EVIDENCE FOR DISTINCT CYTOKINE EXPRESSION IN ALLERGIC VERSUS NONALLERGIC CHRONIC SINUSITIS
EVIDENCE FOR DISTINCT CYTOKINE EXPRESSION IN ALLERGIC VERSUS NONALLERGIC CHRONIC SINUSITIS
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DOI：
10.1016/s0091-6749(95)70298-9
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发表时间：
1995-10-01
影响因子：
14.2
通讯作者：
HAMID, Q
中科院分区：
文献类型：
--
作者：
HAMILOS, DL;LEUNG, DYM;HAMID, Q
背景资料：本研究的目的是描述慢性增生性鼻窦炎伴鼻息肉病（CHS/NP）患者组织细胞因子表达与细胞浸润之间的关系，并比较过敏患者与过敏患者的免疫病理学和细胞因子谱。我们对12例CHS/NP患者的鼻息肉组织样本和10例正常对照患者的鼻甲活检样本进行了研究。用原位杂交法检测IL-4、IL-2和IFN-γ细胞因子mRNA的表达。这些数据与先前报告的细胞因子mRNA种类粒细胞-巨噬细胞集落刺激因子（GM-CSF）、IL-3和IL-5以及炎性细胞浸润的免疫细胞化学特征的数据一起进行分析。结果：组织嗜酸性粒细胞增多是过敏性和非过敏性CHS/NP的一个显著特征，并与GM-CSF和IL-3 mRNA（+）细胞密度相关。与正常对照组相比，过敏性CHS/NP患者具有显著更高的GM-CSF、IL-3、IL-4和IL-5的组织密度（p小于或等于0.025）。相比之下，非过敏性CHS/NP患者的GM-CSF、IL-3和IFN-γ的组织密度显著更高（p小于或等于0.001）。过敏性和非过敏性亚组显示出不同的细胞因子谱，过敏性亚组最显著的细胞因子是IL-4（p = 0.001）和IL-5（p = 0.017），非过敏性亚组最显著的细胞因子是IFN-γ（p = 0.004）。此外，与非过敏性CHS/NP患者的对照组相比，过敏性CHS/NP患者的CD 3（+）T淋巴细胞密度增加（p = 0.03）。CD 3（+）T淋巴细胞密度是过敏性CHS/NP与非过敏性CHS/NP之间唯一有意义的差异。阿司匹林敏感性的临床病史与非过敏性CHS/NP，以及非过敏性CHS/NP的细胞因子，包括IFN-γ的配置文件是密切相关的。结论：我们得出结论，不同的机制嗜酸性粒细胞增多症存在于过敏性与非过敏性CHS/NP患者。过敏性机制涉及浸润T淋巴细胞产生T-H 2型细胞因子，包括GM-CSF、IL-3、IL-4和IL-5。非过敏性机制涉及未知，但确实涉及GM-CSF、IL-3和IFN-γ的产生。然而，非过敏性嗜酸性粒细胞增多症是独立的IL-4和IL-5，细胞因子，有助于组织嗜酸性粒细胞在过敏性炎症。阿司匹林敏感性与非过敏性CHS/NP和细胞因子（包括IFN-γ）的非过敏性CHS/NP谱的产生密切相关。
Background: The purpose of this study was to characterize the relationship between tissue cytokine expression and the cellular infiltrate present in chronic hyperplastic sinusitis with nasal polyposis (CHS/NP) and to compare the immunopathology and cytokine profile of patients with allergy versus patients with allergy.Methods: Nasal polyp tissue samples from 12 patients with CHS/NP and nasal turbinate biopsy specimens from 10 normal control patients we-e examined for the expression of it interleukin (IL)-4, IL-2 and interferon (IFN)-gamma cytokine messenger RNA (mRNA) species by in situ hybridization. These data were analyzed in conjunction with data previously reported for the cytokine mRNA species granulocyte-macrophage colony-stimulating factor (GM-CSF), IL-3, and IL-5 and the immunocytochemical profile of the inflammatory cell infiltrate. Patients with allergy were distinguished from those without allergy on the basis of allergy skin tests.Results: Tissue eosinophilia was a prominent feature of both allergic and nonallergic CHS/NP and correlated in both subgroups with the density of GM-CSF and IL-3 mRNA(+) cells. In comparison with normal controls, patients with allergic CHS/NP had significantly higher tissue densities of GM-CSF, IL-3, IL-4 and IL-5 (p less than or equal to 0.025). In contrast, patients with nonallergic CHS/NP had significantly higher, tissue densities of GM-CSF, IL-3,and IFN-gamma (p less than or equal to 0.001). The allergic and nonallergic subgroups showed distinct cytokine profiles with the most distinguishing cytokines of the allergic subgroup being IL-4 (p = 0.001) and IL-5 (p = 0.017) and of the nonallergic subgroup being IFN-gamma (p = 0.004). Furthermore, patients with allergic CHS/NP showed an increased density of CD3(+) T lymphocytes compared with either controls of patients with nonallergic CHS/NP (p = 0.03). The density of CD3(+) T lymphocytes was the only significant difference between patients with allergic and nonallergic CHS/NP. A clinical history of aspirin sensitivity was strongly correlated with nonallergic CHS/NP, as well as the nonallergic CHS/NP profile of cytokines, including IFN-gamma.Conclusion: We conclude that distinct mechanisms of eosinophilia exist in patients with allergic versus nonallergic CHS/NP. The allergic mechanism involves production of T-H2-type cytokines, including GM-CSF, IL-3, IL-4 and IL-5, bf infiltrating T lymphocytes. The nonallergic mechanism involves unknown but does involve production of GM-CSF, IL-3, and IFN-gamma. However nonallergic eosinophilia is independent of IL-4 and IL-5, cytokines that contribute to tissue eosinophilia in allergic inflammation. Aspirin sensitivity is strongly correlated with nonallergic CHS/NP and production of the nonallergic CHS/NP profile of cytokines, including IFN-gamma.