Interleukin‐8 expression in otitis media
Interleukin‐8 expression in otitis media
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DOI：
10.1288/00005537-199408000-00013
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发表时间：
1994-08
期刊：
影响因子：
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通讯作者：
K. Maxwell;G. Leonard;R. Carpenter;D. Kreutzer;J. E. Fitzgerald;J. Burleson
中科院分区：
文献类型：
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作者：
K. Maxwell;G. Leonard;R. Carpenter;D. Kreutzer;J. E. Fitzgerald;J. Burleson
基于作者实验室最近关于中耳炎 (OM) 中细胞因子与炎症相关性的研究，作者推测，在慢性渗出性中耳炎 (COME) 中，白细胞介素-8 (IL-8) 负责 1. 中耳裂处白细胞的积累，以及 2. 原位白细胞激活以及随后的组织损伤。此外，作者假设 IL-8 表达至少部分受到白介素-1 (IL-1) 和肿瘤坏死因子 (TNF) 的控制。为了开始检验这一假设，我们分析了 2 至 90 个月（平均年龄 29 个月）接受鼓膜置管术的儿童中耳积液 (MEE) 中是否存在这些炎症细胞因子。在这些研究中，通过放射免疫分析 (RIA) 或酶联免疫分析 (ELISA) 测量了 MEE 中的 IL-8、白介素-1 β (IL-1β)、肿瘤坏死因子-α (TNF-α) 和肿瘤坏死因子-β (TNF-β)。 IL-8、IL-1β、TNF-α 和 TNF-β 分别存在于 92%、67%、77% 和 0% 的积液中。 IL-8、IL-1β 和 TNF-α 的平均 (± SEM) 值为 4805 (± 913) pg/mg、4076 (± 1510) pg/mg 和 163 (± 90) pg/mg。进一步分析表明，IL-8 水平与 IL-1β（R2 = .500，P = .000）和 TNF-α（R2 = .387，P = .023）相关。因此，作者的研究清楚地表明，IL-8 始终存在于患有 COME 的儿童的 MEE 中，并且与 IL-1β 和 TNF-α 的水平密切相关，这两种物质都是已知的 IL-8 产生诱导剂。这些结果支持作者的假设，即 IL-1β、TNF-α 和 IL-8 与中耳炎症级联密切相关，并表明这些细胞因子的调节可能是未来渗出性中耳炎 (OME) 治疗干预的可能部位。
Based on recent studies in the authors' laboratory on the correlation of cytokines and inflammation in otitis media (OM), the authors hypothesized that in chronic otitis media with effusion (COME) interleukin‐8 (IL‐8) is responsible for 1. the accumulation of leukocytes in the middle ear cleft and 2. in situ leukocyte activation with subsequent tissue damage. Additionally, the authors hypothesized that IL‐8 expression is at least in part under the control of interleukin‐1 (IL‐1) and tumor necrosis factor (TNF). To begin to test this hypothesis, middle ear effusions (MEE) obtained from children ages 2 to 90 months (mean age, 29 months) undergoing tympanostomy tube placement for the presence of these inflammatory cytokines were analyzed. For these studies, IL‐8, interleukin‐1 β (IL‐1β), tumor necrosis factor‐α (TNF‐α), and tumor necrosis factor‐β (TNF‐β) were measured in MEE by radioimmunoassay (RIA) or enzyme‐linked immunoassay (ELISA). IL‐8, IL‐1β, TNF‐α, and TNF‐β were present in 92%, 67%, 77%, and 0% of effusions, respectively. The mean (± SEM) values for IL‐8, IL‐1β, and TNF‐α were 4805 (± 913) pg/mg, 4076 (± 1510) pg/mg, and 163 (± 90) pg/mg. Further analysis indicated that levels of IL‐8 correlated with IL‐1β (R2 = .500, P = .000) and TNF‐α (R2 = .387, P = .023). Thus the authors' studies clearly demonstrate that IL‐8 is consistently present in the MEE of children with COME and is strongly correlated with levels of IL‐1β and TNF‐α, both known inducers of IL‐8 production. These results support the authors' hypothesis that IL‐1β, TNF‐α, and IL‐8 are intimately involved in the inflammatory cascade in the middle ear and suggest regulation of these cytokines as possible sites of future therapeutic intervention in otitis media with effusion (OME).