Alveolar macrophage-epithelial cell interaction following exposure to atmospheric particles induces the release of mediators involved in monocyte mobilization and recruitment.
Alveolar macrophage-epithelial cell interaction following exposure to atmospheric particles induces the release of mediators involved in monocyte mobilization and recruitment.
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DOI：
10.1186/1465-9921-6-87
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发表时间：
2005-08-01
影响因子：
5.8
通讯作者：
van Eeden SF
中科院分区：
文献类型：
--
作者：
Ishii H;Hayashi S;Hogg JC;Fujii T;Goto Y;Sakamoto N;Mukae H;Vincent R;van Eeden SF
我们实验室的研究表明，体外暴露于周围颗粒物(PM10)的人肺泡巨噬细胞(AM)和支气管上皮细胞(HBEC)可增加其炎症介质的产生，PM10暴露细胞的上清可缩短单核细胞在骨髓中的转运时间，并促进其释放到循环中。本研究涉及PM10(EHC-93)对AM和HBEC的共培养，以及在mRNA和蛋白水平上测量参与单核细胞动力学的介质的产生。这些实验还被设计用来确定这些细胞之间通过细胞间黏附分子(ICAM)-1的黏附相互作用在这些介质的产生中的作用。AM/HBEC与100μg/mlPM10共培养2或24 h后，其粒细胞-巨噬细胞集落刺激因子、M-CSF、巨噬细胞炎性蛋白-1β、单核细胞趋化蛋白-1、白介素6和细胞间黏附分子-1mRNA水平均高于单独培养的AM或HBEC，或对照组。作用24 h后，共培养上清液中GM-CSF、M-CSF、MIP-1β和IL-6水平均高于对照组(P<；0.05)。AM和HBEC在产生GM-CSF、MIP-1β和IL-6方面存在协同作用。但用抗ICAM-1的封闭抗体或在HBEC上交联ICAM-1均不能阻断PM10诱导的共培养的mRNA表达的增加。我们的结论是，AM和HBEC(处理吸入颗粒物的肺细胞)之间的ICAM-1独立相互作用增加了介质的产生和释放，从而提高了单核细胞的骨髓周转和它们在组织中的募集。我们推测，这种相互作用放大了PM10诱导的肺部炎症，并导致了暴露在空气污染中的肺部和全身发病率。
Studies from our laboratory have shown that human alveolar macrophages (AM) and bronchial epithelial cells (HBEC) exposed to ambient particles (PM10) in vitro increase their production of inflammatory mediators and that supernatants from PM10-exposed cells shorten the transit time of monocytes through the bone marrow and promote their release into the circulation. The present study concerns co-culture of AM and HBEC exposed to PM10 (EHC-93) and the production of mediators involved in monocyte kinetics measured at both the mRNA and protein levels. The experiments were also designed to determine the role of the adhesive interaction between these cells via the intercellular adhesion molecule (ICAM)-1 in the production of these mediators. AM/HBEC co-cultures exposed to 100 μg/ml of PM10 for 2 or 24 h increased their levels of granulocyte-macrophage colony-stimulating factor (GM-CSF), M-CSF, macrophage inflammatory protein (MIP)-1β, monocyte chemotactic protein (MCP)-1, interleukin (IL)-6 and ICAM-1 mRNA, compared to exposed AM or HBEC mono-cultures, or control non-exposed co-cultures. The levels of GM-CSF, M-CSF, MIP-1β and IL-6 increased in co-cultured supernatants collected after 24 h exposure compared to control cells (p < 0.05). There was synergy between AM and HBEC in the production of GM-CSF, MIP-1β and IL-6. But neither pretreatment of HBEC with blocking antibodies against ICAM-1 nor cross-linking of ICAM-1 on HBEC blocked the PM10-induced increase in co-culture mRNA expression. We conclude that an ICAM-1 independent interaction between AM and HBEC, lung cells that process inhaled particles, increases the production and release of mediators that enhance bone marrow turnover of monocytes and their recruitment into tissues. We speculate that this interaction amplifies PM10-induced lung inflammation and contributes to both the pulmonary and systemic morbidity associated with exposure to air pollution.
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DOI：
10.1165/ajrcmb.25.3.4445
发表时间：
2001-09-01
影响因子：
6.4
作者：
Fujii, T;Hayashi, S;Van Eeden, SF
通讯作者：
Van Eeden, SF
影响因子：
3.8
作者：
Carter, JD;Ghio, AJ;Devlin, RB
通讯作者：
Devlin, RB
DOI：
10.1164/ajrccm.160.supplement_1.11
发表时间：
1999-11-01
影响因子：
24.7
作者：
Mills, PR;Davies, RJ;Devalia, JL
通讯作者：
Devalia, JL
DOI：
10.1016/1357-4310(95)80019-0
发表时间：
1995-04-01
期刊：
MOLECULAR MEDICINE TODAY
影响因子：
--
作者：
SHANLEY, TP;WARNER, RL;WARD, PA
通讯作者：
WARD, PA
影响因子：
4.4
作者：
Moore, BB;Coffey, MJ;Toews, GB
通讯作者：
Toews, GB