Ambient ozone and pulmonary innate immunity.
Ambient ozone and pulmonary innate immunity.
复制标题
DOI：
10.1007/s12026-010-8180-z
复制
发表时间：
2011-04
影响因子：
4.4
通讯作者：
Hollingsworth, John W.
中科院分区：
文献类型：
--
作者：
Al-Hegelan, Mashael;Tighe, Robert M.;Castillo, Christian;Hollingsworth, John W.
环境臭氧是影响人类发病率和死亡率的标准空气污染物。臭氧吸入的影响包括对肺组织的毒性和宿主免疫反应的改变。先天免疫系统促进对外来病原体和组织损伤的立即识别。新出现的证据支持臭氧可以改变宿主的先天免疫反应，这种对吸入臭氧的反应取决于先天免疫的基因。对环境臭氧和宿主先天免疫之间复杂相互作用的进一步理解将为炎症性气道疾病的发病机制提供基本的见解。我们回顾了目前的证据，支持环境臭氧吸入：（1）修改所需的细胞类型的完整的先天免疫，（2）是部分依赖于先天免疫的基因，（3）引发肺先天免疫反应的LPS，（4）有助于先天适应性免疫系统的串扰。
Ambient ozone is a criteria air pollutant that impacts both human morbidity and mortality. The effect of ozone inhalation includes both toxicity to lung tissue and alteration of the host immunologic response. The innate immune system facilitates immediate recognition of both foreign pathogens and tissue damage. Emerging evidence supports that ozone can modify the host innate immune response and that this response to inhaled ozone is dependent on genes of innate immunity. Improved understanding of the complex interaction between environmental ozone and host innate immunity will provide fundamental insight into the pathogenesis of inflammatory airways disease. We review the current evidence supporting that environmental ozone inhalation: (1) modifies cell types required for intact innate immunity, (2) is partially dependent on genes of innate immunity, (3) primes pulmonary innate immune responses to LPS, and (4) contributes to innate-adaptive immune system cross-talk.
登录
查看更多内容
DOI：
10.1164/rccm.200509-1527oc
发表时间：
2007-04-15
影响因子：
24.7
作者：
Cho, Hye-Youn;Morgan, Daniel L.;Kleeberger, Steven R.
通讯作者：
Kleeberger, Steven R.
影响因子：
15.9
作者：
Andonegui, G;Bonder, CS;Kubes, P
通讯作者：
Kubes, P
影响因子：
3.8
作者：
Devlin, RB;McDonnell, WF;Koren, HS
通讯作者：
Koren, HS
影响因子：
15.9
作者：
Dahl, Morten;Bauer, Alison K.;Kobzik, Lester
通讯作者：
Kobzik, Lester
影响因子：
3.8
作者：
BECKER, S;MADDEN, MC;KOREN, HS
通讯作者：
KOREN, HS