Effect of ozone on leukocyte function in exposed human subjects

Peterson, Mirdza L.; Harder, Shirley; Rummo, Nicholas J.; House, Dennis E.

doi:10.1016/0013-9351(78)90127-5

Cited by 17 publications

(8 citation statements)

References 17 publications

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“…Neutrophils generate both reactive oxygen species and neutrophil elastase, which help facilitate the clearance of bacterial pathogens. Despite increased numbers of neutrophils after ozone inhalation, bacterial clearance is impaired after ozone exposure under some 51 but not all conditions 52 . Furthermore, the role of neutrophils in the development of ozone-induced AHR remains inconsistent.…”

Section: Multiple Cell Types Required For Intact Innate Immunity Are mentioning

confidence: 99%

Ambient ozone and pulmonary innate immunity

et al. 2010

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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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Section: Multiple Cell Types Required For Intact Innate Immunity Are mentioning

confidence: 99%

Ambient ozone and pulmonary innate immunity

et al. 2010

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“…It remains unclear whether recruited neutrophils directly contribute to the biologic response to inhaled O 3 . Early work by Peterson and colleagues demonstrates that human exposure to low levels of ambient O 3 lead to defective neutrophil phagocytosis and intracellular killing (74). It is possible that differences in O 3 exposure protocols or techniques of neutrophil depletion used in these experiments contribute to the divergent observations.…”

Section: Neutrophils and Environmental Airway Injury With Omentioning

confidence: 99%

Ozone and Pulmonary Innate Immunity

Hollingsworth

Kleeberger²,

Foster³

2007

Proceedings of the American Thoracic Society

111

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Ambient ozone (O(3)) is a commonly encountered environmental air pollutant with considerable impact on public health. Many other inhaled environmental toxicants can substantially affect pulmonary immune responses. Therefore, it is of considerable interest to better understand the complex interaction between environmental airway irritants and immunologically based human disease. The innate immune system represents the first line of defense against microbial pathogens. Intact innate immunity requires maintenance of an intact barrier to interface with the external environment, effective phagocytosis of microbial pathogens, and precise detection of pathogen-associated molecular patterns. We use ambient O(3) as a model to highlight the importance of understanding the role of exposure to ubiquitous air toxins and regulation of basic immune function. Inhalation of O(3) is associated with impaired antibacterial host defense, in part related to disruption of epithelial barrier and effective phagocytosis of pathogens. The functional response to ambient O(3) seems to be dependent on many components of the innate immune signaling. In this article, we review the complex interaction between inhalation of O(3) and pulmonary innate immunity.

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“…The mechanisms by which ozone exposure compromises host defense in the lung are not well understood. Reduced bacterial clearance is primarily attributed to ozone-mediated impairment of macrophage phagocytosis [10], although modulation of adaptive immune responses following exposure in humans has also been reported [13], [14].…”

Section: Introductionmentioning

confidence: 99%

Early Life Ozone Exposure Results in Dysregulated Innate Immune Function and Altered microRNA Expression in Airway Epithelium

et al. 2014

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Exposure to ozone has been associated with increased incidence of respiratory morbidity in humans; however the mechanism(s) behind the enhancement of susceptibility are unclear. We have previously reported that exposure to episodic ozone during postnatal development results in an attenuated peripheral blood cytokine response to lipopolysaccharide (LPS) that persists with maturity. As the lung is closely interfaced with the external environment, we hypothesized that the conducting airway epithelium of neonates may also be a target of immunomodulation by ozone. To test this hypothesis, we evaluated primary airway epithelial cell cultures derived from juvenile rhesus macaque monkeys with a prior history of episodic postnatal ozone exposure. Innate immune function was measured by expression of the proinflammatory cytokines IL-6 and IL-8 in primary cultures established following in vivo LPS challenge or, in response to in vitro LPS treatment. Postnatal ozone exposure resulted in significantly attenuated IL-6 mRNA and protein expression in primary cultures from juvenile animals; IL-8 mRNA was also significantly reduced. The effect of antecedent ozone exposure was modulated by in vivo LPS challenge, as primary cultures exhibited enhanced cytokine expression upon secondary in vitro LPS treatment. Assessment of potential IL-6-targeting microRNAs miR-149, miR-202, and miR-410 showed differential expression in primary cultures based upon animal exposure history. Functional assays revealed that miR-149 is capable of binding to the IL-6 3′ UTR and decreasing IL-6 protein synthesis in airway epithelial cell lines. Cumulatively, our findings suggest that episodic ozone during early life contributes to the molecular programming of airway epithelium, such that memory from prior exposures is retained in the form of a dysregulated IL-6 and IL-8 response to LPS; differentially expressed microRNAs such as miR-149 may play a role in the persistent modulation of the epithelial innate immune response towards microbes in the mature lung.

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Effect of ozone on leukocyte function in exposed human subjects

Cited by 17 publications

References 17 publications

Ambient ozone and pulmonary innate immunity

Ambient ozone and pulmonary innate immunity

Ozone and Pulmonary Innate Immunity

Early Life Ozone Exposure Results in Dysregulated Innate Immune Function and Altered microRNA Expression in Airway Epithelium

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