BACKGROUND: Inhaled endotoxin is known to induce airway inflammation, causing bronchial hyperreactivity. OBJECTIVE: We characterized the response to lipopolysaccharide-inhalation by measuring exhaled nitric oxide (eNO) and inflammatory mediators. PATIENTS AND METHODS: A total of 43 adult volunteers (13 asthmatics, 30 healthy controls) inhaled stepwise LPS every 30 min up to a cumulative dose of 100 microg (2.5, 10.5, 42, 45 microg). After each provocation and up to 24 h later, FEV(1) was determined; the procedure was stopped when FEV(1) declined more than 12.5%. We measured eNO, leucocytes, eosinophils, polymorphonuclear neutrophils (PMNs), C-reactive protein (CrP), lipopolysaccharide binding protein (LBP), eosinophilic cationic protein (ECP), leucotriene B4 (LTB4), thromboxane B2 (TXB2), and body temperature. RESULTS: Initial eNO values were higher in asthmatics (P < 0.01), but only increased in an asthmatic subgroup. Marked differences were observed in the systemic response to LPS inhalation. Significant increases were found for CrP, LBP, and PMNs. There was no correlation between FEV(1) decrease and basal eNO levels. CONCLUSIONS: Inhalation of endotoxin was followed by clinical and laboratory signs of systemic inflammation, with asthmatics responding to the challenge similar as healthy subjects. Bronchial eNO increased only temporarily in asthmatics.
BACKGROUND: Inhaled endotoxin is known to induce airway inflammation, causing bronchial hyperreactivity. OBJECTIVE: We characterized the response to lipopolysaccharide-inhalation by measuring exhaled nitric oxide (eNO) and inflammatory mediators. PATIENTS AND METHODS: A total of 43 adult volunteers (13 asthmatics, 30 healthy controls) inhaled stepwise LPS every 30 min up to a cumulative dose of 100 microg (2.5, 10.5, 42, 45 microg). After each provocation and up to 24 h later, FEV(1) was determined; the procedure was stopped when FEV(1) declined more than 12.5%. We measured eNO, leucocytes, eosinophils, polymorphonuclear neutrophils (PMNs), C-reactive protein (CrP), lipopolysaccharide binding protein (LBP), eosinophilic cationic protein (ECP), leucotriene B4 (LTB4), thromboxane B2 (TXB2), and body temperature. RESULTS: Initial eNO values were higher in asthmatics (P < 0.01), but only increased in an asthmatic subgroup. Marked differences were observed in the systemic response to LPS inhalation. Significant increases were found for CrP, LBP, and PMNs. There was no correlation between FEV(1) decrease and basal eNO levels. CONCLUSIONS: Inhalation of endotoxin was followed by clinical and laboratory signs of systemic inflammation, with asthmatics responding to the challenge similar as healthy subjects. Bronchial eNO increased only temporarily in asthmatics.
Authors: Raminder Aul; Jane Armstrong; Annelyse Duvoix; David Lomas; Brian Hayes; Bruce E Miller; Chris Jagger; Dave Singh Journal: Br J Clin Pharmacol Date: 2012-12 Impact factor: 4.335
Authors: Jessica Wiser; Neil E Alexis; Qing Jiang; Weidong Wu; Carole Robinette; Robert Roubey; David B Peden Journal: Free Radic Biol Med Date: 2008-03-12 Impact factor: 7.376
Authors: Elisabet Johansson; Tiina Reponen; Stephen Vesper; Linda Levin; James Lockey; Patrick Ryan; David I Bernstein; Manuel Villareal; Gurjit K Khurana Hershey; Chris Schaffer; Grace Lemasters Journal: Environ Int Date: 2013-06-24 Impact factor: 9.621
Authors: Richard Kitz; Markus A Rose; Katja Placzek; Johannes Schulze; Stefan Zielen; Ralf Schubert Journal: Med Microbiol Immunol Date: 2007-06-12 Impact factor: 3.402