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429 results on '"Chignard M"'

1. A soluble fucose-specific lectin from Aspergillus fumigatus conidia - Structure, specificity and possible role in fungal pathogenicity

Author

Fahy, John, Houser, J, Komarek, J, Kostlanova, N, Cioci, G, Varrot, A, Kerr, SC, Lahmann, M, Balloy, V, Fahy, JV, and Chignard, M

Abstract

Aspergillus fumigatus is an important allergen and opportunistic pathogen. Similarly to many other pathogens, it is able to produce lectins that may be involved in the host-pathogen interaction. We focused on the lectin AFL, which was prepared in recombina

Published
2013

13. Neutrophil recruitment and increased permeability during acute lung injury induced by lipopolysaccharide

Author

CHIGNARD, M. and BALLOY, V.

Subjects
Lungs -- Inflammation, Permeability -- Genetic aspects, Genetic research -- Analysis, Biological sciences
Abstract

Chignard, M., and V. Balloy. Neutrophil recruitment and increased permeability during acute lung injury induced by lipopolysaccharide. Am J Physiol Lung Cell Mol Physiol 279: L1083-L1090, 2000.--The intranasal administration of lipopolysaccharide (LPS) to mice triggers a huge influx of polymorphonuclear neutrophils (PMNs) into the airway spaces, with a peak at 48 h. The increase in protein concentration, an index of microvascular permeability, displayed a different pattern, i.e., a first increase with a plateau between 3 and 24 h followed by a second increase peaking at 72 h. When mice were depleted of circulating PMNs, the increase in protein concentration was inhibited at 3 h but not at 24 h. The lack of PMN involvement at 24 h was confirmed by 1) in situ activation of exudated PMNs present in the air spaces on intranasal administration of LPS and 2) induction of the migration of PMNs sequestered in lung vessels on intraperitoneal administration of LPS. These findings show that the increase in microvascular permeability during lung inflammation is due to at least two distinct mechanisms, an early one related to the neutrophil influx and a delayed one occurring even under neutropenic conditions. mice; pulmonary inflammation; anti-granulocyte antibody; bronchoalveolar fluid

Published
2000

23. Detrimental contribution of the Toll-like receptor (TLR) to influenza A virus-induced acute pneumonia

Author

Le Goffic, Ronan, Balloy, V., Lagranderie, M., Alexopoulou, L., Escriou, N., Flavell, R., Chignard, M., Si-Tahar, Mustapha, Défense innée et inflammation, Institut Pasteur [Paris] (IP)-Institut National de la Santé et de la Recherche Médicale (INSERM), Institut Pasteur [Paris] (IP), Centre d'Immunologie de Marseille - Luminy (CIML), Aix Marseille Université (AMU)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Génétique Moléculaire des Virus Respiratoires, Institut Pasteur [Paris] (IP)-Université Paris Diderot - Paris 7 (UPD7)-Centre National de la Recherche Scientifique (CNRS), Yale School of Medicine [New Haven, Connecticut] (YSM), Guglietta, Noëlle, Institut Pasteur [Paris]-Institut National de la Santé et de la Recherche Médicale (INSERM), Institut Pasteur [Paris], Centre National de la Recherche Scientifique (CNRS)-Université Paris Diderot - Paris 7 (UPD7)-Institut Pasteur [Paris], Yale University School of Medicine, Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Aix Marseille Université (AMU), and Institut Pasteur [Paris]-Université Paris Diderot - Paris 7 (UPD7)-Centre National de la Recherche Scientifique (CNRS)

Subjects
Inflammation, [SDV.IMM] Life Sciences [q-bio]/Immunology, Influenza A virus, T cells, Respiratory infections, Cytokines, [SDV.IMM]Life Sciences [q-bio]/Immunology, chemical and pharmacologic phenomena, Mouse models, Influenza, Toll-like receptors
Abstract

International audience; Influenza A virus (IAV) is the etiological agent of a highly contagious acute respiratory disease that causes epidemics and considerable mortality annually. Recently, we demonstrated, using an in vitro approach, that the pattern recognition Toll-like receptor (TLR)3 plays a key role in the immune response of lung epithelial cells to IAV. In view of these data and the fact that the functional role of TLR3 in vivo is still debated, we designed an investigation to better understand the role of TLR3 in the mechanisms of IAV pathogenesis and host immune response using an experimental murine model. The time-course of several dynamic parameters, including animal survival, respiratory suffering, viral clearance, leukocyte recruitment into the airspaces and secretion of critical inflammatory mediators, was compared in infected wild-type and TLR3−/− mice. First, we found that the pulmonary expression of TLR3 is constitutive and markedly upregulated following influenza infection in control mice. Notably, when compared to wild-type mice, infected TLR3−/− animals displayed significantly reduced inflammatory mediators, including RANTES (regulated upon activation, normal T cell expressed and secreted), interleukin-6, and interleukin-12p40/p70 as well as a lower number of CD8+ T lymphocytes in the bronchoalveolar airspace. More important, despite a higher viral production in the lungs, mice deficient in TLR3 had an unexpected survival advantage. Hence, to our knowledge, our findings show for the first time that TLR3-IAV interaction critically contributes to the debilitating effects of a detrimental host inflammatory response.

Published
2006
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32. Regulation of the structure and activity of platelet adhesion receptors by leukocyte proteinases

Author

Dominique Pidard, Renesto P, Rabhi S, and Chignard M

Subjects
Integrins, Structure-Activity Relationship, Platelet Adhesiveness, Endopeptidases, Leukocytes, Humans, Receptors, Cell Surface, Platelet Membrane Glycoproteins
Abstract

Two major membrane receptors implicated in the adhesive properties of blood platelets are the GPIb-IX complex, a receptor for subendothelial von Willebrand factor, and the alpha IIb beta 3 integrin, the receptor for plasma fibrinogen. We have evaluated how the biological activities of these receptors can be potentially modulated through limited proteolysis when platelets are exposed to the serine-proteinases secreted by activated polymorphonuclear neutrophils, i.e., leukocyte elastase (EL) and cathepsin G (CG). CG can activate the alpha IIb beta 3 integrin through intracellular metabolic pathways, but has no direct proteolytic activity on the receptor subunits. By contrast, EL does not activate the platelet metabolism, but specifically cleaves a short peptide sequence within the alpha IIb subunit, and this cleavage occurs in parallel with an up-regulation of the activity of the fibrinogen receptor. On another hand, both EL and CG cleave the amino-terminal portion of the GPIb alpha subunit of the GPIb-IX receptor, eliminating the binding site for von Willebrand factor and diminishing the capacity of platelets to interact with this adhesion protein. Thus, neutrophil proteinases have the potential to regulate the activity of platelet adhesion receptors, and such experimental observations may prove to be relevant in vivo in various pathological conditions.

Published
1994

38. Critical role of cytosolic phospholipase A2 in bronchial mucus hypersecretion in CFTR-deficient mice

Author

Dif, F., primary, Wu, Y.-Z., additional, Burgel, P.-R., additional, Ollero, M., additional, Leduc, D., additional, Aarbiou, J., additional, Borot, F., additional, Garcia-Verdugo, I., additional, Martin, C., additional, Chignard, M., additional, Israel-Biet, D., additional, Kita, Y., additional, Scholte, B. J., additional, and Touqui, L., additional

Published
2010
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