Tracking of airway and tissue mechanics during TLC maneuvers in mice

Hantos, Zoltán; Collins, Rachel A.; Turner, Debra J.; Jánosi, Tibor Z.; Sly, Peter D.

doi:10.1152/japplphysiol.00104.2003

Cited by 54 publications

(61 citation statements)

References 27 publications

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“…Penh was measured for 3 min in baseline conditions. Mice were then exposed to the inhalation of PBS and subsequent increasing doses of MCh (3,6,12,24, and 48 g/l) during 1 min. Every aerosol was separated by a 15-min recovery period in order to allow airway Penh to go back to baseline level.…”

Section: Bronchial Airway Responsiveness Measurementmentioning

confidence: 99%

“…A tracheotomy was performed by inserting a 20-gauge polyethylene catheter into the trachea and ligating it around the catheter to avoid leaks and disconnections. Mice were ventilated with a FlexiVent small-animal ventilator (SCIREQ, Montreal, Canada) as described by Hantos et al [12]. Following baseline lung-function measurements, mice were exposed to a saline aerosol (PBS) followed by aerosols containing increasing doses (3,6,9, and 12 g/1) of methacholine (ICN Biomedicals, Asse Relegem, Belgium).…”

Section: Bronchial Airway Responsiveness Measurementmentioning

confidence: 99%

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Mouse models of asthma: a comparison between C57BL/6 and BALB/c strains regarding bronchial responsiveness, inflammation, and cytokine production

et al. 2009

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Objective Animal models of asthma mimic major features of human disease. Since the genetic background of experimental animals might affect hyperresponsiveness and inflammation, we studied its potential influence and the mechanisms leading to differences in strains. MethodsWe applied a mouse model of allergic asthma to BALB/c and C57BL/6 mice.Results BALB/c mice displayed greater levels of airway reactivity to methacholine than C57BL/6 mice. Moreover, BALB/c mice exhibited higher numbers of mast cells in lung tissue when compared to C57BL/6. On the contrary, eosinophil and neutrophil counts in bronchoalveolar lavage fluid (BALF) as well as peribronchial eosinophilia were greater in C57BL/6. IL (Interleukin)-4, IL-5, IL-13, and CCL11 levels measured in wholelung extracts were higher in BALB/c, while, in sharp contrast, CCL11 and CCL5 levels were higher in BALF of C57BL/6 mice. ConclusionsWe observed phenotypic differences between C57BL/6 and BALB/c mice in an asthma model with different distributions of pro-inflammatory cytokines and inflammatory cells.

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Section: Bronchial Airway Responsiveness Measurementmentioning

confidence: 99%

Section: Bronchial Airway Responsiveness Measurementmentioning

confidence: 99%

Mouse models of asthma: a comparison between C57BL/6 and BALB/c strains regarding bronchial responsiveness, inflammation, and cytokine production

et al. 2009

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“…AHR to inhaled methacholine (MCh) was measured using a modification of the low-frequency forced oscillation technique as previously described (10). Briefly, mice were anesthetized, tracheostomized and ventilated using a custom built ventilator (flexiVent; Scireq) that functioned both as a ventilator and means of measuring respiratory system input impedance (Zrs).…”

Section: Measurement Of Ahrmentioning

confidence: 99%

Allergic Airways Disease Develops after an Increase in Allergen Capture and Processing in the Airway Mucosa

Garnier

Wikström

Zosky

et al. 2007

The Journal of Immunology

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Airway mucosal dendritic cells (AMDC) and other airway APCs continuously sample inhaled Ags and regulate the nature of any resulting T cell-mediated immune response. Although immunity develops to harmful pathogens, tolerance arises to nonpathogenic Ags in healthy individuals. This homeostasis is thought to be disrupted in allergic respiratory disorders such as allergic asthma, such that a potentially damaging Th2-biased, CD4+ T cell-mediated inflammatory response develops against intrinsically nonpathogenic allergens. Using a mouse model of experimental allergic airways disease (EAAD), we have investigated the functional changes occurring in AMDC and other airway APC populations during disease onset. Onset of EAAD was characterized by early and transient activation of airway CD4+ T cells coinciding with up-regulation of CD40 expression exclusively on CD11b− AMDC. Concurrent enhanced allergen uptake and processing occurred within all airway APC populations, including B cells, macrophages, and both CD11b+ and CD11b− AMDC subsets. Immune serum transfer into naive animals recapitulated the enhanced allergen uptake observed in airway APC populations and mediated activation of naive allergen-specific, airway CD4+ T cells following inhaled allergen challenge. These data suggest that the onset of EAAD is initiated by enhanced allergen capture and processing by a number of airway APC populations and that allergen-specific Igs play a role in the conversion of normally quiescent AMDC subsets into those capable of inducing airway CD4+ T cell activation.

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“…Briefly, Z rs was measured using a wave‐tube system 42 adapted for use in small animals 41 , 43 . Oscillatory signals consisting of nine non‐integer multiple frequency components between 4 and 38 Hz were delivered via a 1 m wave tube (internal diameter = 0·116 cm) to tracheostomized mice during brief apnoeic periods.…”

Section: Methodsmentioning

confidence: 99%

Acute diesel exhaust particle exposure increases viral titre and inflammation associated with existing influenza infection, but does not exacerbate deficits in lung function

Larcombe

Foong

Boylen

et al. 2012

Influenza Resp Viruses

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Please cite this paper as: Larcombe et al. (2012) Acute diesel exhaust particle exposure increases viral titre and inflammation associated with existing influenza infection, but does not exacerbate deficits in lung function. Influenza and Other Respiratory Viruses DOI:10.1111/irv.12012. Background Exposure to diesel exhaust particles (DEP) is thought to exacerbate many pre‐existing respiratory diseases, including asthma, bronchitis and chronic obstructive pulmonary disease, however, there is a paucity of data on whether DEP exacerbates illness due to respiratory viral infection. Objectives To assess the physiological consequences of an acute DEP exposure during the peak of influenza‐induced illness. Methods We exposed adult female BALB/c mice to 100 μg DEP (or control) 3·75 days after infection with 104·5 plaque forming units of influenza A/Mem71 (or control). Six hours, 24 hours and 7 days after DEP exposure we measured thoracic gas volume and lung function at functional residual capacity. Bronchoalveolar lavage fluid was taken for analyses of cellular inflammation and cytokines, and whole lungs were taken for measurement of viral titre. Results Influenza infection resulted in significantly increased inflammation, cytokine influx and impairment to lung function. DEP exposure alone resulted in less inflammation and cytokine influx, and no impairment to lung function. Mice infected with influenza and exposed to DEP had higher viral titres and neutrophilia compared with infected mice, yet they did not have more impaired lung mechanics than mice infected with influenza alone. Conclusions A single dose of DEP is not sufficient to physiologically exacerbate pre‐existing respiratory disease caused by influenza infection in mice.

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Tracking of airway and tissue mechanics during TLC maneuvers in mice

Cited by 54 publications

References 27 publications

Mouse models of asthma: a comparison between C57BL/6 and BALB/c strains regarding bronchial responsiveness, inflammation, and cytokine production

Mouse models of asthma: a comparison between C57BL/6 and BALB/c strains regarding bronchial responsiveness, inflammation, and cytokine production

Allergic Airways Disease Develops after an Increase in Allergen Capture and Processing in the Airway Mucosa

Acute diesel exhaust particle exposure increases viral titre and inflammation associated with existing influenza infection, but does not exacerbate deficits in lung function

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