1998 Fiscal Year Final Research Report Summary
Study on mutual offects of eosinophils and fibroblasts in the pathogenesis of brochial asthma
| Project/Area Number |
09670469
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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 |
内科学一般
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| Research Institution | St.Marianna University School of Medicine |
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Principal Investigator |
TAKAFUJI Shigeru St.Marianna University School of Medicine, Faculty of Medicine, lecturer, 医学部, 講師 (90179549)
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| Project Period (FY) |
1997 – 1998
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| Keywords | eosinophil / fibroblast / degranulation / GM-CSF / adhesion / SCF / IL-4 |
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| Research Abstract |
Although eosinophils (Eos) and fibroblasts (Fb) are closely approximated in the bronchial submucosae of asthmatics, and are believed to play important roles in the pathogenesis of bronchial asthma, the interaction between Eos and Fb has not been thoroughly elucidated. 1n1997, we examined eosinophil cationic protein (ECP) release from human Eos cultured in the presence of human lung Fb. Eos from healthy donors were cultured with or without C5a for 16 h in the presence of human fetal lung Fb which had previously been incubated with or without some cytokines far 4 h. ECP in supernatants was measured by RIA The results were as follows. ECP release was potentiated only when both Eos and Fb were activated by C5a and TNF, respectively, while it was not significantly potentiated when either Eos or Fb were activated. ECP release from Eos activated by Ca was also potentiated when Fb were stimulated by IL-lbeta. The enhancement of ECP release in cocultured Eos and Fb with stimulation was partly inhibited by monoclonal antibodies against GM-CSF and was accompanied by the enhancement of adhesion of Eos to Fb. Anti-ICAM-1 mAb, anti-CDl8 mAb and anti-CD29 mAb significantly inhibited ECP enhancement and the enhancement of adhesion of Eos to Fb.
In 1998, we examined the effect of Eos on SCF production from Fb. The results were as follows. SCF production from Fb was potentiated when Fb were activated by IL-4 of several cytokines. SCF production from Fb were further potentiated when activated Eos were added to culture system, in addition to IL-4. In summary, Fb may influence Eos degranulation, while Eos may have effects on Fb SCF production. It is suggested that the mutual effects of both cells may lead to the exacerbation and chronicity of asthma.
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