Murine mechanical ventilation stimulates alveolar epithelial cell proliferation

Chess, Patricia R.; Benson, Randi Potter; Maniscalco, William M.; Wright, Terry W.; O’Reilly, Michael A.; Johnston, Carl J.

doi:10.3109/01902141003632332

Cited by 8 publications

(5 citation statements)

References 51 publications

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“…The presence of neutrophils in the airspace is a consistent feature of lung injury in animals and humans because these are the first cells of the immune system to be recruited to the site of inflammation [ 37 ]. In addition, we observed that MV led to recruitment of lymphocytes to the lung; our results corroborate the findings of Chess et al [ 38 ] who reported a higher percentage of lymphocytes in ventilated animals with a moderate tidal volume.…”

Section: Discussionsupporting

confidence: 92%

High‐Fat Diet Increases HMGB1 Expression and Promotes Lung Inflammation in Mice Subjected to Mechanical Ventilation

Souza

Chírico

Cartelle

et al. 2018

Oxidative Medicine and Cellular Longevity

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This study aims to evaluate the effects of a high-fat diet and mechanical ventilation on the pulmonary and systemic inflammatory response in C57BL/6 mice. Male C57BL/6 mice were divided into two groups: one received a standard diet, and the other received a high-fat diet. After 10 weeks, the groups were further divided into two groups each: control group (CG), mechanical ventilation group (MVG), diet group (DG), and diet mechanical ventilation group (DMVG). MVG and DMVG underwent mechanical ventilation for 60 minutes. All animals were euthanized for subsequent analysis. Animals receiving a high-fat diet presented higher body mass, adipose index, and greater adipocyte area. In the lung, the expression of HMGB1 was greater in DG and DMVG than in CG and MVG. CCL2 and IL-22 levels in MVG and DMVG were increased compared to those in CG and DG, whereas IL-10 and IL-17 were decreased. Superoxide dismutase activity was higher in MVG and DMVG than in CG. Catalase activity was lower in DG than in CG, and in MV groups, it was lower than that in CG and DG. MV and obesity promote inflammation and pulmonary oxidative stress in adult C57BL/6 mice.

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Section: Discussionsupporting

confidence: 92%

High‐Fat Diet Increases HMGB1 Expression and Promotes Lung Inflammation in Mice Subjected to Mechanical Ventilation

Souza

Chírico

Cartelle

et al. 2018

Oxidative Medicine and Cellular Longevity

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“…These differences were likely caused by variability introduced by both ventilation and smoke exposure, resulting in an interactive effect after combination of the two stimuli. Our findings after mechanical ventilation confirm those of a previous study in mice exposed to mechanical ventilation for 6 hours with 10 ml/kg tidal volume and PEEP of 3 cmH 2 O [ 42 ]. The results of that suggested that ventilation induced low-level BALF neutrophilia and proliferation of ATII cells, whereas ventilation did not increase apoptosis in ATII cells, as measured by terminal deoxynucleotidyl transferase deoxyuridine triphosphate nick-end labeling staining.…”

Section: Discussionsupporting

confidence: 91%

Double impact of cigarette smoke and mechanical ventilation on the alveolar epithelial type II cell

et al. 2014

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IntroductionVentilator-induced lung injury (VILI) impacts clinical outcomes in acute respiratory distress syndrome (ARDS), which is characterized by neutrophil-mediated inflammation and loss of alveolar barrier function. Recent epidemiological studies suggest that smoking may be a risk factor for the development of ARDS. Because alveolar type II cells are central to maintaining the alveolar epithelial barrier during oxidative stress, mediated in part by neutrophilic inflammation and mechanical ventilation, we hypothesized that exposure to cigarette smoke and mechanical strain have interactive effects leading to the activation of and damage to alveolar type II cells.MethodsTo determine if cigarette smoke increases susceptibility to VILI in vivo, a clinically relevant rat model was established. Rats were exposed to three research cigarettes per day for two weeks. After this period, some rats were mechanically ventilated for 4 hours. Bronchoalveolar lavage (BAL) and differential cell count was done and alveolar type II cells were isolated. Proteomic analysis was performed on the isolated alveolar type II cells to discover alterations in cellular pathways at the protein level that might contribute to injury. Effects on levels of proteins in pathways associated with innate immunity, oxidative stress and apoptosis were evaluated in alveolar type II cell lysates by enzyme-linked immunosorbent assay. Statistical comparisons were performed by t-tests, and the results were corrected for multiple comparisons using the false discovery rate.ResultsTobacco smoke exposure increased airspace neutrophil influx in response to mechanical ventilation. The combined exposure to cigarette smoke and mechanical ventilation significantly increased BAL neutrophil count and protein content. Neutrophils were significantly higher after smoke exposure and ventilation than after ventilation alone. DNA fragments were significantly elevated in alveolar type II cells. Smoke exposure did not significantly alter other protein-level markers of cell activation, including Toll-like receptor 4; caspases 3, 8 and 9; and heat shock protein 70.ConclusionsCigarette smoke exposure may impact ventilator-associated alveolar epithelial injury by augmenting neutrophil influx. We found that cigarette smoke had less effect on other pathways previously associated with VILI, including innate immunity, oxidative stress and apoptosis.

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“…[ 16 ] Mouse studies have focused on supraphysiologic tidal volumes of 20 to 45 ml/kg to stimulate an injurious response with durations of ventilation varying from two to six hours. [ 17 , 18 , 19 , 20 , 21 , 22 , 23 ] and lung injury has been shown to occur with short-term ventilation. However, a direct comparison between short-term and long-term ventilation in a translational model is currently lacking in the literature and it is also unknown at what time point ventilation becomes injurious.…”

Section: Introductionmentioning

confidence: 99%

Effects of positive end-expiratory pressure and recruitment maneuvers in a ventilator-induced injury mouse model

et al. 2017

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BackgroundPositive-pressure mechanical ventilation is an essential therapeutic intervention, yet it causes the clinical syndrome known as ventilator-induced lung injury. Various lung protective mechanical ventilation strategies have attempted to reduce or prevent ventilator-induced lung injury but few modalities have proven effective. A model that isolates the contribution of mechanical ventilation on the development of acute lung injury is needed to better understand biologic mechanisms that lead to ventilator-induced lung injury.ObjectivesTo evaluate the effects of positive end-expiratory pressure and recruitment maneuvers in reducing lung injury in a ventilator-induced lung injury murine model in short- and longer-term ventilation.Methods5–12 week-old female BALB/c mice (n = 85) were anesthetized, placed on mechanical ventilation for either 2 hrs or 4 hrs with either low tidal volume (8 ml/kg) or high tidal volume (15 ml/kg) with or without positive end-expiratory pressure and recruitment maneuvers.ResultsAlteration of the alveolar-capillary barrier was noted at 2 hrs of high tidal volume ventilation. Standardized histology scores, influx of bronchoalveolar lavage albumin, proinflammatory cytokines, and absolute neutrophils were significantly higher in the high-tidal volume ventilation group at 4 hours of ventilation. Application of positive end-expiratory pressure resulted in significantly decreased standardized histology scores and bronchoalveolar absolute neutrophil counts at low- and high-tidal volume ventilation, respectively. Recruitment maneuvers were essential to maintain pulmonary compliance at both 2 and 4 hrs of ventilation.ConclusionsSigns of ventilator-induced lung injury are evident soon after high tidal volume ventilation (as early as 2 hours) and lung injury worsens with longer-term ventilation (4 hrs). Application of positive end-expiratory pressure and recruitment maneuvers are protective against worsening VILI across all time points. Dynamic compliance can be used guide the frequency of recruitment maneuvers to help ameloriate ventilator-induced lung injury.

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Murine mechanical ventilation stimulates alveolar epithelial cell proliferation

Cited by 8 publications

References 51 publications

High‐Fat Diet Increases HMGB1 Expression and Promotes Lung Inflammation in Mice Subjected to Mechanical Ventilation

High‐Fat Diet Increases HMGB1 Expression and Promotes Lung Inflammation in Mice Subjected to Mechanical Ventilation

Double impact of cigarette smoke and mechanical ventilation on the alveolar epithelial type II cell

Effects of positive end-expiratory pressure and recruitment maneuvers in a ventilator-induced injury mouse model

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