近日，國際雜志Journal of Allergy and Clinical Immunology在線刊登了日本研究人員的最新研究成果“A critical role of IL-33 in experimental allergic rhinitis,，”，文章中,，研究者發(fā)現(xiàn)了花粉癥的主要導(dǎo)火索。
每年春季日本大街上的“口罩族”蔚為壯觀,，花粉癥成為很多人一年一季的“洗禮”,。日本一個研究小組最新研究發(fā)現(xiàn)，一種作為免疫調(diào)節(jié)物質(zhì)的白細胞介素發(fā)揮了花粉癥主要“導(dǎo)火索”的作用。
據(jù)日本媒體5日報道,，花粉癥可導(dǎo)致眼睛和鼻子等出現(xiàn)過敏癥狀,。研究人員已知在花粉癥患者的血清中，白細胞介素－33的濃度很高,。它是由鼻粘膜釋放出來的,，在白細胞介素－33的刺激下，組織胺大量增加,，而組織胺是引起噴嚏,、鼻涕和鼻塞的物質(zhì)。
在動物實驗中,，研究人員培養(yǎng)了體內(nèi)不能產(chǎn)生白細胞介素－33的實驗鼠,，和普通實驗鼠相比，它們感染花粉癥后打噴嚏的次數(shù)減少了三分之二,，癥狀也沒有惡化,。不過由于并非完全沒有花粉癥癥狀，研究小組認為小鼠體內(nèi)應(yīng)該還有其他物質(zhì)與花粉癥有關(guān),。
兵庫醫(yī)科大學(xué)教授善本知廣說,，雖然單靠遏制白細胞介素－33尚不能完全控制花粉癥,，但這是與發(fā)病相關(guān)的最主要原因,，這項研究也許有助于開發(fā)有效的治療藥物。（生物谷Bioon.com）
doi:10.1016/j.jaci.2012.02.013
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A critical role of IL-33 in experimental allergic rhinitis
Yoko Haenuki, MDa, b, c, Kazufumi Matsushita, PhDa, Shizue Futatsugi-Yumikura, BPharma, Ken J. Ishii, MD, PhDd, e, Tatsukata Kawagoe, MD, PhDe, Yoshimasa Imoto, MD, PhDf, Shigeharu Fujieda, MD, PhDf, Makoto Yasuda, MD, PhDc, Yasuo Hisa, MD, PhDc, Shizuo Akira, MD, PhDe, Kenji Nakanishi, MD, PhDb, Tomohiro Yoshimoto, MD, PhDa,
Background We reported previously that serum levels of IL-33 are significantly increased in patients with allergic rhinitis (AR). However, very little is known about the role of IL-33 for the development of AR.
Objective We thought to develop a novel murine model of ragweed pollen–specific AR and examined the pathologic role for ragweed-induced IL-33 in the development of AR manifestation using IL-33–deficient (il33−/−) mice. Methods Ragweed-immunized and ragweed-challenged mice were examined for early- and late-phase nasal responses. IL-33 protein expression in the nasal epithelial cells of the AR murine model and patients with AR were assessed by using confocal microscopy.
Results After nasal challenge with ragweed pollen, ragweed-immunized wild-type mice manifested early-phase (sneezing) and late-phase (eosinophilic and basophilic accumulation) responses. In contrast, il33−/− and FcεRI−/− mice did not have both early- and late-phase AR responses. IL-33 protein was constitutively expressed in the nucleus of nasal epithelial cells and was promptly released into nasal fluids in response to nasal exposure to ragweed pollen. In human subjects we revealed constitutive expression of IL-33 protein in the nasal epithelial cells of healthy control subjects and downregulated expression of IL-33 protein in inflamed nasal epithelial cells of patients with AR. IL-33–stimulated mast cells and basophils contributed to the early- and late-phase AR manifestation through increasing histamine release and production of chemoattractants for eosinophils/basophils, respectively.
Conclusions Ragweed pollen–driven endogenous IL-33 contributed to the development of AR responses. IL-33 might present an important therapeutic target for the prevention of AR.
