1992 Fiscal Year Final Research Report Summary
Peptide Histidine Isoleucine (PHI) in the Respiratory Tract
| Project/Area Number |
02670336
|
|---|
| Research Category |
Grant-in-Aid for General Scientific Research (C)
|
| Allocation Type | Single-year Grants |
|---|
| Research Field |
Respiratory organ internal medicine
|
|---|
| Research Institution | Gunma University School of Medicine |
|---|
Principal Investigator |
KUROSAWA Motohiro Gunma University School of Medicine First Department of Internal Medicine Lecturer in Medicine, 医学部, 助手 (10170119)
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
HISADA Takeshi Gunma University School of Medicine First Department of Internal Medicine Postgr
|
|---|
| Project Period (FY) |
1990 – 1992
|
| Keywords | PHI / VIP / immunoreactivity / respiratory tract / airway resistance / superoxide anion / inflammatory cells / leukotriene C_4 / rat / guinea pig |
|---|
| Research Abstract |
(1) A high titer of peptide histidine isoleucine (PHI) antiserum which did not react with vasoactive intestinal peptide (VIP) was obtained from a rabbit immunized with rat PHI and rat PHI radioimmunoassay was established with this antiserum. Tracheas, extrapulmonary bronchi and lungs were dissected from rats sacrificed by microwave irradiation. They were homoginized with 0.5 N acetic acid and centrifuged. Lyophilized supernates were used as samples for the radioimmunoassay. PHI immunoreactivity occurred more in the central airways than in the peripheral ones. VIP immunoreactivity in rat respiratory tracts, assayed simultaneously by radioimmunoassay using commercialized VIPantiserum, was as strong as that of PHI, suggesting that PHI and VIP may be produced from the same precursor at the ratio of 1:1 in rat respiratory tracts.
(2) Intravenous administration of VIP or PHI reduced dynamic respiratory resistance; however, the effect was significantly less than that of isoprenaline. VIP and P
… More
HI inhibited the increase in dynamic respiratory resistance by intravenous administration of histamine in a dose-dependent manner, suggesting that VIP and PHI may be involved in the pathogenesis of airway hyperresponsiveness through inhibiting the effect of mediator release on the airway.
(3) VIP inhibited superoxide anion production in a dose- dependent manner by the activated peripheral blood neutrophils, mononuclear cells and also by the human monoblast cell line U937, the capacity of which for superoxide anion formation was induced by the pretreatment of interferon-gamma. 3x10^<-6> M VIP also inhibited superoxide anion generation by the activated peripheral blood eosinophils and alveolar macrophages obtained by bronchoalveolar lavage, suggesting VIP may serve as an endogenous modulator of inflammatory reactions in the respiratory tract.
(4) A high titer of PHI antiserum which did not react with VIP was obtained from a rabbit immunized with rat PHI and PHI like immunoreactivity in the respiratory tract from guinea pigs was measured by radioimmunoassay. Tracheas, extrapulmonary bronchi and lungs were dissected and treated by microwave irradiation. They were homogenized with 0.5 N acetic acid and centrifuged. Lyophilized supernates were used as samples for the radioimmunoassay. PHI like immunoreactivity was present more in the central airways than in the peripheral ones. Intravenous administration of leukotriene C_4 reduced significantly PHI like immunoreactivity in the tracheas and the extrapulmonary bronchi in parallel with the significant increase of dynamic respiratory resistance. Less
|
