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Review
. 2011 Apr;49(1-3):173-91.
doi: 10.1007/s12026-010-8180-z.

Ambient ozone and pulmonary innate immunity

Mashael Al-Hegelan  1 , Robert M Tighe, Christian Castillo, John W Hollingsworth
Affiliations
Review

Ambient ozone and pulmonary innate immunity

Mashael Al-Hegelan et al. Immunol Res. 2011 Apr.

Abstract

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.

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Figures

Figure 1
Figure 1. Ozone alters many cell types in the lung and modifies pulmonary innate immunity
(A) Many cell types are modified by inhalation of ozone. Inhalation of ozone can lead to increase numbers of macrophages, neutrophils, and dendritic cells in the lung. Ozone disrupts airway epithelia cells including; impaired barrier function, injury to cilia, impaired mucociliary clearance, and alters production of cytokines. Ozone can impair macrophage phagocytosis, induce cytokine expression, induce apoptosis, and alter expression of genes of innate immunity. (B) The response to ozone is dependent on genes of innate immunity and can enhance surface expression of TLR4 on macrophages. Current evidence supports a role of both macrophages and airway epithelia in the complete innate immune response to ozone. Ozone induces fragmentation of extracellular matrix hyaluronan (HA) into low molecular weight (LMW). HA fragments result in TLR4-dependent and CD44-dependent production of pro-inflammatory cytokines. The response to ozone supports a role of both MyD88 and NF-kB in the production of pro-inflammatory cytokines.
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