A5072778963- Asthma and respiratory diseases
- Chronic Obstructive Pulmonary Disease (COPD) Research
- Phosphodiesterase function and regulation
- Neuropeptides and Animal Physiology
- Protease and Inhibitor Mechanisms
- Nitric Oxide and Endothelin Effects
- Pulmonary Hypertension Research and Treatments
- Receptor Mechanisms and Signaling
- Respiratory and Cough-Related Research
- Neonatal Respiratory Health Research
- Interstitial Lung Diseases and Idiopathic Pulmonary Fibrosis
- Mast cells and histamine
- Peptidase Inhibition and Analysis
- Neuroscience of respiration and sleep
- Food Allergy and Anaphylaxis Research
- Inhalation and Respiratory Drug Delivery
- Inflammasome and immune disorders
- Respiratory Support and Mechanisms
- Immune Response and Inflammation
- Adenosine and Purinergic Signaling
- Allergic Rhinitis and Sensitization
- Immune cells in cancer
- Liver Disease Diagnosis and Treatment
- Pharmacological Effects and Assays
- Alcohol Consumption and Health Effects
Inserm
2015-2025
Université de Rennes
2015-2025
Centre Hospitalier Universitaire de Rennes
2006-2025
Institut National de Recherche pour l'Agriculture, l'Alimentation et l'Environnement
2020-2025
Nutrition, métabolismes et cancer
2017-2021
Foie, Métabolisme, Cancer
2011-2021
Université Bretagne Loire
2017-2018
Hôpital Pontchaillou
2006-2016
Laboratoire de Recherche sur la Croissance Cellulaire, la Réparation et la Régénération Tissulaires
2006-2009
University of Cape Town
2009
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...
Abstract The NLR pyrin domain containing 3 (NLRP3) inflammasome is a major component of the innate immune system, but its mechanism activation by wide range molecules remains largely unknown. Widely used nano-sized inorganic metal oxides such as silica dioxide (nano-SiO 2 ) and titanium (nano-TiO activate NLRP3 in macrophages similarly to or asbestos micro-sized particles. By investigating towards molecular mechanisms response nanoparticles, we show here that active adenosine triphosphate...
Idiopathic pulmonary fibrosis is a devastating as yet untreatable disease. We demonstrated recently the predominant role of NLRP3 inflammasome activation and IL-1β expression in establishment inflammation mice.The contribution IL-23 or IL-17 was assessed using bleomycin model deficient mice.We show that IL-1β-induced lung injury leads to increased early IL-23p19, IL-17A IL-17F expression. Early IL-23p19 IL-17A, but not IL-17F, IL-17RA signaling are required for inflammatory response BLM...
Abstract Background Reactive oxygen species and tissue remodeling regulators, such as metalloproteinases (MMPs) their inhibitors (TIMPs), are thought to be involved in the development of pulmonary fibrosis. We investigated these factors fibrotic response bleomycin p47 phox -/- (KO) mice, deficient for ROS production through NADPH-oxidase pathway. Methods Mice administered by intranasal instillation 0.1 mg bleomycin. Either 24 h or 14 days after, mice were anesthetized underwent either...
Inflammation has an important role in the development of liver fibrosis general and activation hepatic stellate cells (HSCs) particular. It is known that HSCs are themselves able to produce cytokines chemokines, this production may be a key event initiation fibrogenesis. However, direct involvement chemokines HSC (self-)activation remains uncertain. In study, effects pro-inflammatory IL-1α β, TNF-α, IL-8 on state were examined, comparison pro-fibrogenic mediator TGF-β1. LX-2 stimulated for...
The Nod-like receptor family protein 3 (NLRP3)-inflammasome pathway is known to be activated by danger signals such as monosodium urate (MSU). We investigated the role of P2 purinergic receptors in activation NLRP3-inflammasome after MSU treatment primary human monocyte-derived macrophages (MDMs). After initial stimulation with a low concentration LPS (0.1 μg/ml), 6 h crystals (250, 500, and 1000 μg/ml) induced MDMs release IL-1β, IL-1α, IL-6 dose-dependent manner. Moreover, caspase 1...
Bleomycin-induced pulmonary fibrosis is known to be associated with the increased activity of two gelatinases, matrix metalloproteinase (MMP)-2 and MMP-9, in bronchoalveolar lavage (BAL). This study has investigated effect a synthetic inhibitor MMP, batimastat, on development induced by bleomycin administration mice. Animals wereintranasally instilled saline or (0.5 mg 100 µl per mouse). Batimastat (30 mg/kg) vehicle alone was administered intraperitoneal injection 24 h 1 before...
The effects of three endothelins: (i) the classical or human/porcine endothelin (ET‐1); (ii) [Trp 6 , Leu 7 ] (ET‐2) and (iii) [Thr 2 Phe 4 Thr 5 Tyr Lys 14 rat (ET‐3) were tested on human isolated bronchus. ET‐1 produced a concentration‐dependent contraction bronchus that proceeded in two different steps. first step was observed at very low concentrations (pD = 11.01 ± 0.17, n 10) but corresponded to intrinsic activity (E max 15.6 1.8% E induced by acetylcholine (ACh) 3 × 10 −3 m 10). This...
Abstract The need to develop a blood substitute is now urgent because of the increasing concern over Europe's BSE outbreak and worldwide HIV/AIDS epidemic, which have cut supplies. Extracellular soluble hemoglobin has long been studied for its possible use as safe effective alternative transfusion, but this met with little success. Clinical trials revealed undesirable side effects–oxidative damage vasoconstriction–that hamper application cellfree substitute. We addressed these problems found...
Abstract Lung emphysema and fibrosis are severe complications of chronic obstructive pulmonary disease, uncontrolled protease activation may be involved in the pathogenesis. Using experimental elastase-induced acute inflammation, we demonstrate here that inflammation development is IL-1R1 Toll/IL-1R signal transduction adaptor MyD88 dependent; however, TLR recognition dispensable this model. Elastase induces IL-1β, TNF-α, keratinocyte-derived chemokine, IL-6 secretion neutrophil recruitment...