Experimental lung injury promotes alterations in energy metabolism and respiratory mechanics in the lungs of rats: prevention by exercise

Cunha, Maira J. da; Cunha, Aline Andrea da; Scherer, Emilene B. S.; Machado, Fernando Machado; Loureiro, Samanta Oliveira; Jaenisch, Rodrigo Boemo; Guma, Fátima Costa Rodrigues; Lago, Pedro Dal; Wyse, Ângela T. S.

doi:10.1007/s11010-013-1944-8

Cited by 11 publications

(14 citation statements)

References 66 publications

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“…This model allowed us to evaluate the utility of HMPAO lung uptake not only for pre-clinical detection of lung injury, but also, as stated above, for tracking the reversibility of the injury (Figure 5). Common findings of LPS injury include lung influx of neutrophils (5,23,24), bronchoalveolar lavage fluid with increased protein and neutrophils (5,23), decreased lung compliance (12), and decreased oxygenation with high doses of LPS (24), some of which we have corroborated here (Table 7). Several authors reported increased lung wet-to-dry weight ratio 24 hrs after endotoxin (23,24), which was not the case in the present study (Table 1).…”

Section: Discussionsupporting

confidence: 79%

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99MTc-Hexamethylpropyleneamine Oxime Imaging for Early Detection of Acute Lung Injury in Rats Exposed to Hyperoxia or Lipopolysaccharide Treatment

Audi

Clough

Haworth

et al. 2016

Shock

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99mTc-Hexamethylpropyleneamine oxime (HMPAO) is a clinical single-photon emission computed tomography biomarker of tissue oxidoreductive state. Our objective was to investigate whether HMPAO lung uptake can serve as a pre-clinical marker of lung injury in two well-established rat models of human acute lung injury (ALI). Rats were exposed to >95% O2 (hyperoxia) or treated with intratracheal lipopolysaccharide (LPS), with first endpoints obtained 24 hours later. HMPAO was administered intravenously before and after treatment with the glutathione-depleting agent diethyl maleate (DEM), scintigraphy images were acquired, and HMPAO lung uptake was quantified from the images. We also measured breathing rates, heart rates, oxygen saturation, bronchoalveolar lavage (BAL) cell counts and protein, lung homogenate glutathione (GSH) content, and pulmonary vascular endothelial filtration coefficient (Kf). For hyperoxia rats, HMPAO lung uptake increased after 24 hours (134%) and 48 hours (172%) of exposure. For LPS-treated rats, HMPAO lung uptake increased (188%) 24 hours after injury and fell with resolution of injury. DEM reduced HMPAO uptake in hyperoxia and LPS rats by a greater fraction than in normoxia rats. Both hyperoxia exposure (18%) and LPS treatment (26%) increased lung homogenate GSH content, which correlated strongly with HMPAO uptake. Neither of the treatments had an effect on Kf at 24 hours. LPS-treated rats appeared healthy but exhibited mild tachypnea, BAL and histological evidence of inflammation, and increased wet and dry lung weights. These results suggest the potential utility of HMPAO as a tool for detecting ALI at a phase likely to exhibit minimal clinical evidence of injury.

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Section: Discussionsupporting

confidence: 79%

“…In particular, endothelial apoptosis (7–9), mitochondrial dysfunction (7–12), and altered lung tissue oxidoreductive state (13,14) are features of both disorders. Furthermore, there is strong evidence that the pulmonary capillary endothelium is a primary and initial site of both hyperoxia- and LPS-induced ALI (4,7,11).…”

Section: Introductionmentioning

confidence: 99%

99MTc-Hexamethylpropyleneamine Oxime Imaging for Early Detection of Acute Lung Injury in Rats Exposed to Hyperoxia or Lipopolysaccharide Treatment

Audi

Clough

Haworth

et al. 2016

Shock

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“…Asthma is characterized by the enhancement in inflammatory cells in the lung such as eosinophil (Lambrecht & Hammad, ). Although there is an enhancement in DNA extracellular traps formation by eosinophils, mechanism of EETs release and their pathophysiologic role in asthma are poorly understood (Cunha et al, ; Dworski et al, ). Moreover, evidence has been observed the participation of autophagy in asthma immunopathology (Liu et al, ; Poon et al, ).…”

Section: Discussionmentioning

confidence: 99%

Autophagy induces eosinophil extracellular traps formation and allergic airway inflammation in a murine asthma model

Silveira

Antunes

Kaiber

et al. 2019

Journal Cellular Physiology

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Studies have shown autophagy participation in the immunopathology of inflammatory diseases. However, autophagy role in asthma and in eosinophil extracellular traps (EETs) release is poorly understood. Here, we attempted to investigate the autophagy involvement in EETs release and in lung inflammation in an experimental asthma model. Mice were sensitized with ovalbumin (OVA), followed by OVA challenge.Before the challenge with OVA, mice were treated with an autophagy inhibitor, 3-methyladenine (3-MA). We showed that 3-MA treatment decreases the number of eosinophils, eosinophil peroxidase (EPO) activity, goblet cells hyperplasia, proinflammatory cytokines, and nuclear factor kappa B (NFκB) p65 immunocontent in the lung. Moreover, 3-MA was able to improve oxidative stress, mitochondrial energy metabolism, and Na + , K + -ATPase activity. We demonstrated that treatment with autophagy inhibitor 3-MA reduced EETs formation in the airway. On the basis of our results, 3-MA treatment can be an interesting alternative for reducing lung inflammation, oxidative stress, mitochondrial damage, and EETs formation in asthma. K E Y W O R D Sasthma, autophagy, eosinophil extracellular traps, eosinophils, inflammation

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“…Acute and chronic physical exercise in rats on a high-fat diet induced an important suppression in the TLR4 signaling pathway in the liver, muscle, and adipose tissue, reducing LPS serum levels and improved insulin signaling and sensitivity (Oliveira et al, 2011 ). Moreover, exercise prevented lung injury and associated oxidative stress provoked by instillation of LPS (Reis Goncalves et al, 2012 ; da Cunha et al, 2013 , 2014 ) and LPS-induced depressive-like behavior in rats (Martin et al, 2014 ).…”

Section: Potential Mechanism By Which Exercise Influences Gut Microbimentioning

confidence: 99%

Gut Microbiota Modification: Another Piece in the Puzzle of the Benefits of Physical Exercise in Health?

et al. 2016

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Regular physical exercise provides many health benefits, protecting against the development of chronic diseases, and improving quality of life. Some of the mechanisms by which exercise provides these effects are the promotion of an anti-inflammatory state, reinforcement of the neuromuscular function, and activation of the hypothalamic–pituitary–adrenal (HPA) axis. Recently, it has been proposed that physical exercise is able to modify gut microbiota, and thus this could be another factor by which exercise promotes well-being, since gut microbiota appears to be closely related to health and disease. The purpose of this paper is to review the recent findings on gut microbiota modification by exercise, proposing several mechanisms by which physical exercise might cause changes in gut microbiota.

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Experimental lung injury promotes alterations in energy metabolism and respiratory mechanics in the lungs of rats: prevention by exercise

Cited by 11 publications

References 66 publications

99MTc-Hexamethylpropyleneamine Oxime Imaging for Early Detection of Acute Lung Injury in Rats Exposed to Hyperoxia or Lipopolysaccharide Treatment

99MTc-Hexamethylpropyleneamine Oxime Imaging for Early Detection of Acute Lung Injury in Rats Exposed to Hyperoxia or Lipopolysaccharide Treatment

Autophagy induces eosinophil extracellular traps formation and allergic airway inflammation in a murine asthma model

Gut Microbiota Modification: Another Piece in the Puzzle of the Benefits of Physical Exercise in Health?

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