Alterations in the pulmonary histoarchitecture of neonatal mice exposed to hyperoxia

Reis, Renata Brito dos; Nagato, Akinori Cardozo; Nardeli, Clarissa Rodrigues; Matias, Isadora C.P.; Lima, Wanderson Geraldo de; Bezerra, Frank Silva

doi:10.1016/j.jped.2012.10.003

Cited by 6 publications

(6 citation statements)

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“…We speculate that the low expression of Nrf2 reveals a relationship between reductions to the neutrophil population by oxidative damage (with reduced total numbers of cells present) because oxidative damage with increased levels of malondialdehyde was observed only in the OVA + O 2 group. These findings are consistent with previous studies conducted by our group that has shown the potential of the hyperoxia to reduce the population of inflammatory cells 102, as well as inducing apoptosis mainly through oxidative stress 103.…”

Section: Discussionsupporting

confidence: 93%

“…In the absence of this activation, there is an increased severity of asthma and inflammation of the airways in mice model [101]. Besides, Potteti et al demonstrated that chronic hyperoxia does not involve the Nrf2 signaling pathways [102]. In the present study, the highest levels of Nrf2 correlated with hyperoxia and whith the greatest numbers of neutrophils.…”

Section: Groupssupporting

confidence: 50%

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Hyperoxia promotes polarization of the immune response in ovalbumin‐induced airway inflammation, leading to a TH₁₇ cell phenotype

Nagato

Bezerra²,

Talvani

et al. 2015

Immunity Inflam & Disease

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Previous studies have demonstrated that hyperoxia-induced stress and oxidative damage to the lungs of mice lead to an increase in IL-6, TNF-α, and TGF-β expression. Together, IL-6 and TGF-β have been known to direct T cell differentiation toward the TH17 phenotype. In the current study, we tested the hypothesis that hyperoxia promotes the polarization of T cells to the TH17 cell phenotype in response to ovalbumin-induced acute airway inflammation. Airway inflammation was induced in female BALB/c mice by intraperitoneal sensitization and intranasal introduction of ovalbumin, followed by challenge methacholine. After the methacholine challenge, animals were exposed to hyperoxic conditions in an inhalation chamber for 24 h. The controls were subjected to normoxia or aluminum hydroxide dissolved in phosphate buffered saline. After 24 h of hyperoxia, the number of macrophages and lymphocytes decreased in animals with ovalbumin-induced airway inflammation, whereas the number of neutrophils increased after ovalbumin-induced airway inflammation. The results showed that expression of Nrf2, iNOS, T-bet and IL-17 increased after 24 of hyperoxia in both alveolar macrophages and in lung epithelial cells, compared with both animals that remained in room air, and animals with ovalbumin-induced airway inflammation. Hyperoxia alone without the induction of airway inflammation lead to increased levels of TNF-α and CCL5, whereas hyperoxia after inflammation lead to decreased CCL2 levels. Histological evidence of extravasation of inflammatory cells into the perivascular and peribronchial regions of the lungs was observed after pulmonary inflammation and hyperoxia. Hyperoxia promotes polarization of the immune response toward the TH17 phenotype, resulting in tissue damage associated with oxidative stress, and the migration of neutrophils to the lung and airways. Elucidating the effect of hyperoxia on ovalbumin-induced acute airway inflammation is relevant to preventing or treating asthmatic patients that require oxygen supplementation to reverse the hypoxemia.

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Section: Discussionsupporting

confidence: 93%

Section: Groupssupporting

confidence: 50%

Hyperoxia promotes polarization of the immune response in ovalbumin‐induced airway inflammation, leading to a TH₁₇ cell phenotype

Nagato

Bezerra²,

Talvani

et al. 2015

Immunity Inflam & Disease

Self Cite

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“…The number of macrophages, the surface volume of gas exchange and the volume of lung parenchyma are decreased, while the area of atelectasis is increased (17). Hyperoxia induces the production of ROS, which subsequently activates several downstream pathways, represented by the MAPK and NF-κB cascades (4,18).…”

Section: Discussionmentioning

confidence: 99%

Vitamin D attenuates hyperoxia-induced lung injury through downregulation of Toll-like receptor 4

Yao

Shi

Zhao

et al. 2017

International Journal of Molecular Medicine

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With considerable morbidity and mortality, bron-chopulmonary dysplasia (BPD) is a focus of attention in neonatology. Hyperoxia-induced lung injury has long been used as a model of BPD. Among all the signaling pathways involved, Toll-like receptor 4 (TLR4) has been demonstrated to play an important role, and is known to be regulated by vitamin D. This study aimed at elucidating the effect of vitamin D on hyperoxia-induced lung injury and the role of TLR4 in the process. Vitamin D was administered to hyperoxia-treated neonatal rats to investigate changes in the morphology of lungs and expression of pro-inflammatory cytokines, apoptotic proteins and TLR4. Vitamin D attenuated hyperoxia-induced lung injury by protecting the integrity of the lung structure, decreasing extracellular matrix deposition and inhibiting inflammation. The upregulation of TLR4 by hyperoxia was ameliorated by vitamin D and apoptosis was reduced. Vitamin D administration antagonized the activation of TLR4 and therefore alleviated inflammation, reduced apoptosis and preserved lung structure.

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“…The increase in the level of MDA was identified in both the diabetes-induced hyperoxia group and in the control hyperoxia group. Reis et al 25 observed that hyperoxia (100% oxygen for 24 h) induced a decrease in the number of alveolar macrophages in the alveolar lumen, modified pulmonary histoarchitecture and raised the amount of red blood cells in the air spaces of the experimental group hyperoxia in relation to the control group. In the pulmonary histopathologic analysis of the hyperoxic control group, it was also possible to identify the presence of extensive abnormalities in lung architecture and inflammation in comparison with the other groups of control animals (p=0.014 and p=0.012, respectively; data not shown) (Figure 3).…”

Section: ■ Discussionmentioning

confidence: 99%

Pulmonary oxidative stress in diabetic rats exposed to hyperoxia

Paiva

Silva²,

Souza³

et al. 2017

Acta Cir. Bras.

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Pulmonary oxidative stress in diabetic rats exposed to hyperoxia 1 1-Experimental SurgeryActa Cir Bras. 2017;32(7):503-514 AbstractPurpose: To evaluate the pulmonary oxidative stress in diabetic rats exposed to hyperoxia for 90 minutes. Methods: Forty male Wistar rats were divided into four groups, each one containing 10 animals, according to the oxygen concentration to which they were exposed: 21%, 50%, 75% and 100% (hyperoxia). In each group five animals were randomly induced to diabetes by means of at a dose of 55 mg/kg of streptozotocin (STZ). Results: Seventy two hours after diabetes induction, a significant difference was seen in blood glucose in the experimental groups in comparison with the control. In the experimental groups a significant difference was observed in the concentration of malondialdehyde (MDA) in lung tissue and blood plasma (p<0.05), except the 50% group. In the control group, significant differences in the MDA concentration in plasma and lung tissue were also observed (p<0.05), except the 75% group. The MDA concentration in lung tissue in comparison with the diabetic and non-diabetic groups showed a significant difference in the 21% group; however, no difference was seen in the 75 and 100% groups. Conclusion:In diabetic animals high oxygen concentrations (75 and 100%) do not appear to exert deleterious effects on lipid peroxidation in lung tissue.

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Alterations in the pulmonary histoarchitecture of neonatal mice exposed to hyperoxia

Abstract: The present results indicate that hyperoxia caused alterations in lung histoarchitecture, increasing areas of atelectasis and diffuse alveolar hemorrhage.

Cited by 6 publications

References 27 publications

Hyperoxia promotes polarization of the immune response in ovalbumin‐induced airway inflammation, leading to a TH₁₇ cell phenotype

Hyperoxia promotes polarization of the immune response in ovalbumin‐induced airway inflammation, leading to a TH₁₇ cell phenotype

Vitamin D attenuates hyperoxia-induced lung injury through downregulation of Toll-like receptor 4

Pulmonary oxidative stress in diabetic rats exposed to hyperoxia

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Alterations in the pulmonary histoarchitecture of neonatal mice exposed to hyperoxia

Abstract: The present results indicate that hyperoxia caused alterations in lung histoarchitecture, increasing areas of atelectasis and diffuse alveolar hemorrhage.

Cited by 6 publications

References 27 publications

Hyperoxia promotes polarization of the immune response in ovalbumin‐induced airway inflammation, leading to a TH17 cell phenotype

Hyperoxia promotes polarization of the immune response in ovalbumin‐induced airway inflammation, leading to a TH17 cell phenotype

Vitamin D attenuates hyperoxia-induced lung injury through downregulation of Toll-like receptor 4

Pulmonary oxidative stress in diabetic rats exposed to hyperoxia

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Resources

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Hyperoxia promotes polarization of the immune response in ovalbumin‐induced airway inflammation, leading to a TH₁₇ cell phenotype

Hyperoxia promotes polarization of the immune response in ovalbumin‐induced airway inflammation, leading to a TH₁₇ cell phenotype