Effects of Ozone Exposure on Nuclear Factor-kappaB Activation and Tumor Necrosis Factor-alpha Expression in Human Nasal Epithelial Cells

Nichols, Brenda G.

doi:10.1093/toxsci/60.2.356

Cited by 49 publications

(25 citation statements)

References 27 publications

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“…Lack of JNK (Jnk1 or Jnk2) inhibited neutrophilic influx and chemokine expression after mechanical ventilation (40). These two redox-sensitive transcription factor signaling pathways have also been shown to be induced by O 3 in airway cells and tissues (41)(42)(43)(44). More recently, Fakhrzadeh and colleagues (45) determined a functional role of pulmonary NF-B in the increase of inducible nitric oxide synthase and TNF-␣ levels by inhaled O 3 .…”

Section: Discussionmentioning

confidence: 99%

Signal Transduction Pathways of Tumor Necrosis Factor–mediated Lung Injury Induced by Ozone in Mice

Cho¹,

Morgan²,

Bauer³

et al. 2007

Am J Respir Crit Care Med

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Section: Discussionmentioning

confidence: 99%

Signal Transduction Pathways of Tumor Necrosis Factor–mediated Lung Injury Induced by Ozone in Mice

Cho¹,

Morgan²,

Bauer³

et al. 2007

Am J Respir Crit Care Med

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“…Isolated human alveolar macrophages and THP-1 cells derived from monocytic leukemic cells also fail to secrete chemokines in response to ozone (11,12). However, others have shown a modest secretion of chemokines and cytokines by epithelial cells in response to ozone in A549 cells, BEAS-2B cells, and human nasal epithelial cells (12)(13)(14)(15). Hence, there appears to be a discrepancy between the limited chemokine production by direct ozone exposure in vitro and the obvious neutrophil influx in vivo (16).…”

mentioning

confidence: 99%

Ozone Exposure of Macrophages Induces an Alveolar Epithelial Chemokine Response through IL-1α

Manzer

Dinarello²,

McConville³

et al. 2008

Am J Respir Cell Mol Biol

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Ozone is known to produce an acute influx of neutrophils, and alveolar epithelial cells can secrete chemokines and modulate inflammatory processes. However, direct exposure of alveolar epithelial cells and macrophages to ozone (O 3 ) produces little chemokine response. To determine if cell-cell interactions might be responsible, we investigated the effect of alveolar macrophage-conditioned media after ozone exposure (MO 3 CM) on alveolar epithelial cell chemokine production. Serum-free media were conditioned by exposing a rat alveolar macrophage cell line NR8383 to ozone for 1 hour. Ozone stimulated secretion of IL-1a, IL-1b, and IL-18 from NR8383 cells, but there was no secretion of chemokines or TNF-a. Freshly isolated type II cells were cultured, so as to express the biological markers of type I cells, and these cells are referred to as type I-like cells. Type I-like cells were exposed to diluted MO 3 CM for 24 hours, and this conditioned medium stimulated secretion of cytokine-induced neutrophil chemattractant-1 (CXCL1) and monocyte chemoattractant protein-1 (CCL2). Secretion of these chemokines was inhibited by the IL-1 receptor antagonist. Although both recombinant IL-1a and IL-1b stimulated alveolar epithelial cells to secrete chemokines, recombinant IL-1a was 100-fold more potent than IL-1b. Furthermore, neutralizing anti-rat IL-1a antibodies inhibited the secretion of chemokines by alveolar epithelial cells, whereas neutralizing anti-rat IL-1b antibodies had no effect. These observations indicate that secretion of IL-1a from macrophages stimulates alveolar epithelial cells to secrete chemokines that can elicit an inflammatory response.

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“…The alveolar epithelial cell, a rich source of proinflammatory cytokines, may be one of the contributors to this O 3 -induced inflammation (2,47). Recent work done with human nasal epithelial cells shows that O 3 exposure resulted in NF-B activation and increased production of TNF-␣ by these cells (55). Thus the same may be true for the alveolar epithelial cells (8).…”

Section: Discussionmentioning

confidence: 99%

Modulatory effects of ozone on THP-1 cells in response to SP-A stimulation

Janic

Umstead

Phelps

et al. 2005

American Journal of Physiology-Lung Cellular and Molecular Phys

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, a major component of air pollution and a strong oxidizing agent, can lead to lung injury associated with edema, inflammation, and epithelial cell damage. The effects of O 3 on pulmonary immune cells have been studied in various in vivo and in vitro systems. We have shown previously that O 3 exposure of surfactant protein (SP)-A decreases its ability to modulate proinflammatory cytokine production by cells of monocyte/macrophage lineage (THP-1 cells). In this report, we exposed THP-1 cells and/or native SP-A obtained from bronchoalveolar lavage of patients with alveolar proteinosis to O 3 and studied cytokine production and NF-B signaling. The results showed 1) exposure of THP-1 cells to O 3 significantly decreased their ability to express TNF-␣ in response to SP-A; TNF-␣ production, under these conditions, was still significantly higher than basal (unstimulated) levels in filtered air-exposed THP-1 cells; 2) exposure of both THP-1 cells and SP-A to O 3 did not result in any significant differences in TNF-␣ expression compared with basal levels; 3) O 3 exposure of SP-A resulted in a decreased ability of SP-A to activate the NF-B pathway, as assessed by the lack of significant increase and decrease of the nuclear p65 subunit of NF-B and cytoplasmic I B␣, respectively; and 4) O 3 exposure of THP-1 cells resulted in a decrease in SP-A-mediated THP-1 cell responsiveness, which did not seem to be mediated via the classic NF-B pathway. These findings indicate that O 3 exposure may mediate its effect on macrophage function both directly and indirectly (via SP-A oxidation) and by involving different mechanisms.inflammation; tumor necrosis factor-␣; nuclear factor-B; I B␣; surfactant protein A OZONE (O 3 ) IS A MAJOR COMPONENT of photochemical air pollution. Approximately 113 million people live in areas with O 3 levels above the National Ambient Air Quality (NAAQ) standards for the daily exposure limit, noted as a maximum of 0.12 ppm for 1 h or 0.08 ppm cumulative for 8 consecutive hours (1). O 3 is a strong oxidizing agent that can be rapidly converted into a number of reactive oxygen species (ROS). O 3 exposure has been associated with impaired lung function (53) and with the majority of pathological changes localized in the lower airways. Due to its very low water solubility, O 3 cannot effectively penetrate through the thick epithelial lining fluid in the upper airways. However, the thinner lining in the lower airways allows O 3 to interact with various elements of the fluid and the underlying cells.O 3 and other oxidants exhibit their toxicity by reacting with cell proteins and lipids. This interaction often results in edema, inflammation, and epithelial cell damage causing lung injury and surfactant derangement (66, 67). Furthermore, both morphological (6, 7) and biochemical (26, 27) changes in surfactant are observed following O 3 exposure. An extensive body of work has been generated by various groups to support the hypothesis that O 3 -induced changes lead to a compromised immune response in the lung. However,...

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Effects of Ozone Exposure on Nuclear Factor-kappaB Activation and Tumor Necrosis Factor-alpha Expression in Human Nasal Epithelial Cells

Cited by 49 publications

References 27 publications

Signal Transduction Pathways of Tumor Necrosis Factor–mediated Lung Injury Induced by Ozone in Mice

Signal Transduction Pathways of Tumor Necrosis Factor–mediated Lung Injury Induced by Ozone in Mice

Ozone Exposure of Macrophages Induces an Alveolar Epithelial Chemokine Response through IL-1α

Modulatory effects of ozone on THP-1 cells in response to SP-A stimulation

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