2001 Fiscal Year Final Research Report Summary
Protective mechanisms in inflammatory lung diseases at airway and alveolar area
| Project/Area Number |
12670557
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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 | KYOTO UNIVERSITY |
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Principal Investigator |
NAGAI Sonoko Assoc. Prof., Reap. Med., Kyoto Univ., 医学研究科, 助教授 (30217955)
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| Co-Investigator(Kenkyū-buntansha) |
NIIMI Akio Assist. Prof., Resp. Med., Kyoto Univ., 医学研究科, 助手 (30252513)
KITAICHI Masanori Assoc. Prof., Pathol., Kyoto Univ., 医学研究科, 助教授 (00161464)
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| Project Period (FY) |
2000 – 2001
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| Keywords | interstitial pneumonia / collagen-vascular disease / fibroblast / cytokine / protease / T-lymphocyte / TGFB / apoptosis |
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| Research Abstract |
We investigated on the pathogenesis of inflammatory lung diseases (interstitial pneumonias) using clinical samples, aiming at progressive or protective cytokine profiles and protease-antiprotease imbalance. We scored histopathological findings of lung specimens obtaind from 31 cases (16 IPF, 9 CVD other than SSc and 6 SSc) using a semiquaqntitative scoring method. Fewer macrophages in the alveolar spaces and a decrease in the degree of fibrosis may contribute to BALF lymphocytosis more in patients with in the degree of fibrosis may contribute to BALF lymphocytosis more in patients with UIP/CVD non-SSc than in patients with IPF/UIP and UIP-SSc. We examined mRNA expressions of MMP-3 and TIMP-3 in a cell line (A549) and in primary culture of normal adult human type II pneumocytes using RT-PCR. The matrix degradation is enhanced by IL-1beta and suppressed by TGF-betal via regulations in the balance between MMP-3 and TIMP-3. We investigated the cytotoxic effects of cigarette smoke extract (
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CSE) on an alveolar type II cell-derived cell line (A549). Apoptosis of alveolar epithelial cells may be one of the mechanisms of lung injuury induced by cigarette smoking. This cytotoxic effect might be due to an interaction between aldehydes and oxidants present in CSE or formed in CSE-exposed cells. We compared the function of lung fibroblasts obtained from surgically biopsied cells. We compared the function of lung fibroblasts obtained from surgically biopsied specimens of patients with UIP (n=5), NSIP (n=5), and normal control (n=5). Fibroblasts obtained from UIP showed increased contractility compared with those obtained from NSIP or controls with enhanced F-action content in fibroblasts. The products representing the contractility were identified as fibronectin (ED-A domain) and TGF-betal by immunoblots. The contractility positively korrelated with the amount of either fibronectin or TGF-beta 1. Thus, UIP fibroblasts showed greater contractility than did NSIP fibroblasts or TGF-beta 1. Thus, UIP fibroblasts showed greater contractility than did NSIP fibroblasts and up-regulated control fibroblasts. Less
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