1989 Fiscal Year Final Research Report Summary
Mucosal Immunity in the Nose
| Project/Area Number |
63570819
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
Otorhinolaryngology
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| Research Institution | Nippon Medical School |
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Principal Investigator |
OKUDA Minoru Nippon Medical School, Faculty of Medicine, Professor, 医学部, 教授 (70073731)
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| Co-Investigator(Kenkyū-buntansha) |
TOMIYAMA Shuninchi Nippon Medical School, Faculty of Medicine, Assistant Professor, 医学部, 講師 (00094665)
YEN Chen-Hsien Nippon Medical School, Faculty of Medicine, Assistant, 医学部, 助手 (10214735)
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| Project Period (FY) |
1988 – 1989
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| Keywords | nasal allergy / chemical substance in nasal fluid / passive glandular secretion / nasal intraepithelial lymphocyte / nasal surface mast cell / interleukin |
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| Research Abstract |
Different chemical substances in the nasal fluid play an important role in nasal mucosal immunity. To verify the sources of these substances we carried out a biochemical analysis of nasal fluid collected bilaterally but separately, after allergen provocation only unilaterally. The nasal fluid collected from the unprovoked side is a reflex-mediated,, glandular secretion, which consists of active and passive secretion. Passive secretion from the nasal secretory glands was noted to be important as the source of nasal fluid component.
Cellular component in the nasal epithelium is also essential for nasal mucosal immunity. We examined the nature of nasal epithelial lymphocytes by FACS after increasing their number by cell culture. The lymphocytes consisted of activated Ts/Tc, activated Th/Ti, suppresser inducer T, helper inducer T and natural killer cell.
Recently the effect of interleukins and colony stimulating factor (CSF) on proliferation of mast cells, the most important effector cells in Type I allergy, is of interest to many researchers. We provoked the nasal mucosa of patients of nasal allergy with interleukin 2,3,4 and CSF and followed up the changes in the number of nasal surface mast cells. The increase in mast cells was minimal, on challenge with interleukin 4.
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