TY - JOUR
T1 - Role of lysophosphatidylcholine in eosinophil infiltration and resistance in airways
AU - Nishiyama, Osamu
AU - Kume, Hiroaki
AU - Kondo, Masashi
AU - Ito, Yasushi
AU - Ito, Masafumi
AU - Yamaki, Kenichi
PY - 2004/3
Y1 - 2004/3
N2 - 1. Lysophosphatidylcholine (Lyso-PC), which is synthesized by phospholipase A2, is generally considered to induce adhesion molecules. However, little is known about the involvement of Lyso-PC in the pathogenesis of bronchial asthma. The present study was designed to examine whether pre-exposure to Lyso-PC causes eosinophil recruitment and an increase in resistance in airways. 2. Eosinophils in bronchoalveolar lavage fluid (BALF) and the airway walls were enumerated after inhalation of 0.5 mg/mL Lyso-PC to guinea-pigs for 10 min. Respiratory resistance (Rrs) was recorded continuously over 6 h after inhalation of an equi-dose of Lyso-PC for an equivalent period. 3. The proportion of eosinophils was increased from 10.7 ± 3.3 to 27.5 ± 3.1% (P < 0.0001) in BALF 6 h after inhalation of Lyso-PC, whereas the proportion of neutrophils and lymphocytes was not increased. Histological examination also showed uniform distribution of eosinophils in the airway wall of bronchi and bronchioles 6 h after inhalation of Lyso-PC. The number of eosinophils (/10 h.p.f.) in the bronchi and bronchioles was increased from 43.5 ± 16.8 to 154.8 ± 21.7 (P < 0.0001) and from 34.8 ± 0.7 to 106.0 ± 26.6 (P < 0.01), respectively. This eosinophil infiltration was similarly observed 24 h later. 4. Next, we examined the effects of eosinophil infiltration induced by Lyso-PC on Rrs. Inhalation of Lyso-PC caused a slow increase in Rrs and the percentage increase in Rrs, was 19.8 ± 1.9% (P < 0.0001) 6 h later. Eosinophil infiltration and an increase in Rrs, did not occur after inhalation of physiological saline. These phenomena induced by Lyso-PC were diminished by pretreatment with dexamethasone (6 μg/kg per day for 3 days). 5. Lysophosphatidylcholine causes eosinophil infiltration and a subsequent increase in resistance in airways. Our results indicate that Lyso-PC may be involved in the pathophysiology of bronchial asthma.
AB - 1. Lysophosphatidylcholine (Lyso-PC), which is synthesized by phospholipase A2, is generally considered to induce adhesion molecules. However, little is known about the involvement of Lyso-PC in the pathogenesis of bronchial asthma. The present study was designed to examine whether pre-exposure to Lyso-PC causes eosinophil recruitment and an increase in resistance in airways. 2. Eosinophils in bronchoalveolar lavage fluid (BALF) and the airway walls were enumerated after inhalation of 0.5 mg/mL Lyso-PC to guinea-pigs for 10 min. Respiratory resistance (Rrs) was recorded continuously over 6 h after inhalation of an equi-dose of Lyso-PC for an equivalent period. 3. The proportion of eosinophils was increased from 10.7 ± 3.3 to 27.5 ± 3.1% (P < 0.0001) in BALF 6 h after inhalation of Lyso-PC, whereas the proportion of neutrophils and lymphocytes was not increased. Histological examination also showed uniform distribution of eosinophils in the airway wall of bronchi and bronchioles 6 h after inhalation of Lyso-PC. The number of eosinophils (/10 h.p.f.) in the bronchi and bronchioles was increased from 43.5 ± 16.8 to 154.8 ± 21.7 (P < 0.0001) and from 34.8 ± 0.7 to 106.0 ± 26.6 (P < 0.01), respectively. This eosinophil infiltration was similarly observed 24 h later. 4. Next, we examined the effects of eosinophil infiltration induced by Lyso-PC on Rrs. Inhalation of Lyso-PC caused a slow increase in Rrs and the percentage increase in Rrs, was 19.8 ± 1.9% (P < 0.0001) 6 h later. Eosinophil infiltration and an increase in Rrs, did not occur after inhalation of physiological saline. These phenomena induced by Lyso-PC were diminished by pretreatment with dexamethasone (6 μg/kg per day for 3 days). 5. Lysophosphatidylcholine causes eosinophil infiltration and a subsequent increase in resistance in airways. Our results indicate that Lyso-PC may be involved in the pathophysiology of bronchial asthma.
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U2 - 10.1111/j.1440-1681.2004.03973.x
DO - 10.1111/j.1440-1681.2004.03973.x
M3 - Article
C2 - 15008962
AN - SCOPUS:1542512185
SN - 0305-1870
VL - 31
SP - 179
EP - 184
JO - Clinical and Experimental Pharmacology and Physiology
JF - Clinical and Experimental Pharmacology and Physiology
IS - 3
ER -