Bronchiolar chemokine expression is different after single versus repeated cigarette smoke exposure.
Bronchiolar chemokine expression is different after single versus repeated cigarette smoke exposure.
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单一与反复的香烟烟雾暴露后，支气管趋化因子表达不同。
DOI：
10.1186/1465-9921-9-7
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发表时间：
2008-01-21
影响因子：
5.8
通讯作者：
Nishimura, Masaharu
中科院分区：
文献类型：
--
作者：
Betsuyaku, Tomoko;Hamamura, Ichiro;Hata, Junko;Takahashi, Hiroshi;Mitsuhashi, Hiroaki;Adair-Kirk, Tracy L.;Senior, Robert M.;Nishimura, Masaharu
细支气管是香烟烟雾（CS）引起的肺部炎症的关键区域。然而，关于细支气管上皮细胞响应CS的细胞因子基因表达的体内动态的研究很少。我们对 C57BL/6J 小鼠进行不同时期的 CS（全身暴露，90 分钟/天），并使用激光捕获显微切割分离细支气管上皮细胞，通过定量逆转录聚合酶链反应分析 mRNA。我们检测到连续 10 天接触 CS 后，支气管上皮细胞角质形成细胞衍生趋化因子 (KC)、巨噬细胞炎症蛋白 2 (MIP-2)、肿瘤坏死因子 α (TNF-α) 和白细胞介素 1β (IL-1β) 的表达增强。支气管肺泡灌洗 (BAL) 液中中性粒细胞和 KC、MIP-2、TNF-α 和 IL-1β 蛋白的增加反映了这一点。最初吸入 CS 导致 KC 和 MIP-2 快速而强劲地上调，并在 1 小时内伴随 DNA 氧化，随后在 3 小时内恢复到对照值。相反，在CS暴露10天后，没有观察到这种最初的激增。随着CS暴露延长至4、12、18和24周，细支气管KC和MIP-2表达及其在BAL液中的水平与10天时相比相对减弱。然而，BAL 液中的中性粒细胞持续增加长达 24 周，表明长期 CS 暴露导致的中性粒细胞积累变得独立于 KC 和 MIP-2。这些发现表明细支气管上皮细胞因子表达的不同模式取决于CS暴露的持续时间，并且复杂的机制控制体内细支气管分子动力学。
Bronchioles are critical zones in cigarette smoke (CS)-induced lung inflammation. However, there have been few studies on the in vivo dynamics of cytokine gene expression in bronchiolar epithelial cells in response to CS. We subjected C57BL/6J mice to CS (whole body exposure, 90 min/day) for various periods, and used laser capture microdissection to isolate bronchiolar epithelial cells for analysis of mRNA by quantitative reverse transcription-polymerase chain reaction. We detected enhanced expression of keratinocyte-derived chemokine (KC), macrophage inflammatory protein-2 (MIP-2), tumor necrosis factor-α (TNF-α), and interleukin-1β (IL-1β) by bronchial epithelial cells after 10 consecutive days of CS exposure. This was mirrored by increases in neutrophils and KC, MIP-2, TNF-α, and IL-1β proteins in the bronchoalveolar lavage (BAL) fluid. The initial inhalation of CS resulted in rapid and robust upregulation of KC and MIP-2 with concomitant DNA oxidation within 1 hr, followed by a return to control values within 3 hrs. In contrast, after CS exposure for 10 days, this initial surge was not observed. As the CS exposure was extended to 4, 12, 18 and 24 weeks, the bronchiolar KC and MIP-2 expression and their levels in BAL fluid were relatively dampened compared to those at 10 days. However, neutrophils in BAL fluid continuously increased up to 24 weeks, suggesting that neutrophil accumulation as a result of long-term CS exposure became independent of KC and MIP-2. These findings indicate variable patterns of bronchiolar epithelial cytokine expression depending on the duration of CS exposure, and that complex mechanisms govern bronchiolar molecular dynamics in vivo.
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影响因子：
15.9
作者：
Cataisson, Christophe;Pearson, Andrea J.;Yuspa, Stuart H.
通讯作者：
Yuspa, Stuart H.
影响因子：
3.1
作者：
d'Empaire, Gabriela;Baer, Michael T.;Gibson, Frank C., III
通讯作者：
Gibson, Frank C., III
影响因子：
4.7
作者：
Jarvis, MJ;Primatesta, P;Bryant, A
通讯作者：
Bryant, A
影响因子：
5.8
作者：
Kode, Aruna;Yang, Se-Ran;Rahman, Irfan
通讯作者：
Rahman, Irfan
影响因子：
4.4
作者：
Belperio, JA;Keane, MP;Strieter, RM
通讯作者：
Strieter, RM