Gingival epithelial cells increase interleukin-8 secretion in response to Actinobacillus actinomycetemcomitans challenge
Gingival epithelial cells increase interleukin-8 secretion in response to Actinobacillus actinomycetemcomitans challenge
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DOI：
10.1902/jop.1998.69.10.1105
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发表时间：
1998-10-01
影响因子：
4.3
通讯作者：
Park, NH
中科院分区：
文献类型：
--
作者：
Huang, GTJ;Haake, SK;Park, NH
牙周疾病是由细菌病原体与宿主牙龈组织相互作用引起的。牙龈上皮细胞在遇到口腔细菌后启动宿主防御机制中的作用尚未研究。伴放线放线杆菌是一种重要的牙周致病菌，可粘附并侵入口腔上皮细胞。因此，我们研究了牙龈上皮细胞是否增加分泌的有效中性粒细胞趋化因子白细胞介素-8（IL-8）后，A。伴放线菌挑战。将从牙龈组织中分离的正常人口腔角质形成细胞（NHOK）和3种口腔上皮细胞系（HOK-18 A、HOK-16 B-BaP-T1和HEp-2）与A.放线菌共生菌培养2小时，以允许细菌-上皮细胞相互作用。然后洗涤上皮细胞，并加入含有庆大霉素的新鲜培养基以杀死细胞外细菌。将细胞培养物进一步孵育24小时，然后收集上清液用于用ELISA检测IL-8。结果显示，在细菌攻击后24小时，IL-8分泌增加2至7倍。在使用HOK-16 B-BaP-T1细胞的细菌剂量反应研究中，最高的IL-8分泌是在1，000：1的感染复数（MOI）下。时程研究表明，IL-8分泌迅速达到最高水平后6小时细菌的挑战，随后下降到基础水平。这些数据表明牙龈上皮细胞能够响应于A.伴随放线菌挑战并因此可促进作为宿主防御机制的中性粒细胞的募集。
PERIODONTAL DISEASES RESULT FROM THE INTERACTION Of bacterial pathogens with the host gingival tissues. The role of gingival epithelial cells in the initiation of host defense mechanisms after encountering oral bacteria has not been investigated. Actinobacillus actinomycetemcomitans is a key periodontal pathogen that adheres to and invades oral epithelial cells. Thus, we examined whether gingival epithelial cells increase secretion of the potent neutrophil chemoattractant interleukin-8 (IL-8) following A. actinomycetemcomitans challenge. Normal human oral keratinocytes (NHOK), isolated from gingival tissue, and 3 oral epithelial cell lines (HOK-18A, HOK-16B-BaP-T1, and HEp-2) were co-cultured with A. actinomycetemcomitans for 2 hours to allow bacteria-epithelial cell interactions. The epithelial cells were then washed, and fresh medium with gentamicin was added to kill extracellular bacteria. Cell cultures were further incubated for 24 hours before the supernatant was collected for IL-8 detection with ELISA. The results showed that IL-8 secretion increased 2- to 7-fold 24 hours after bacterial challenge. The highest IL-8 secretion was at the multiplicity of infection (MOI) of 1,000:1 in bacterial dose response studies using HOK-16B-BaP-T1 cells. Time-course studies revealed that IL-8 secretion rapidly reached a maximum level 6 hours after bacterial challenge and subsequently decreased to basal levels. These data indicate that gingival epithelial cells are capable of upregulating IL-8 expression rapidly in response to A. actinomycetemcomitans challenge and thus may facilitate the recruitment of neutrophils as a host defense mechanism.