Whole cigarette smoke increased the expression of TLRs, HBDs, and proinflammory cytokines by human gingival epithelial cells through different signaling pathways.
Whole cigarette smoke increased the expression of TLRs, HBDs, and proinflammory cytokines by human gingival epithelial cells through different signaling pathways.
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DOI：
10.1371/journal.pone.0052614
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发表时间：
2012
期刊：
影响因子：
3.7
通讯作者：
Rouabhia M
中科院分区：
文献类型：
--
作者：
Semlali A;Witoled C;Alanazi M;Rouabhia M
牙龈上皮被认为是口腔先天性免疫反应的调节器，对各种各样的侮辱，如细菌和化学品，包括香烟烟雾中发现的那些化学品。我们研究了香烟烟雾对原代人牙龈上皮细胞中细胞表面表达的Toll样受体（TLR）-2，-4和-6，人β-防御素（HBD）和促炎细胞因子表达和产生的影响。全香烟烟雾显示增加TLR 2、TLR 4和TLR 6表达。香烟烟雾导致ERK 1/2、p38和JNK磷酸化，并与核因子-κB（NFκB）易位到细胞核中。使用ERK 1/2、p38、JNK MAP激酶和NFκB抑制剂可下调香烟烟雾暴露后TLR的表达，提示这些信号通路参与了对香烟烟雾的细胞反应。香烟烟雾还通过ERK 1/2和NFκB途径促进HBD 2、HBD 3、IL-1β和IL-6的表达。有趣的是，TLR，HBD和细胞因子表达的调节在牙龈上皮细胞暴露于烟雾后很长时间内保持不变。通过促进TLR、HBD和促炎细胞因子的表达和产生，香烟烟雾可能导致先天免疫失调，这可能对人类健康产生负面影响。
The gingival epithelium is becoming known as a regulator of the oral innate immune responses to a variety of insults such as bacteria and chemicals, including those chemicals found in cigarette smoke. We investigated the effects of whole cigarette smoke on cell-surface-expressed Toll-like receptors (TLR)-2, −4 and −6, human β-defensin (HBD) and proinflammatory cytokine expression and production in primary human gingival epithelial cells. Whole cigarette smoke was shown to increase TLR2, TLR4 and TLR6 expression. Cigarette smoke led to ERK1/2, p38 and JNK phosphorylation in conjunction with nuclear factor-κB (NFκB) translocation into the nucleus. TLR expression following cigarette smoke exposure was down regulated by the use of ERK1/2, p38, JNK MAP kinases, and NFκB inhibitors, suggesting the involvement of these signaling pathways in the cellular response against cigarette smoke. Cigarette smoke also promoted HBD2, HBD3, IL-1β, and IL-6 expression through the ERK1/2 and NFκB pathways. Interestingly, the modulation of TLR, HBD, and cytokine expression was maintained long after the gingival epithelial cells were exposed to smoke. By promoting TLR, HBDs, and proinflammatory cytokine expression and production, cigarette smoke may contribute to innate immunity dysregulation, which may have a negative effect on human health.
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