1998 Fiscal Year Final Research Report Summary
Immunological-molecular biological analysis of the developmental mechanisms by using a newly established murinemodel of chronic Pseudomona saeruginosa respiratory infection.
| Project/Area Number |
08670668
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Respiratory organ internal medicine
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| Research Institution | Nagasaki University |
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Principal Investigator |
MIYAHARA Yoshiki Nagasaki University, School of Medicine Hospital Lecturer, 医学部・附属病院, 講師 (20253643)
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| Co-Investigator(Kenkyū-buntansha) |
KOHNO Shigeru Nagasaki University, School of Medicene Professor, 医学部, 教授 (80136647)
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| Project Period (FY) |
1996 – 1998
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| Keywords | Chronic infection / Pseudomonas aeruginosa / cytokine / Diffuse panbronchiolitis / Cystic fibrosis |
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| Research Abstract |
The patho-physiology of chronic infection was defined by pathological or bacterial examination. It was difficult that analysis of the developmental process of chronic respiratory infection. We analyzed the immunological and pathological process of chronic pseudomonas respiratory infection by using our newly established murine model.
The animals were infected with mucoid P.aervginosa NUS10 isolated from patient's sputum. This bacteria were suspended in saline (Lo^9CFU/ml). Disposable sterile plastic cut-down intravenous catheters was cut 2mm - length and used for intubation. The intubation tube was then immersed in the bacterial saline suspention for 3 days at 37ﾟC.This intubation tube was inserted through the murine (ddy male 6ws) oral cavity. BAL was performed infected mice. BALF samples were cultured quantitatively , counted the total leukocyre and measured by ELISA.
The numbers of polymorphonuclear leukocytes increased at the early phase of infection and rapidly decreased till 3day s after infection . After 10days, numbers of PMN were constantly larger than the control mice. This percentage was 5O - 6O%. This kinetics of PMN and MIP-2 were correlated. We classified these cyrokine kinetics to four phase, acute, subacute, subchronic, chronic for convenience. At the acute phase, all cytokines were significantry elevated. TNF alpha was elevated at subacute phase transiently. At the chronic phase, except MIP-2, these cytokines were decreased at the control level. From our study of cytokine profile of chronic bacterial respiratory infection in mice, MIP-2 from Cystic fibrosis patients or DPB patients are not specific for Cystic fibrosis or DPB , but the profiles as common to the chronic bacterial infections. However, IL-10 is specific for Cystic fibrosis.
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