J Alle Clin Immun：日科学家发现花粉症的主要“导火索”

近日，国际杂志Journal of Allergy and Clinical Immunology在线刊登了日本研究人员的最新研究成果“A critical role of IL-33 in experimental allergic rhinitis，”，文章中，研究者发现了花粉症的主要导火索。

每年春季日本大街上的“口罩族”蔚为壮观，花粉症成为很多人一年一季的“洗礼”。日本一个研究小组最新研究发现，一种作为免疫调节物质的白细胞介素发挥了花粉症主要“导火索”的作用。

据日本媒体5日报道，花粉症可导致眼睛和鼻子等出现过敏症状。研究人员已知在花粉症患者的血清中，白细胞介素－33的浓度很高。它是由鼻粘膜释放出来的，在白细胞介素－33的刺激下，组织胺大量增加，而组织胺是引起喷嚏、鼻涕和鼻塞的物质。

在动物实验中，研究人员培养了体内不能产生白细胞介素－33的实验鼠，和普通实验鼠相比，它们感染花粉症后打喷嚏的次数减少了三分之二，症状也没有恶化。不过由于并非完全没有花粉症症状，研究小组认为小鼠体内应该还有其他物质与花粉症有关。

兵库医科大学教授善本知广说，虽然单靠遏制白细胞介素－33尚不能完全控制花粉症，但这是与发病相关的最主要原因，这项研究也许有助于开发有效的治疗药物。（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.