A noninvasive technique for measurement of changes in specific airway resistance

Pennock, Bernard E.; Cox, CM; Rogers, Robert M.; Cain, William A.; Wells, Jason

doi:10.1152/jappl.1979.46.2.399

Cited by 278 publications

(161 citation statements)

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“…Pulmonary Function Measurements sRaw was measured in conscious guinea pigs by a two-chambered, doubleflow plethysmograph system in accordance with the method of Pennock et al 29) In brief, an animal was placed with its neck extending through the partition of a two-chambered box, and after detection of airflow by sensors attached to both the front and rear chambers, sRaw was then measured using a Data Analyzer Pulmos-I device (M.I.P.S., Osaka).…”

Section: Methodsmentioning

confidence: 99%

Pulmonary Emphysema Induced by Cigarette Smoke Solution and Lipopolysaccharide in Guinea Pigs

Mizutani

Fuchikami²,

Takahashi³

et al. 2009

Biological & Pharmaceutical Bulletin

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Chronic obstructive pulmonary disease (COPD) is a major global health problem that is predicted to become the third most common cause of death by 2020.1,2) Nearly 90% of COPD patients are smokers.3) COPD is a condition characterized by airway obstruction due to narrowing of the small airways that is not fully reversible, airway inflammation, and emphysema-related loss of the elastic recoil of the lung. [4][5][6] Pulmonary emphysema is a major component of COPD and is defined by a destructive change of the pulmonary alveoli and enlargement of the respiratory region of the lung distal to the terminal bronchioles. In addition, residual volume (RV) and functional residual capacity (FRC) are characteristically increased in COPD and are related to the degree of hyperinflation of the lungs, especially when there is predominately emphysema. 7,8) Still, the detailed sequence of events leading to the onset of pulmonary emphysema is not yet fully elucidated.On the other hand, it has been suggested that the morbidity and mortality of COPD are associated with acute exacerbations.9,10) Some exacerbations of COPD are undoubtedly related to respiratory bacteria, which infect the lower airways and increase overall airway inflammation. 11,12) In addition, meta-analyses of antibiotic therapy have indicated an advantage for the use of such interventions, which confirms that bacteria are responsible for the exacerbations in COPD. 13,14) In studies using guinea pigs and mice, it has been reported that repeated exposure of the animals to lipopolysaccharide (LPS) results in persistent chronic pulmonary inflammation observed in human subjects with COPD. 15,16) The use of appropriate experimental COPD animal models is indispensable for the development of new therapeutic drugs and for the analysis of the pathogenesis of the disease. By exposing animals to 3 or more months of cigarette smoke, various experimental COPD models have been developed in guinea pigs, rats and mice. [17][18][19][20][21][22][23][24] Although all of these models have emphysematous airspace enlargement, studies on the clinical pathogenesis of COPD would be much more efficient if the emphysematous condition could be experimentally reproduced within a much shorter time period.In order to shorten the period of development of an experimental COPD model, a more efficient delivery system of the constituents of cigarette smoke into the lung is required. To bypass the problem of using inhaled smoke, which is spontaneously exhaled, we attempted to intratracheally instill a cigarette smoke solution (CSS) over several weeks. Since respiratory infections are assumed to be the main risk factors for exacerbation of COPD, we decided to add LPS to the protocol of the multiple CSS administrations. Through the use of these multiple intratracheal administrations of CSS and LPS, we succeeded in inducing airway obstruction, bronchitis and emphysema over a considerably shorter term as compared to that seen for the other models that are currently in use. On the other hand, theophylline is ...

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Section: Methodsmentioning

confidence: 99%

Pulmonary Emphysema Induced by Cigarette Smoke Solution and Lipopolysaccharide in Guinea Pigs

Mizutani

Fuchikami²,

Takahashi³

et al. 2009

Biological & Pharmaceutical Bulletin

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“…To evaluate the degree of early-and late-phase increases in airway resistance, specific airway resistance [sRaw; cmH 2 O 3 mL/(mL/s)] was measured in conscious mice before and 10 min to 5 h after the first and fourth challenges using a two-chambered, double-flow plethysmograph system (Pulmos-I; M.I.P.S., Osaka, Japan) according to the method of Pennock et al (32).…”

Section: Measurement Of Airway Resistancementioning

confidence: 99%

Complement C3a-Induced IL-17 Plays a Critical Role in an IgE-Mediated Late-Phase Asthmatic Response and Airway Hyperresponsiveness via Neutrophilic Inflammation in Mice

Mizutani

Goshima

Nabe

et al. 2012

The Journal of Immunology

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Allergen-specific IgE plays an essential role in the pathogenesis of allergic asthma. Although there has been increasing evidence suggesting the involvement of IL-17 in the disease, the relationship between IL-17 and IgE-mediated asthmatic responses has not yet been defined. In this study, we attempted to elucidate the contribution of IL-17 to an IgE-mediated late-phase asthmatic response and airway hyperresponsiveness (AHR). BALB/c mice passively sensitized with an OVA-specific IgE mAb were challenged with OVA intratracheally four times. The fourth challenge caused a late-phase increase in airway resistance associated with elevated levels of IL-17+CD4+ cells in the lungs. Multiple treatments with a C3a receptor antagonist or anti-C3a mAb during the challenges inhibited the increase in IL-17+CD4+ cells. Meanwhile, a single treatment with the antagonist or the mAb at the fourth challenge suppressed the late-phase increase in airway resistance, AHR, and infiltration by neutrophils in bronchoalveolar lavage fluid. Because IL-17 production in the lungs was significantly repressed by both treatments, the effect of an anti–IL-17 mAb was examined. The late-phase increase in airway resistance, AHR, and infiltration by neutrophils in bronchoalveolar lavage fluid was inhibited. Furthermore, an anti–Gr-1 mAb had a similar effect. Collectively, we found that IgE mediated the increase of IL-17+CD4+ cells in the lungs caused by repeated Ag challenges via C3a. The mechanisms leading to the IgE-mediated late-phase asthmatic response and AHR are closely associated with neutrophilic inflammation through the production of IL-17 induced by C3a.

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“…The noninvasive technique is based on measurement of the time delay between thoracic and mouth volume changes, and we calculated the airway resistance (30,31). Airway responsiveness to i.v.…”

Section: Measurement Of Specific Airway Responsiveness (Sraw)mentioning

confidence: 99%

Intervention of Thymus and Activation-Regulated Chemokine Attenuates the Development of Allergic Airway Inflammation and Hyperresponsiveness in Mice

Kawasaki

Takizawa²,

Yoneyama

et al. 2001

The Journal of Immunology

245

168

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Thymus- and activation-regulated chemokine (TARC; CCL17) is a lymphocyte-directed CC chemokine that specifically chemoattracts CC chemokine receptor 4-positive (CCR4+) Th2 cells. To establish the pathophysiological roles of TARC in vivo, we investigated here whether an mAb against TARC could inhibit the induction of asthmatic reaction in mice elicited by OVA. TARC was constitutively expressed in the lung and was up-regulated in allergic inflammation. The specific Ab against TARC attenuated OVA-induced airway eosinophilia and diminished the degree of airway hyperresponsiveness with a concomitant decrease in Th2 cytokine levels. Our results for the first time indicate that TARC is a pivotal chemokine for the development of Th2-dominated experimental allergen-induced asthma with eosinophilia and AHR. This study also represents the first success in controlling Th2 cytokine production in vivo by targeting a chemokine.

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A noninvasive technique for measurement of changes in specific airway resistance

Cited by 278 publications

References 0 publications

Pulmonary Emphysema Induced by Cigarette Smoke Solution and Lipopolysaccharide in Guinea Pigs

Pulmonary Emphysema Induced by Cigarette Smoke Solution and Lipopolysaccharide in Guinea Pigs

Complement C3a-Induced IL-17 Plays a Critical Role in an IgE-Mediated Late-Phase Asthmatic Response and Airway Hyperresponsiveness via Neutrophilic Inflammation in Mice

Intervention of Thymus and Activation-Regulated Chemokine Attenuates the Development of Allergic Airway Inflammation and Hyperresponsiveness in Mice

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