TY - JOUR
T1 - PAF responsiveness in Japanese subjects with plasma PAF acetylhydrolase deficiency
AU - Naoki, Katsuhiko
AU - Asano, Koichiro
AU - Satoh, Nagato
AU - Fukunaga, Kouichi
AU - Oguma, Tsuyoshi
AU - Shiomi, Tetsuya
AU - Suzuki, Yusuke
AU - Nakajima, Takeshi
AU - Niimi, Kyoko
AU - Shiraishi, Yoshiki
AU - Ishizaka, Akitoshi
AU - Yamaguchi, Kazuhiro
N1 - Funding Information:
We thank Akiko Tanabe, Morimi Kinebuchi, and Makiko Iwata for their excellent technical assistance. This study was partially supported by Grants-in-Aid from the Japanese Ministry of Education, Science and Culture, the Japanese Ministry of Health, Labour and Welfare, the Keio University Fukuzawa Foundation, and the Keio University Medical Science Fund.
PY - 2004/4/23
Y1 - 2004/4/23
N2 - Approximately 4% of the Japanese population genetically lack plasma platelet activating factor acetylhydrolase (PAF-AH) and show a higher prevalence of thromboembolic disease, but whether they are susceptible to another PAF-related disease, asthma, remains controversial. To determine the role of plasma PAF-AH in airway physiology, we performed PAF bronchoprovocation tests in 8 plasma PAF-AH-deficient subjects and 16 control subjects. Serial inhalation of PAF (1-1000μg/ml) concentration-dependently induced acute bronchoconstriction, but there was no significant difference between PAF-AH-deficient and control subjects (11.7±4.6% vs. 9.6±2.8% decrease in forced expiratory volume in 1s). Transient neutropenia after single inhalation of PAF (1000μg/ml) showed no significant difference between the groups either in its magnitude (72±11% vs. 65±9% decrease) or duration (4.1±1.0 vs. 3.3±0.8min). In conclusion, a lack of plasma PAF-AH activity alone does not augment physiological responses to PAF in the airway.
AB - Approximately 4% of the Japanese population genetically lack plasma platelet activating factor acetylhydrolase (PAF-AH) and show a higher prevalence of thromboembolic disease, but whether they are susceptible to another PAF-related disease, asthma, remains controversial. To determine the role of plasma PAF-AH in airway physiology, we performed PAF bronchoprovocation tests in 8 plasma PAF-AH-deficient subjects and 16 control subjects. Serial inhalation of PAF (1-1000μg/ml) concentration-dependently induced acute bronchoconstriction, but there was no significant difference between PAF-AH-deficient and control subjects (11.7±4.6% vs. 9.6±2.8% decrease in forced expiratory volume in 1s). Transient neutropenia after single inhalation of PAF (1000μg/ml) showed no significant difference between the groups either in its magnitude (72±11% vs. 65±9% decrease) or duration (4.1±1.0 vs. 3.3±0.8min). In conclusion, a lack of plasma PAF-AH activity alone does not augment physiological responses to PAF in the airway.
KW - Airway responsiveness
KW - Asthma
KW - Neutrophil
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U2 - 10.1016/j.bbrc.2004.03.031
DO - 10.1016/j.bbrc.2004.03.031
M3 - Article
C2 - 15047169
AN - SCOPUS:12144291364
SN - 0006-291X
VL - 317
SP - 205
EP - 210
JO - Biochemical and Biophysical Research Communications
JF - Biochemical and Biophysical Research Communications
IS - 1
ER -