The effect of ozone exposure on the release of eicosanoids in guinea‐pig BAL fluid in relation to cellular damage and inflammation

Hoof, H.J.M. van; Zijlstra, Freek J.; Voss, Hans–Peter; Garrelds, Ingrid M.; Dormans, J. A. M. A.; Bree, L. van; Bast, Aalt

doi:10.1080/09629359791497

Cited by 6 publications

(4 citation statements)

References 36 publications

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“…Perhaps because of interspecies differences in epithelial cell composition, analytical approaches, lipid membrane resident arachidonic acid (AA) stores, and COX-1/2 profiles, the effects of ozone in modulating prostanoid secretion remain contradictory (22,60). We investigated the effects of ozone in modulating prostanoids in basal and TNF-treated cultures.…”

Section: Ozone Markedly Increases Pge 2 Levels In Tnftreated Nhbe-asmmentioning

confidence: 98%

Ozone modulates IL-6 secretion in human airway epithelial and smooth muscle cells

Damera¹,

Zhao²,

Wang³

et al. 2009

American Journal of Physiology-Lung Cellular and Molecular Phys

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Although ozone enhances leukocyte function and recruitment in airways, the direct effect of ozone in modulating structural cell-derived inflammatory mediators remains unknown. Using a coculture model comprised of differentiated human airway epithelial cells (NHBE) and smooth muscle cells (ASM), we postulate that ozone regulates IL-6 secretion in basal and cytokine-primed structural cells. Air-liquid interface (ALI) cultures of NHBE cells underwent differentiation as determined by mucin secretion, transepithelial electrical resistance (TEER), and ultrastructure parameters. Whereas TNF enhanced basal secretion of IL-6 (57 +/- 3%), ozone exposure at 0.6 ppm for 6 h augmented IL-6 levels in basal (41 +/- 3%) and TNF- (50 +/- 5%) primed cocultures compared with that derived from NHBE or ASM monolayers alone. Levels of PGE(2), 6-keto-PGF(1alpha), PGF(2alpha), and thromboxane B(2) (TxB(2)) levels in basal and TNF-primed cocultures revealed that ozone selectively enhanced PGE(2) production in TNF- (6 +/- 3-fold) primed cocultures, with little effect (P > 0.05) on diluent-treated cultures. In accordance with ozone-induced increases in PGE(2) levels, cyclooxygenase inhibition with indomethacin partially abolished IL-6 secretion. Surprisingly, indomethacin had little effect on constitutive secretion of IL-6 in cocultures, whereas indomethacin completely restored ozone-mediated TEER reduction in TNF-primed cocultures. Collectively, our data for the first time suggest a dual role of ozone in modulating IL-6 secretion and TEER outcomes in a PGE(2)-dependent (in presence of TNF stimulus) and -independent manner (in absence of cytokine stimulus).

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Section: Ozone Markedly Increases Pge 2 Levels In Tnftreated Nhbe-asmmentioning

confidence: 98%

Ozone modulates IL-6 secretion in human airway epithelial and smooth muscle cells

Damera¹,

Zhao²,

Wang³

et al. 2009

American Journal of Physiology-Lung Cellular and Molecular Phys

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“…However, there are no significant differences between ozone therapy and low-level laser therapy 25) . [26][27] nor by ozonated autohaemotherapy for technical difficulties. however the colorectal tract, although somewhat empirical, is easy, nontoxic and has the rationale that ozonated products reach the liver via portal circulation -28) .…”

Section: Discussionmentioning

confidence: 99%

Effects of Gaseous Ozone Treatment on Bone Regeneration in Femoral Defect Model in Rats

Duman

Davul

Gökçe

et al. 2017

J. Hard Tissue Biology.

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The purpose of this study was to investigate the effect of ozone therapy in rat femoral fractures.Following the right open femoral fractures and intramedullary Kirschner wire fixation of the fracture in 60 male Wistar albino rats, the animals were divided into two groups of 30 animals each: ozone therapy group (n=30); non-treatment (control) group (n=30). Ozone was administered by rectal insufflation. After the rats were sacrified fracture healing was assessed by biomechanical and histopathologic evaluation. Histological and mechanical findings indicated that the ozone therapy had a significantly positive effect on bone healing.

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“…Previously, studies have reported that a wide variety of eicosanoids (PGE 2 , PGD 2 , PGF 2α , TXB 2 , LTB 4 , HETEs, and LTC 4 ) is increased in the bronchoalveolar lavage fluid following ozone exposure. − Reports also have been published on the production of eicosanoids (TXB 2 , PGE 2 , cysteinyl leukotrienes, and LTB 4 ) upon the exposure of airway and tracheal epithelial cells to ozone. , Other studies have shown that ozone exposure increases eicosanoid production upon activation of the eicosanoid pathway by calcium ionophore in AM and airway segments. , More relevant to the work reported herein, the effects of ozonized lipid products on activation of the eicosanoid pathway have been examined to some extent. Arachidonic acid release by BEAS-2B cells and PGE 2 production in primary human bronchial epithelial cells were observed in the presence of the ozonized lipid product, 16:0/9al-PC. , Additionally, the ozonolysis products of membrane fatty acids, unsaturated C3-, C6-, and C9-aldehydes released from phospholipids upon ozone exposure, induced the release of AA and the subsequent formation of PGE 2 , PGF 2α , and 15-HETE in human airway epithelial cells .…”

Section: Discussionmentioning

confidence: 99%

Phospholipid Ozonation Products Activate the 5-Lipoxygenase Pathway in Macrophages

Berry

Murphy

2016

Chem. Res. Toxicol.

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Ozone is a highly reactive environmental toxicant that can react with the double bonds of lipids in pulmonary surfactant. This study was undertaken to investigate the proinflammatory properties of the major lipid-ozone product in pulmonary surfactant, 1-palmitoyl-2-(9’-oxo-nonanoyl)-glycerophosphocholine (16:0/9al-PC), with respect to eicosanoid production. A dose-dependent increase in the formation of 5-lipoxygenase (5-LO) products was observed in murine resident peritoneal macrophages (RPM) and alveolar macrophages (AM) upon treatment with 16:0/9al-PC. In contrast, the production of cyclooxygenase (COX) derived eicosanoids did not change from basal levels in the presence of 16:0/9al-PC. When 16:0/9al-PC and the TLR2 ligand, zymosan, were added to RPM or AM, an enhancement of 5-LO product formation along with a concomitant decrease in COX product formation was observed. Neither intracellular calcium levels or arachidonic acid release were influenced by the addition of 16:0/9al-PC to RPM. Results from mitogen-activated protein kinase (MAPK) inhibitor studies and direct measurement of phosphorylation of MAPKs revealed that 16:0/9al-PC activates the p38 MAPK pathway in RPM, which results in activation of 5-LO. Our results indicate that 16:0/9al-PC has a profound effect on the eicosanoid pathway, which may have implications in inflammatory pulmonary disease states where eicosanoids have been shown to play a role.

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The effect of ozone exposure on the release of eicosanoids in guinea‐pig BAL fluid in relation to cellular damage and inflammation

Cited by 6 publications

References 36 publications

Ozone modulates IL-6 secretion in human airway epithelial and smooth muscle cells

Ozone modulates IL-6 secretion in human airway epithelial and smooth muscle cells

Effects of Gaseous Ozone Treatment on Bone Regeneration in Femoral Defect Model in Rats

Phospholipid Ozonation Products Activate the 5-Lipoxygenase Pathway in Macrophages

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