Ozone-induced Inflammation in the Lower Airways of Human Subjects

Koren, Hillel S.; Devlin, Robert B.; Graham, Delores E.; Mann, Richard H.; McGee, Maria P.; Horstman, Donald H.; Kozumbo, Walter J.; Becker, Susanne; House, Dennis E.; McDonnell, William F.; Bromberg, Philip A.

doi:10.1164/ajrccm/139.2.407

Cited by 475 publications

(230 citation statements)

References 9 publications

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“…Acute ozone inhalation in humans has been shown to result in the elevation in BAL fluid of several macromolecules normally restricted to the vascular compartment that may contribute to cellular injury and necrosis, including complement 3a (39). Interestingly, Park and colleagues (40) have recently demonstrated that either depleting and/or antagonizing complement in mice significantly reduces ozoneinduced airway hyperresponsiveness.…”

Section: Discussionmentioning

confidence: 99%

Activation of Neurokinin-1 Receptors during Ozone Inhalation Contributes to Epithelial Injury and Repair

Oslund¹,

Hyde

Putney³

et al. 2008

Am J Respir Cell Mol Biol

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We investigated the importance of neurokinin (NK)-1 receptors in epithelial injury and repair and neutrophil function. Conscious Wistar rats were exposed to 1 ppm ozone or filtered air for 8 hours, followed by an 8-hour postexposure period. Before exposure, we administered either the NK-1 receptor antagonist, SR140333, or saline as a control. Ethidium homodimer was instilled into lungs as a marker of necrotic airway epithelial cells. After fixation, whole mounts of airway dissected lung lobes were immunostained for 5-bromo-29-deoxyuridine, a marker of epithelial proliferation. Both ethidium homodimer and 5-bromo-29-deoxyuridine-positive epithelial cells were quantified in specific airway generations. Rats treated with the NK-1 receptor antagonist had significantly reduced epithelial injury and epithelial proliferation compared with control rats. Sections of terminal bronchioles showed no significant difference in the number of neutrophils in airways between groups. In addition, staining ozone-exposed lung sections for active caspase 3 showed no apoptotic cells, but ethidium-positive cells colocalized with the orphan nuclear receptor, Nur77, a marker of nonapoptotic, programmed cell death mediated by the NK-1 receptor. An immortalized human airway epithelial cell line, human bronchial epithelial-1, showed no significant difference in the number of oxidant stresspositive cells during exposure to hydrogen peroxide and a range of SR140333 doses, demonstrating no antioxidant effect of the receptor antagonist. We conclude that activation of the NK-1 receptor during acute ozone inhalation contributes to epithelial injury and subsequent epithelial proliferation, a critical component of repair, but does not influence neutrophil emigration into airways.

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Section: Discussionmentioning

confidence: 99%

Activation of Neurokinin-1 Receptors during Ozone Inhalation Contributes to Epithelial Injury and Repair

Oslund¹,

Hyde

Putney³

et al. 2008

Am J Respir Cell Mol Biol

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“…A complex sequence of events is involved in the inflammatory process, each step of which can have detrimental effects on the lung and its host defense functions (62 (64). Mineral dust particles such as quartz, asbestos, and silica induce pulmonary inflammation and activate immune cells to produce ROS.…”

Section: Airway Inflammationmentioning

confidence: 99%

Interactions of oxygen radicals with airway epithelium.

Wright

Cohn

et al. 1994

Environ Health Perspect

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Reactive oxygen species (ROS) have been implicated in the pathogenesis of numerous disease processes. Epithelial cells lining the respiratory airways are uniquely vulnerable regarding potential for oxidative damage due to their potential for exposure to both endogenous (e.g., mitochondrial respiration, phagocytic respiratory burst, cellular oxidases) and exogenous (e.g., air pollutants, xenobiotics, catalase negative organisms) oxidants. Airway epithelial cells use several nonenzymatic and enzymatic antioxidant mechanisms to protect against oxidative insult. Nonenzymatic defenses include certain vitamins and low molecular weight compounds such as thiols. The enzymes superoxide dismutase, catalase, and glutatione peroxidase are major sources of antioxidant protection. Other materials associated with airway epithelium such as mucus, epithelial lining fluid, and even the basement membrane/extracellular matrix may have protective actions as well. When the normal balance between oxidants and antioxidants is upset, oxidant stress ensues and subsequent epithelial cell alterations or damage may be a critical component in the pathogenesis of several respiratory diseases. Oxidant stress may profoundly alter lung physiology including pulmonary function (e.g., forced expiratory volumes, flow rates, and maximal inspiratory capacity), mucociliary activity, and airway reactivity. ROS may induce airway inflammation; the inflammatory process may serve as an additional source of ROS in airways and provoke the pathophysiologic responses described. On a more fundamental level, cellular mechanisms in the pathogenesis of ROS may involve activation of intracellular signaling enzymes including phospholipases and protein kinases stimulating the release of inflammatory lipids and cytokines. Respiratory epithelium may be intimately involved in defense against, and pathophysiologic changes invoked by, ROS. -Environ Health Perspect 1 02(Suppl 1 0): 85-90 (1994)

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“…In addition, increased exposure to O3 has been linked to increased incidences of diabetes mellitus type I [18] . Moreover, inflammation induced by exposure to O3 in humans has been reported [19] . Although most of the damage by O3 occurs in the lungs due to inhalation, it has been shown to cause oxidation or peroxidation of biomolecules such as DNA, proteins, lipids, leading to a vicious cycle of chronic inflammation and oxidative stress commonly seen in diabetes [13] .…”

Section: Climate Change and Diabetes Mellitusmentioning

confidence: 99%

Untitled

2017

RJLBPCS

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ABSTRACT:Climate change through its effect on weather, anthropogenic emissions, distribution and types of air irritants is expected to increase exposure to air pollutants such as Carbon monoxide, Sulphur dioxide and Ozone. In addition, climate change is proposed to increase the risk of cardiovascular diseases (CVDs) directly through air pollution, extreme temperatures and indirectly via changes in diets. This is projected to increase morbidity and mortality from NCDs tremendously in low and middle income Countries. The purpose of this study was to review existing literature on impact of climate change on NCDs, identify gaps in existing studies, to stimulate further research interest in the field. This was a literature survey in which PubMed, ScienceDirect and Google scholar databases were searched using keywords; Climate change, Mitigation, Health, Non-Communicable Diseases, Diabetes, Cancers and Cardiovascular diseases (CVDs). Little research has been done on climate change and NCDs; therefore, data is lacking or inadequate if at all. Out of a total of 3,204,565 hits only 65,815 articles were specific to climate change and health, out of which only 35 were directly relevant to the survey. Results from this review indicated that climate change has led to increased or extreme temperatures, which can be directly or indirectly attributed to the increased NCDs prevalence. Furthermore, inhalation and or exposure to acute ozone exposure leads to oxidative stress, inflammation, ultimately leading to diabetes mellitus I & II, CVDs and cancers.Oxidative stress is also associated with DNA damage, endothelium dysfunction, damage to blood cells leading to high blood pressure, arteriosclerosis, myocardial infarction among other cardiovascular conditions. However, further research is required to strengthen this hypothesis. This information will help in attainment of sustainable development goal (SDG) number 3 on ensuring health for all, promotion of wellbeing for all at all ages and number 13 on combating climate

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Ozone-induced Inflammation in the Lower Airways of Human Subjects

Cited by 475 publications

References 9 publications

Activation of Neurokinin-1 Receptors during Ozone Inhalation Contributes to Epithelial Injury and Repair

Activation of Neurokinin-1 Receptors during Ozone Inhalation Contributes to Epithelial Injury and Repair

Interactions of oxygen radicals with airway epithelium.

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