2004 Fiscal Year Final Research Report Summary
Distinct role of nasal tibroblasts in the initiation of eosinophilic inflammatory response
| Project/Area Number |
14571643
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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 |
Otorhinolaryngology
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| Research Institution | Nippon Medical School |
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Principal Investigator |
NONAKA Manabu Nippon Medical School, ENT, Assistant Professor, 医学部, 講師 (70271351)
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| Project Period (FY) |
2002 – 2004
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| Keywords | fibroblast / eotaxin / RANTES / TARC / airway |
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| Research Abstract |
Rationale : It is now generally accepted type 2 T helper(Th2) cytokines and some chemoattractants play an essential role in the pathogenesis of the nasal polyposis. Nasal polyposis is characterized by chronic eosinophil inflammation and varying degrees of structural abnormalities. The mechanisms that cause the predominance of eosinophil infiltration in nasal polyposis has yet to be clarified. There is growing evidence that fibroblasts could be a major source of chemotactic factors for eosinophils. As the nasal mucosa is the first respiratory tissue that environmental agents encounter, it is exposed to many potentially injurious agents including microorganisms and their breakdown products including LPS. We investigated whether nasal fibroblasts produce CC chemokines (RANTES, eotaxin, TARC) when stimulated with the breakdown products of microorganisms and several cytokines (IL-4,IL-13).
Methods : Fibroblasts lines were established from nasal polyp tissue. The expression of those chemokine mRNAs was evaluated by RT-PCR or real-time PCR. The amount of chemokines in the supernatants was measured by ELISA.
Results : LPS induced RANTES, and synergized with IFN-γ to produce RANTES in nasal fibroblasts. Combined stimulation with LPS and IL-4 synergistically induced eotaxin and TARC in nasal fibroblasts.
Conclusions : These results indicate that nasal fibroblasts contribute to innate immunity and eosinophilic inflammation like nasal polyposis in the human upper airway.
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