Toll-like receptor (TLR) expression and TLR‑mediated interleukin-8 production by human submandibular gland epithelial cells.
Toll-like receptor (TLR) expression and TLR‑mediated interleukin-8 production by human submandibular gland epithelial cells.
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DOI：
10.3892/mmr.2014.2507
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发表时间：
2014-11
影响因子：
3.4
通讯作者：
K. Ohta;Y. Ishida;A. Fukui;K. Mizuta;H. Nishi;M. Takechi;N. Kamata
中科院分区：
文献类型：
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作者：
K. Ohta;Y. Ishida;A. Fukui;K. Mizuta;H. Nishi;M. Takechi;N. Kamata
Toll样受体（TLR）家族成员是在先天性和适应性免疫应答的激活中必不可少的模式识别受体。下颌下腺上皮细胞（SMGC）可能通过TLR识别微生物成分，并参与下颌下腺炎症反应的发生。因此，在本研究中，TLRs在SMGC中的功能表达进行了研究。RT-PCR检测SMGC和整个颌下组织中TLRs的mRNA表达。随后，使用ELISA检查各种TLR激动剂和肿瘤坏死因子α（TNF-α）对IL-8产生的影响。SMGC和整个下颌下组织均表达TLR 1 -10 mRNA。此外，SMGC产生的白细胞介素（IL）-8（IL）-8增加Pam 3CSK 4（TLR 1/2激动剂），poly I：C（TLR 3激动剂），E。大肠杆菌脂多糖（LPS; TLR 4激动剂）、鞭毛蛋白（TLR 5激动剂）和巨噬细胞活化脂肽（MALP）-2（TLR 2/6激动剂）治疗以剂量依赖性方式，而咪喹莫特（TLR 7激动剂）或CpG-寡脱氧核苷酸（TLR 9激动剂）给药无明显作用。Pam 3CSK 4、poly I：C、LPS、鞭毛蛋白和MALP-2也增强了TNF-α诱导的SMGC中IL-8的产生。这些结果表明，先天性免疫反应对微生物成分的TNF-α介导的自身免疫性炎症性疾病的发展在下颌下腺的结果。
Toll-like receptor (TLR) family members are pattern recognition receptors that are essential in the activation of innate and adaptive immune responses. Submandibular gland epithelial cells (SMGCs) may recognize microbial components through TLRs and be involved in the development of inflammatory reactions in the submandibular glands. Therefore, the functional expression of TLRs in SMGCs was investigated in the present study. The mRNA expression of TLRs in SMGC and whole submandibular tissues was determined by RT-PCR. Subsequently, the effects of various TLR agonists and tumor necrosis factor alpha (TNF-α) on IL-8 production were examined using an ELISA. SMGCs, as well as whole submandibular tissues, expressed TLR1-10 mRNA. Furthermore, interleukin (IL)-8 production in SMGCs was increased by Pam3CSK4 (TLR1/2 agonist), poly I:C (TLR3 agonist), E. coli lipopolysaccharide (LPS; TLR4 agonist), flagellin (TLR5 agonist) and macrophage‑activating lipopeptide (MALP)-2 (TLR2/6 agonist) treatments in a dose‑dependent manner, whereas administration of either imiquimod (TLR7 agonist) or CpG-oligodeoxynucletide (TLR9 agonist) exerted no evident effect. Pam3CSK4, poly I:C, LPS, flagellin and MALP-2 also enhanced TNF‑α‑induced IL-8 production in SMGCs. These findings suggest that innate immune responses against microbial components result in the development of TNF-α-mediated autoimmune inflammatory disease in the submandibular glands.