Effects of hydrogen peroxide on mucociliary transport in human airway epithelial cells

Honda, Akira; Murayama, Rumiko; Matsuda, Yasutaka; Tsuji, Kenshi; Sawahara, Takahiro; Fukushima, Wataru; Hayashi, Tomohiro; Shimada, Akinori; Takano, Hirohisa

doi:10.3109/15376516.2013.876136

Cited by 6 publications

(11 citation statements)

References 35 publications

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“…Recently, polarized human airway epithelial cells in air-liquid interface (ALI) cultures are developing as a respiratory model, they enable mucociliary transport. 46,47 The mucus on the apical side of airway epithelial cells protects from environmental stimuli. These characteristics may have impacts on metal toxicity as involves the production of ROS.…”

Section: Discussionmentioning

confidence: 99%

Effects of Air Pollution-Related Heavy Metals on the Viability and Inflammatory Responses of Human Airway Epithelial Cells

et al. 2015

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Various metals produced from human activity are ubiquitously detected in ambient air. The metals may lead to induction and/or exacerbation of respiratory diseases, but the significant metals and factors contributing to such diseases have not been identified. To compare the effects of each metal and different oxidation states of metals on human airway, we examined the viability and production of interleukin (IL)-6 and IL-8 using BEAS-2B cell line, derived from human airway epithelial cells. Airway epithelial cells were exposed to Mn(2+), V(4+), V(5+), Cr(3+), Cr(6+), Zn(2+), Ni(2+), and Pb(2+) at a concentration of 0.5, 5, 50, or 500 μmol/L for 24 hours. Mn and V decreased the cell viability in a concentration-dependent manner, and V(5+) tended to have a greater effect than V(4+). The Cr decreased the cell viability, and (Cr(+6)) at concentrations of 50 and 500 μmol/L was more toxic than (Cr(+3)). Zn at a concentration of 500 μmol/L greatly decreased the cell viability, whereas Ni at the same concentration increased it. Pb produced fewer changes. Mn and Ni at a concentration of 500 μmol/L induced the significant production of IL-6 and IL-8. However, most of the metals including (V(+4), V(+5)), (Cr(+3), Cr(+6)), Zn, and Pb inhibited the production of both IL-6 and IL-8. The present results indicate that various heavy metals have different effects on toxicity and the proinflammatory responses of airway epithelial cells, and those influences also depend on the oxidation states of the metals.

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Section: Discussionmentioning

confidence: 99%

Effects of Air Pollution-Related Heavy Metals on the Viability and Inflammatory Responses of Human Airway Epithelial Cells

et al. 2015

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“…The polypeptide pneumolysin is a pore-forming cytolytic toxin that can slow CBF and cause cellular damage ( 44 , 178 ). H 2 O 2 is a potent oxidant that also slows CBF ( 45 , 77 ).…”

Section: Bacterial Infectionsmentioning

confidence: 99%

First contact: the role of respiratory cilia in host-pathogen interactions in the airways

Kuek

Lee

2020

American Journal of Physiology-Lung Cellular and Molecular Phys

117

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Respiratory cilia are the driving force of the mucociliary escalator, working in conjunction with secreted airway mucus to clear inhaled debris and pathogens from the conducting airways. Respiratory cilia are also one of the first contact points between host and inhaled pathogens. Impaired ciliary function is a common pathological feature in patients with chronic airway diseases, increasing susceptibility to respiratory infections. Common respiratory pathogens including viruses, bacteria and fungi have been shown to target cilia and/or ciliated airway epithelial cells, resulting in a disruption of mucociliary clearance that may facilitate host infection. Despite being an integral component of airway innate immunity, the role of respiratory cilia and their clinical significance during airway infections is still poorly understood. This review examines the expression, structure, and function of respiratory cilia during pathogenic infection of the airways. This review also discusses specific known points of interaction of bacteria, fungi, and viruses with respiratory cilia function. The emerging biological functions of motile cilia relating to intracellular signaling and their potential immuno-regulatory roles during infection will also be discussed.

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“…Direct exposure to X/XO or H 2 O 2 results in ciliary slowing [[83], [84], [85], [86]]. Interestingly, slowing by X/XO further declines upon preincubation with SOD.…”

Section: Cilia-localized Redox-sensitive Thiol-regulatory Proteinsmentioning

confidence: 99%

Redox regulation of motile cilia in airway disease

Price

Sisson

2019

Redox Biology

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Motile cilia on airway cells are necessary for clearance of mucus-trapped particles out of the lung. Ciliated airway epithelial cells are uniquely exposed to oxidants through trapping of particles, debris and pathogens in mucus and the direct exposure to inhaled oxidant gases. Dynein ATPases, the motors driving ciliary motility, are sensitive to the local redox environment within each cilium. Several redox-sensitive cilia-localized proteins modulate dynein activity and include Protein Kinase A, Protein Kinase C, and Protein Phosphatase 1. Moreover, cilia are rich in known redox regulatory proteins and thioredoxin domain-containing proteins that are critical in maintaining a balanced redox environment. Importantly, a nonsense mutation in TXNDC3, which contains a thioredoxin motif, has recently been identified as disease-causing in Primary Ciliary Dyskinesia, a hereditary motile cilia disease resulting in impaired mucociliary clearance. Here we review current understanding of the role(s) oxidant species play in modifying airway ciliary function. We focus on oxidants generated in the airways, cilia redox targets that modulate ciliary beating and imbalances in redox state that impact health and disease. Finally, we review disease models such as smoking, asthma, alcohol drinking, and infections as well as the direct application of oxidants that implicate redox balance as a modulator of cilia motility.

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Effects of hydrogen peroxide on mucociliary transport in human airway epithelial cells

Cited by 6 publications

References 35 publications

Effects of Air Pollution-Related Heavy Metals on the Viability and Inflammatory Responses of Human Airway Epithelial Cells

Effects of Air Pollution-Related Heavy Metals on the Viability and Inflammatory Responses of Human Airway Epithelial Cells

First contact: the role of respiratory cilia in host-pathogen interactions in the airways

Redox regulation of motile cilia in airway disease

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