2002-2010
The tyrosine kinase inhibitor nintedanib (BIBF 1120) is in clinical development for the treatment of idiopathic pulmonary fibrosis. To explore its mode action, was tested human lung fibroblasts and mouse models Human expressing platelet-derived growth factor (PDGF) receptor-<i>α</i> -<i>β</i> were stimulated with BB (homodimer) (PDGF-BB). Receptor activation assessed by autophosphorylation cell proliferation bromodeoxyuridine incorporation. Transforming <i>β</i> (TGF<i>β</i>)-induced...
The molecular mechanisms of acute lung injury resulting in inflammation and fibrosis are not well established. Here we investigate the roles IL-1 receptor 1 (IL-1R1) common adaptor for Toll/IL-1R signal transduction, MyD88, this process using a murine model pulmonary injury. Bleomycin insult results expression neutrophil lymphocyte chemotactic factors, chronic inflammation, remodeling, fibrosis. We demonstrate that these end points were attenuated lungs IL-1R1– MyD88-deficient mice. Further,...
Lung injury leads to pulmonary inflammation and fibrosis through myeloid differentiation primary response gene 88 (MyD88) the IL-1 receptor 1 (IL-1R1) signaling pathway. The molecular mechanisms by which lung triggers IL-1beta production, inflammation, remain poorly understood.To determine if depends on NALP3 inflammasome bleomycin (BLM)-induced local production of uric acid, thereby activating in lung.Inflammation upon BLM administration was evaluated vivo inflammasome-deficient mice....
Abstract Acute cigarette smoke exposure of the airways (two cigarettes twice daily for three days) induces acute inflammation in mice. In this study, we show that airway is dependent on Toll-like receptor 4 and IL-1R1 signaling. Cigarette induced a significant recruitment neutrophils bronchoalveolar space pulmonary parenchyma, which was reduced TLR4-, MyD88-, IL-1R1-deficient Diminished neutrophil influx associated with IL-1, IL-6, keratinocyte-derived chemokine levels matrix...
MyD88, the common adapter involved in TLR, IL-1, and IL-18 receptor signaling, is essential for control of acute Mycobacterium tuberculosis (MTB) infection. Although TLR2, TLR4, TLR9 have been implicated response to mycobacteria, gene disruption these TLRs impairs only long-term MTB Here, we addressed respective role IL-1 pathways MyD88-dependent Mice deficient IL-1R1, IL-18R, or Toll-IL-1R domain-containing adaptor protein (TIRAP) were compared with MyD88-deficient mice an model aerogenic...
IL-33, a new member of the IL-1 family cytokine, is involved in Th2-type responses wide range diseases and signals through ST2 receptor expressed on many immune cells. Since effects IL-33 DCs remain controversial, we investigated ability to modulate DC functions vitro vivo. Here, report that activates myeloid produce IL-6, IL-1b, TNF, CCL17 express high levels CD40, CD80 OX40L CCR7. Importantly, IL-33-activated prime naive lymphocytes Th2 cytokines IL-5 IL-13, but not IL-4. In vivo, exposure...
Abstract Silica particles induce lung inflammation and fibrosis. Here we show that stimulator of interferon genes (STING) is essential for silica-induced inflammation. In mice, silica induces cell death self-dsDNA release in the bronchoalveolar space activates STING pathway. Degradation extracellular by DNase I inhibits activation downstream type IFN response. Patients with silicosis have increased circulating dsDNA CXCL10 sputum, patients fibrotic interstitial disease display lung. vitro,...
Abstract Stimulator of interferon genes (STING) contributes to immune responses against tumors and may control viral infection including SARS-CoV-2 infection. However, activation the STING pathway by airway silica or smoke exposure leads cell death, self-dsDNA release, STING/type I IFN dependent acute lung inflammation/ARDS. The inflammatory response induced a synthetic non-nucleotide-based diABZI agonist, in comparison natural cyclic dinucleotide cGAMP, is unknown. A low dose (1 µg...
Toll-like receptors (TLRs) such as TLR2 and TLR4 have been implicated in host response to mycobacterial infection. Here, mice deficient the TLR adaptor molecule myeloid differentiation factor 88 (MyD88) were infected with Mycobacterium tuberculosis (MTB). While primary MyD88(-/-) macrophages DCs are defective TNF, IL-12, NO production stimulation, upregulation of costimulatory molecules CD40 CD86 is unaffected. Aerogenic infection MTB lethal within 4 weeks 2 log(10) higher CFU lung; high...
Toll-like receptors (TLRs) such as TLR2 and TLR4 have been implicated in host response to mycobacterial infection. Here, mice deficient the TLR adaptor molecule myeloid differentiation factor 88 (MyD88) were infected with Mycobacterium tuberculosis (MTB). While primary MyD88–/– macrophages DCs are defective TNF, IL-12, NO production stimulation, upregulation of costimulatory molecules CD40 CD86 is unaffected. Aerogenic infection MTB lethal within 4 weeks 2 log10 higher CFU lung; high...
The dimannoside (PIM2) and hexamannoside (PIM6) phosphatidyl-myo-inositol mannosides are the two most abundant classes of PIM found in Mycobacterium bovis bacillus Calmette Guérin, tuberculosis H37Rv, smegmatis 607. Recently, these long known molecules received a renewed interest due to fact that PIM2 constitute anchor motif an important constituent mycobacterial cell wall, lipoarabinomannans (LAM), both LAM (phosphoinositol-capped LAM) agonists Toll-like receptor 2 (TLR2), pattern...
<h3>Objective</h3> Inflammatory bowel diseases (IBD) have been intrinsically linked to a deregulated cytokine network, but novel therapeutic principles are urgently needed. Here we identify the interleukin (IL)-33 and its receptor ST2 as key negative regulators of wound healing permeability in colon mice. <h3>Design</h3> Expression IL-33 was determined by qRT-PCR, ELISA, immunohistochemistry western-blot analysis. Wild-type <i>St2</i><sup>−/−</sup> mice were used experiments two experimental...
Macrophages play crucial roles in innate immune response and the priming of adaptive immunity, are characterized by their phenotypic heterogeneity plasticity. Reprogramming intracellular metabolism to microenvironmental signals is required for M1/M2 macrophage polarization function. Here we assessed influence iron on vivo vitro. Iron-enriched diet increased M2 marker Arg1 Ym1 expression liver peritoneal macrophages, while deficiency decreased expression. Under LPS-induced inflammatory...
Transferred CD4+CD25+FoxP3+ Treg cells can prevent autoimmune disease, but generally fail to ameliorate established disease. This study was undertaken compare the effects of antigen-specific induced with interleukin-2 (IL-2) and transforming growth factor β (TGFβ) ex vivo (induced [iTreg] cells) equivalent expanded thymus-derived natural (nTreg) on collagen-induced arthritis (CIA).CIA in DBA/1 mice by immunization type II collagen (CII), before or shortly after immunization, were treated...
IL-33 plays a critical role in regulation of tissue homeostasis, injury, and repair. Whether regulates neutrophil recruitment functions independently airways hyperresponsiveness (AHR) the setting ozone-induced lung injury inflammation is unclear.We sought to examine IL-33/ST2 axis on acute ozone exposure mice.ST2- Il33-deficient, citrine reporter, C57BL/6 (wild-type) mice underwent single (1 ppm for 1 hour) all studies. Cell bronchoalveolar space, inflammatory parameters, epithelial barrier...
Tumour Necrosis Factor (TNF) is critical for host control of M. tuberculosis, but the relative contribution TNF from innate and adaptive immune responses during tuberculosis infection unclear. Myeloid versus T-cell-derived function in was investigated using cell type-specific deletion. Mice deficient expression macrophages/neutrophils displayed early, transient susceptibility to recruited activated, TNF-producing CD4+ CD8+ T-cells controlled chronic infection. Strikingly, resulted early...
The cysteine protease caspase-1 (Casp-1) contributes to innate immunity through the assembly of NLRP3, NLRC4, AIM2, and NLRP6 inflammasomes. Here we ask whether activation plays a regulatory role in house dust mite (HDM)-induced experimental allergic airway inflammation. We report enhanced inflammation caspase-1-deficient mice exposed HDM with marked eosinophil recruitment, increased expression IL-4, IL-5, IL-13, as well full-length bioactive IL-33. Furthermore, deficient for NLRP3 failed...
Synthesis of acetylcholine by group 2 innate lymphoid cells is important for optimal immune responses to helminth infection.
Cyclosporins, in particular the nonimmunosuppressive derivative SDZ NIM 811, exhibit potent anti-human immunodeficiency virus type 1 (HIV-1) activity vitro. 811 interferes at two stages of viral replication cycle: (i) translocation preintegration complex to nucleus and (ii) production infectious particles. Immunosuppressive is not correlated with anti-HIV-1 cyclosporins. However, binding cyclophilin A, major cellular receptor protein cyclosporins, a prerequisite for HIV inhibition: all...