Lipopolysaccharide-induced inflammation attenuates taste progenitor cell proliferation and shortens the life span of taste bud cells.
Lipopolysaccharide-induced inflammation attenuates taste progenitor cell proliferation and shortens the life span of taste bud cells.
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DOI：
10.1186/1471-2202-11-72
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发表时间：
2010-06-10
期刊：
影响因子：
2.4
通讯作者：
Wang H
中科院分区：
文献类型：
--
作者：
Cohn ZJ;Kim A;Huang L;Brand J;Wang H
哺乳动物味蕾是味觉感觉细胞、支持细胞和未成熟基底细胞的复杂集合，是口腔中检测味觉刺激的结构单位。尽管味蕾细胞不断更新，但味蕾的结构动态平衡是通过平衡细胞增殖和细胞死亡来维持的。与无味觉舌上皮细胞相比，味觉细胞表达更高水平的几种炎症受体和信号蛋白。炎症是与味觉障碍相关的一些疾病的基础条件，是否干扰味觉细胞的更新和周转尚不清楚。在这里，我们报告了脂多糖（LPS）诱导的炎症对小鼠味觉组织中味觉祖细胞增殖和味蕾细胞更新的影响。腹腔注射LPS可迅速诱导小鼠轮廓乳头和叶状乳头表达多种炎性细胞因子，包括肿瘤坏死因子（TNF）-α、干扰素（IFN）-γ和白细胞介素（IL）-6。TNF-α和IFN-γ免疫反应性优先定位于味蕾细胞亚群。LPS诱导的炎症在LPS注射后1-3天显著减少5-溴-2 '-脱氧尿苷（BrdU）标记的新生味蕾细胞的数量，表明味蕾细胞更新的抑制。BrdU脉冲追踪实验表明，BrdU标记的味觉细胞在LPS处理的小鼠中的平均寿命比对照组短。为了研究LPS是否通过抑制味觉祖细胞增殖来抑制味觉细胞更新，我们研究了细胞增殖标志物Ki 67的表达。实时荧光定量RT-PCR结果显示，LPS显著降低了轮廓上皮和叶状上皮中Ki 67 mRNA的水平。使用抗Ki 67抗体的免疫荧光染色显示，LPS减少了周围的轮廓味蕾，味觉祖细胞的生态位的基底区域的Ki 67阳性细胞的数量。PCR芯片实验显示，LPS可显著下调周纹状上皮和叶状上皮细胞周期调控因子cyclin B2和E2 F1的表达。我们的研究结果表明，LPS诱导的炎症抑制味觉祖细胞增殖，干扰味觉细胞更新。LPS加速细胞更新并适度缩短味觉细胞的平均寿命。炎症的这些影响可能有助于与感染相关的味觉障碍的发展。
The mammalian taste bud, a complex collection of taste sensory cells, supporting cells, and immature basal cells, is the structural unit for detecting taste stimuli in the oral cavity. Even though the cells of the taste bud undergo constant turnover, the structural homeostasis of the bud is maintained by balancing cell proliferation and cell death. Compared with nongustatory lingual epithelial cells, taste cells express higher levels of several inflammatory receptors and signalling proteins. Whether inflammation, an underlying condition in some diseases associated with taste disorders, interferes with taste cell renewal and turnover is unknown. Here we report the effects of lipopolysaccharide (LPS)-induced inflammation on taste progenitor cell proliferation and taste bud cell turnover in mouse taste tissues. Intraperitoneal injection of LPS rapidly induced expression of several inflammatory cytokines, including tumor necrosis factor (TNF)-α, interferon (IFN)-γ, and interleukin (IL)-6, in mouse circumvallate and foliate papillae. TNF-α and IFN-γ immunoreactivities were preferentially localized to subsets of cells in taste buds. LPS-induced inflammation significantly reduced the number of 5-bromo-2'-deoxyuridine (BrdU)-labeled newborn taste bud cells 1-3 days after LPS injection, suggesting an inhibition of taste bud cell renewal. BrdU pulse-chase experiments showed that BrdU-labeled taste cells had a shorter average life span in LPS-treated mice than in controls. To investigate whether LPS inhibits taste cell renewal by suppressing taste progenitor cell proliferation, we studied the expression of Ki67, a cell proliferation marker. Quantitative real-time RT-PCR revealed that LPS markedly reduced Ki67 mRNA levels in circumvallate and foliate epithelia. Immunofluorescent staining using anti-Ki67 antibodies showed that LPS decreased the number of Ki67-positive cells in the basal regions surrounding circumvallate taste buds, the niche for taste progenitor cells. PCR array experiments showed that the expression of cyclin B2 and E2F1, two key cell cycle regulators, was markedly downregulated by LPS in the circumvallate and foliate epithelia. Our results show that LPS-induced inflammation inhibits taste progenitor cell proliferation and interferes with taste cell renewal. LPS accelerates cell turnover and modestly shortens the average life span of taste cells. These effects of inflammation may contribute to the development of taste disorders associated with infections.
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