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Praticien-chercheur
8 articles scientifiques publiés — formation continue solide
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166.7 rhumatos / 100 000 hab. — département bien doté
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13 AV DE L'INTERNE JACQUES LOEB BP 8, 64109 BAYONNE CEDEX
CENTRE HOSPITALIER DE SAINT-PALAIS
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Lien Doctolib = recherche Google site:doctolib.fr (le 1er résultat est presque toujours le profil correct s'il existe).
Critical care medicine · 2005
American journal of respiratory and critical care medicine · 2008
Abstract Rationale High-mobility group box 1 (HMGB1) is a potent inflammatory mediator elevated in sepsis and rheumatoid arthritis, although its role in cystic fibrosis (CF) lung disease is unknown. Objectives To determine whether HMGB1 contributes to CF lung inflammation, including neutrophil chemotaxis and lung matrix degradation. Methods We used sputum and serum from subjects with CF and a Scnn1b-transgenic (Scnn1b-Tg) mouse model that overexpresses β-epithelial Na+ channel in airways and mimics the CF phenotype, including lung inflammation. Human secretions and murine bronchoalveolar lavage fluid (BALF) was assayed for HMGB1 by Western blot and ELISA. Neutrophil chemotaxis was measured in vitro after incubation with human neutrophils. The collagen fragment proline-glycine-proline (PGP) was measured by tandem mass spectroscopy. Measurements and Main Results HMGB1 was detected in CF sputum at higher levels than secretions from normal individuals. Scnn1b-Tg mice had elevated levels of HMGB1 by Western blot and ELISA. We demonstrated that dose-dependent chemotaxis of human neutrophils stimulated by purified HMGB1 was partially dependent on CXC chemokine receptors and that this could be duplicated in CF sputum and BALF from Scnn1b-Tg mice. Neutralization by anti-HMGB1 antibody, in both the sputum and BALF-reduced chemotaxis, which suggested that HMGB1 contributed to the chemotactic properties of these samples. Intratracheal administration of purified HMGB1 induced neutrophil influx into the airways of mice and promoted the release of PGP. PGP was also elevated in Scnn1b-Tg mice and CF serum. Conclusions HMGB1 expression contributes to pulmonary inflammation and lung matrix degradation in CF airway disease and deserves further investigation as a biomarker and potential therapeutic target.
Journal of pediatric orthopedics · 2007
Source PubMed · Recherche par auteur (homonymes possibles, vérifier l'affiliation).
Cureus · 2021 · Case Reports
Sebastian KK, Alzayer H, Abraham E, Roche D, et al.
American journal of respiratory and critical care medicine · 2008 · Comparative Study
Rowe SM, Jackson PL, Liu G, Hardison M, et al.
Critical care medicine · 2005 · Consensus Statement
Marshall JC, Vincent JL, Guyatt G, Angus DC, et al.
Physical therapy · 1986 · Journal Article
Abraham E, Knecht HG, Koenig C
Cureus · 2025 · Case Reports
C P, Ann Jose J, Verma G, Priya V L, et al.
Journal of pediatric orthopedics · 2007 · Journal Article
Abraham E, Gonzalez MH, Pratap S, Amirouche F, et al.
The spine journal : official journal of the North American Spine Society · 2011 · Comparative Study
Rampersaud YR, Wai EK, Fisher CG, Yee AJ, et al.
PloS one · 2015 · Journal Article
Chen X, Giambini H, Ben-Abraham E, An KN, et al.