Ambient ozone and pulmonary innate immunity

被引:58
作者
Al-Hegelan, Mashael [1 ]
Tighe, Robert M. [1 ]
Castillo, Christian [1 ]
Hollingsworth, John W. [1 ]
机构
[1] Duke Univ, Med Ctr, Dept Med, Div Pulm Allergy & Crit Care Med, Durham, NC 27710 USA
关键词
Environmental; Toll-like receptor; TLR4; CD44; Hyaluronan; Asthma; Genetic; Gene x environment; SURFACTANT PROTEIN-A; NITRIC-OXIDE SYNTHASE; TOLL-LIKE RECEPTOR-4; INDUCED AIRWAY HYPERRESPONSIVENESS; INDUCED LUNG INFLAMMATION; ANTIGEN-PRESENTING ACTIVITY; T-CELL ACTIVATION; FACTOR-KAPPA-B; EPITHELIAL-CELLS; IN-VITRO;
D O I
10.1007/s12026-010-8180-z
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
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.
引用
收藏
页码:173 / 191
页数:19
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