Expression of cytokine genes during pneumococcal and nontypeable Haemophilus influenzae acute otitis media in the rat
Expression of cytokine genes during pneumococcal and nontypeable Haemophilus influenzae acute otitis media in the rat
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DOI：
10.1128/iai.68.7.4024-4031.2000
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发表时间：
2000-07-01
影响因子：
3.1
通讯作者：
Ryan, AF
中科院分区：
文献类型：
--
作者：
Melhus, Å;Ryan, AF
急性冲刺培养基（AOM）引起了中耳粘膜细胞以及浸润白细胞的有效炎症反应，以探索3型肺炎链球菌诱导的实验性AOM期间的宿主反应，并探索3型的肺炎链球菌和不可抑制的血红素嗜血杆菌（Nthi）（Nthi）（Nthi），nthi（Nthi），eosroscopy，otomicroscopy otomososocy otomicosocy otomicososocy，在接种后1个月内，监测中耳中中耳的细胞因子基因的。粘液和浸润细胞对细菌挑战的反应迅速。耳鼻镜，AOM在nTHI接种后1天出现，肺炎球菌接种后3天。肺炎球菌AOM比NTHI耳炎更严重，但通常，在肺炎球菌感染的肺炎球菌中检测到较低的转录物水平，而不是nTHI感染的动物，两种肺炎球菌的脑线内6（IL-6）mRNA水平在3至6 h的峰值下峰值峰值。和nthi感染的动物。 IL-1α，肿瘤坏死因子α和IL-10 mRNA水平在6小时以nthi耳炎的峰值，肺炎球菌炎的1至3天。比较耳鼻镜与表达谱进行比较，似乎大多数细胞因子mRNA在临床上进行了AOM诊断之前已经通过了峰值。仅转化生长因子βmRNA之后的时间疗程较慢，即使在耳鼻镜上分辨出AOM后，峰值也很晚并持续表达。在任何时候，在任何动物中均未检测到IL-2和IL-4 mRNA。大多数研究的细胞因子是AOM的早期标志物，可能参与炎症的开始，但由于出现临床体征之前的水平下降，因此它们的药理操作靶标会很差。
Acute otitis media (AOM) elicits potent inflammatory responses from the cells of the middle ear mucosa as well as from infiltrating leukocytes, To explore host responses during experimental AOM induced by Streptococcus pneumoniae type 3 and nontypeable Haemophilus influenzae (NTHi), otomicroscopy findings and expression of cytokine genes in the middle ear were monitored up to 1 month postinoculation. The mucose and infiltrating cells responded rapidly to the bacterial challenge. Otomicroscopically, AOM appeared 1 day after NTHi inoculation and 3 days after pneumococcus inoculation. Pneumococcal AOM was more severe than NTHi otitis, but in general, lower transcript levels were detected in pneumococcus-infected than in NTHi-infected animals, Interleukin-6 (IL-6) mRNA levels peaked at 3 to 6 h for both pneumococcus-infected and NTHi-infected animals. IL-1 alpha, tumor necrosis factor alpha, and IL-10 mRNA levels peaked at 6 h for NTHi otitis and 1 to 3 days for pneumococcal otitis. Comparing otomicroscopy with expression profiles, it would appear that the majority of cytokine mRNAs had passed their peak before the AOM diagnosis could be made clinically. Only transforming growth factor beta mRNA followed a slower time course, peaking very late and continuing expression even after the AOM was otomicroscopically resolved. IL-2 and IL-4 mRNAs were not detected in any animal at any time. Most of the investigated cytokines are very early markers for AOM and may be involved in initiation of inflammation, but they would be poor targets for pharmacological manipulation since their levels decline before clinical signs appear.