Comparative study of three<i>flexiVent</i>system configurations using mechanical test loads

Robichaud, Annette; Fereydoonzad, Liah; Urovitch, Ilan Benjamin

doi:10.3109/01902148.2014.971921

Cited by 15 publications

(11 citation statements)

References 10 publications

(27 reference statements)

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“…Our data indicate differences in measurements between the FV-M2 and FX3 flexivent systems, a difference that has also been observed by other groups [ 48 ]. One study found that there was no difference in precision or accuracy in resistance between the models; however, the FX system resulted in more accurate compliance measurements [ 48 ]. Therefore, the difference in significance in the parameters measured in 4DPI RSV infected female cotton rats between the different instruments may have been partly attributed due to their varying configuration.…”

Section: Discussionsupporting

confidence: 86%

Pulmonary function analysis in cotton rats after respiratory syncytial virus infection

et al. 2020

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The cotton rat (Sigmodon hispidus) is an excellent small animal model for human respiratory viral infections such as human respiratory syncytial virus (RSV) and human metapneumovirus (HMPV). These respiratory viral infections, as well as other pulmonary inflammatory diseases such as asthma, are associated with lung mechanic disturbances. So far, the pathophysiological effects of viral infection and allergy on cotton rat lungs have not been measured, although this information might be an important tool to determine the efficacy of vaccine and drug candidates. To characterize pulmonary function in the cotton rat, we established forced oscillation technique in uninfected, RSV infected and HDM sensitized cotton rats, and characterized pulmonary inflammation, mucus production, pulmonary edema, and oxygenation. There was a gender difference after RSV infection, with females demonstrating airway hyper-responsiveness while males did not. Female cotton rats 2dpi had a mild increase in pulmonary edema (wet: dry weight ratios). At day 4 post infection, female cotton rats demonstrated mild pulmonary inflammation, no increase in mucus production or reduction in oxygenation. Pulmonary function was not significantly impaired after RSV infection. In contrast, cotton rats sensitized to HDM demonstrated airway hyperresponsiveness with a significant increase in pulmonary inflammation, increase in baseline tissue damping, and a decrease in baseline pulmonary compliance. In summary, we established baseline data for forced oscillation technique and other respiratory measures in the cotton rat and used it to analyze respiratory diseases in cotton rats.

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Section: Discussionsupporting

confidence: 86%

Pulmonary function analysis in cotton rats after respiratory syncytial virus infection

et al. 2020

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“…3t), which together indicated reduced lung compliance and distensibility. Further analysis using broadband forced oscillation maneuvers 16 revealed that SARS-CoV-2-infected mice at 7 dpi had relatively normal Newtonian resistance ( Fig. 3u), which is primarily a reflection of resistance in larger conducting airways.…”

Section: Pathophysiology Of Sars-cov-2 Infectionmentioning

confidence: 97%

SARS-CoV-2 infection of human ACE2-transgenic mice causes severe lung inflammation and impaired function

et al. 2020

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Although animal models have been evaluated for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, none have fully recapitulated the lung disease phenotypes seen in humans who have been hospitalized. Here, we evaluate transgenic mice expressing the human angiotensin I-converting enzyme 2 (ACE2) receptor driven by the cytokeratin-18 (K18) gene promoter (K18-hACE2) as a model of SARS-CoV-2 infection. Intranasal inoculation of SARS-CoV-2 in K18-hACE2 mice results in high levels of viral infection in lungs, with spread to other organs. A decline in pulmonary function occurs 4 days after peak viral titer and correlates with infiltration of monocytes, neutrophils and activated T cells. SARS-CoV-2-infected lung tissues show a massively upregulated innate immune response with signatures of nuclear factor-κB-dependent, type I and II interferon signaling, and leukocyte activation pathways. Thus, the K18-hACE2 model of SARS-CoV-2 infection shares many features of severe COVID-19 infection and can be used to define the basis of lung disease and test immune and antiviral-based countermeasures.

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“…Oxygen saturations were measured using the MouseOx Plus pulse oximeter (Starr Life Sciences, Oakmont, PA, USA) via the thigh sensor. Lung mechanic parameters were generated from the flexiVent rodent ventilator using the forced oscillation technique as previously described [ 10 ].…”

Section: Methodsmentioning

confidence: 99%

GM-CSF overexpression after influenza a virus infection prevents mortality and moderates M1-like airway monocyte/macrophage polarization

et al. 2018

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BackgroundInfluenza A viruses cause life-threatening pneumonia and lung injury in the lower respiratory tract. Application of high GM-CSF levels prior to infection has been shown to reduce morbidity and mortality from pathogenic influenza infection in mice, but the mechanisms of protection and treatment efficacy have not been established.MethodsMice were infected intranasally with influenza A virus (PR8 strain). Supra-physiologic levels of GM-CSF were induced in the airways using the double transgenic GM-CSF (DTGM) or littermate control mice starting on 3 days post-infection (dpi). Assessment of respiratory mechanical parameters was performed using the flexiVent rodent ventilator. RNA sequence analysis was performed on FACS-sorted airway macrophage subsets at 8 dpi.ResultsSupra-physiologic levels of GM-CSF conferred a survival benefit, arrested the deterioration of lung mechanics, and reduced the abundance of protein exudates in bronchoalveolar (BAL) fluid to near baseline levels. Transcriptome analysis, and subsequent validation ELISA assays, revealed that excess GM-CSF re-directs macrophages from an “M1-like” to a more “M2-like” activation state as revealed by alterations in the ratios of CXCL9 and CCL17 in BAL fluid, respectively. Ingenuity pathway analysis predicted that GM-CSF surplus during IAV infection elicits expression of anti-inflammatory mediators and moderates M1 macrophage pro-inflammatory signaling by Type II interferon (IFN-γ).ConclusionsOur data indicate that application of high levels of GM-CSF in the lung after influenza A virus infection alters pathogenic “M1-like” macrophage inflammation. These results indicate a possible therapeutic strategy for respiratory virus-associated pneumonia and acute lung injury.Electronic supplementary materialThe online version of this article (10.1186/s12931-017-0708-5) contains supplementary material, which is available to authorized users.

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Comparative study of threeflexiVentsystem configurations using mechanical test loads

Cited by 15 publications

References 10 publications

Pulmonary function analysis in cotton rats after respiratory syncytial virus infection

Pulmonary function analysis in cotton rats after respiratory syncytial virus infection

SARS-CoV-2 infection of human ACE2-transgenic mice causes severe lung inflammation and impaired function

GM-CSF overexpression after influenza a virus infection prevents mortality and moderates M1-like airway monocyte/macrophage polarization

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