Animal models of smoke inhalation induced injuries

Moochhala, Shabbir

doi:10.2741/3554

Cited by 6 publications

(1 citation statement)

References 85 publications

(48 reference statements)

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“…According to a follow-up investigation, the chest computed tomography (CT) examination of firefighters with high-intensity World Trade Center (WTC) exposure showed that they were with bronchial wall thickening, emphysema and respiratory symptoms (Liu et al, 2019b). Studies have demonstrated that the stimulation of the respiratory system by a range of harmful chemicals such as carbon monoxide, cyanide and malondialdehyde, can lead to dyspnea and even suffocation, which is linked to oxidative stress/ antioxidant stress imbalance and inflammatory cascades (David et al, 2009). In this paper, it was found that rhKGF-2 exerts its anti-inflammatory and antioxidant effects, thus reducing SILI through both in-vitro and in-vivo experiments.…”

Section: Discussionmentioning

confidence: 82%

rhKGF-2 Attenuates Smoke Inhalation Lung Injury of Rats via Activating PI3K/Akt/Nrf2 and Repressing FoxO1-NLRP3 Inflammasome

Jiang

Guo

et al. 2021

Front. Pharmacol.

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Smoke inhalation injury is an acute pathological change caused by thermal stimulation or toxic substance absorption through respiratory epithelial cells. This study aims to probe the protective effect and mechanism of recombinant human keratinocyte growth factor 2 (rhKGF-2) against smoke inhalation-induced lung injury (SILI) in rats. The SILI was induced in rats using a smoke exposure model, which were then treated with rhKGF-2. The rat blood was collected for blood-gas analysis, and the levels of inflammatory factors and oxidative stress markers in the plasma were measured. The rat lung tissues were collected. The pathological changes and cell apoptosis were determined by hematoxylin-eosin (HE) staining and TdT-mediated dUTP nick end labeling (TUNEL) assay, and the PI3K/Akt/Nrf2/HO-1/NQO1, and FoxO1-NLRP3 inflammasome expression were verified by western blot (WB). Both of the human alveolar epithelial cell (HPAEpiC) and primary rat alveolar epithelial cell were exposed to lipopolysaccharide (LPS) for making in-vitro alveolar epithelial cell injury model. After treatment with rhKGF-2, GSK2126458 (PI3K inhibitor) and AS1842856 (FoxO1 inhibitor), the cell viability, apoptosis, inflammation, oxidative stress, reactive oxygen species (ROS), PI3K/Akt/Nrf2, HO-1/NQO1, and FoxO1-NLRP3 in HPAEpiC and primary rat alveolar epithelial cell were examined. The data suggested that rhKGF-2 reduced LPS-induced HPAEpiC cell and primary rat alveolar epithelial cell apoptosis and the expression of inflammatory factors and oxidative stress factors. Moreover, rhKGF-2 improved the blood gas and alleviated SILI-induced lung histopathological injury in vivo via repressing inflammation, NLRP3 inflammasome activation and oxidative stress. Mechanistically, rhKGF-2 activated PI3K/Akt pathway, enhanced Nrf2/HO-1/NQO1 expression, and attenuated FoxO1-NLRP3 inflammasome both in vitro and in vivo. However, pharmaceutical inhibition of PI3K/Akt pathway attenuated rhKGF-2-mediated protective effects against SILI, while suppressing FoxO1 promoted rhKGF-2-mediated protective effects. Taken together, this study demonstrated that rhKGF-2 mitigated SILI by regulating the PI3K/Akt/Nrf2 pathway and the FoxO1-NLRP3 axis, which provides new reference in treating SILI.

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Section: Discussionmentioning

confidence: 82%

rhKGF-2 Attenuates Smoke Inhalation Lung Injury of Rats via Activating PI3K/Akt/Nrf2 and Repressing FoxO1-NLRP3 Inflammasome

Jiang

Guo

et al. 2021

Front. Pharmacol.

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Bone marrow mesenchymal stem cells protect lungs from smoke inhalation injury by differentiating into alveolar epithelial cells via Notch signaling

Liang

Yin

et al. 2019

J Biosci

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A review of the effects of wildfire smoke on the health and behavior of wildlife

Sanderfoot

Bassing

Brusa

et al. 2021

Environ. Res. Lett.

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Climate change is intensifying global wildfire activity, and people and wildlife are increasingly exposed to hazardous air pollution during large-scale smoke events. Although wildfire smoke is considered a growing risk to public health, few studies have investigated the impacts of wildfire smoke on wildlife, particularly among species that are vulnerable to smoke inhalation. In this review, we synthesized research to date on how wildfire smoke affects the health and behavior of wildlife. After executing a systematic search using Web of Science, we found only 41 relevant studies. We synthesized findings from this literature and incorporated knowledge gained from fields outside wildlife science, specifically veterinary medicine and air pollution toxicology. Although studies that directly investigated effects of smoke on wildlife were few in number, they show that wildfire smoke contributes to adverse acute and chronic health outcomes in wildlife and influences animal behavior. Our review demonstrates that smoke inhalation can lead to carbon monoxide poisoning, respiratory distress, neurological impairment, respiratory and cardiovascular disease, oxidative stress, and immunosuppression in wildlife, including terrestrial and aquatic species, and these health effects can contribute to changes in movement and vocalization. Some species also use smoke as a cue to engage in fire-avoidance behaviors or to conserve energy. However, our review also highlights significant gaps in our understanding of the impacts of wildfire smoke on wildlife. Most notably, the lack of robust air pollution measurements in existing studies limits meta-analyses and hinders construction of dose-response relationships, thereby precluding predictions of health outcomes and behaviors under different air quality conditions, especially during extreme smoke events. We recommend that future studies leverage existing data sets, infrastructure, and tools to rapidly advance research on this important conservation topic and highlight the potential value of interdisciplinary collaborations between ecologists and atmospheric chemists.

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Animal models of smoke inhalation induced injuries

Cited by 6 publications

References 85 publications

rhKGF-2 Attenuates Smoke Inhalation Lung Injury of Rats via Activating PI3K/Akt/Nrf2 and Repressing FoxO1-NLRP3 Inflammasome

rhKGF-2 Attenuates Smoke Inhalation Lung Injury of Rats via Activating PI3K/Akt/Nrf2 and Repressing FoxO1-NLRP3 Inflammasome

Bone marrow mesenchymal stem cells protect lungs from smoke inhalation injury by differentiating into alveolar epithelial cells via Notch signaling

A review of the effects of wildfire smoke on the health and behavior of wildlife

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