Measurement of low-frequency respiratory impedance in infants.

Sly, Peter D.; Hayden, Mark J.; Peták, Ferenc; Hantos, Zoltán

doi:10.1164/ajrccm.154.1.8680673

Cited by 79 publications

(61 citation statements)

References 31 publications

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“…Airway reactivity (resistance: Raw) was also measured using a modification of the low-frequency forced oscillation technique as described previously (33,34).…”

Section: Measurement Of Airway Resistancementioning

confidence: 99%

Inhibition of Arginase I Activity by RNA Interference Attenuates IL-13-Induced Airways Hyperresponsiveness

Yang

Rangasamy²,

Matthaei³

et al. 2006

The Journal of Immunology

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Increased arginase I activity is associated with allergic disorders such as asthma. How arginase I contributes to and is regulated by allergic inflammatory processes remains unknown. CD4+ Th2 lymphocytes (Th2 cells) and IL-13 are two crucial immune regulators that use STAT6-dependent pathways to induce allergic airways inflammation and enhanced airways responsiveness to spasmogens (airways hyperresponsiveness (AHR)). This pathway is also used to activate arginase I in isolated cells and in hepatic infection with helminths. In the present study, we show that arginase I expression is also regulated in the lung in a STAT6-dependent manner by Th2-induced allergic inflammation or by IL-13 alone. IL-13-induced expression of arginase I correlated directly with increased synthesis of urea and with reduced synthesis of NO. Expression of arginase I, but not eosinophilia or mucus hypersecretion, temporally correlated with the development, persistence, and resolution of IL-13-induced AHR. Pharmacological supplementation with l-arginine or with NO donors amplified or attenuated IL-13-induced AHR, respectively. Moreover, inducing loss of function of arginase I specifically in the lung by using RNA interference abrogated the development of IL-13-induced AHR. These data suggest an important role for metabolism of l-arginine by arginase I in the modulation of IL-13-induced AHR and identify a potential pathway distal to cytokine receptor interactions for the control of IL-13-mediated bronchoconstriction in asthma.

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“…Airway reactivity (resistance: Raw) was also measured using a modification of the low-frequency forced oscillation technique as described previously (33,34).…”

Section: Measurement Of Airway Resistancementioning

confidence: 99%

Inhibition of Arginase I Activity by RNA Interference Attenuates IL-13-Induced Airways Hyperresponsiveness

Yang

Rangasamy²,

Matthaei³

et al. 2006

The Journal of Immunology

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“…Lung function was measured in anesthetized, tracheostomized mice using a modification of the low-frequency forced oscillation technique (flexiVent; Scireg) as described previously (25). Following measurement of baseline lung function, mice sensitized to OVA were challenged with an aerosol of 1% OVA w/v in saline.…”

Section: Lung Function and Airway Physiologymentioning

confidence: 99%

“…Because mast cell mediators are potent bronchoconstrictors, we assessed lung function in Lyn Ϫ/Ϫ mice (25). Lyn Ϫ/Ϫ mice showed significantly enhanced bronchoconstriction following inhalation of OVA compared with similarly treated control animals ( Fig.…”

Section: Enhanced Bronchospasm In Lyn ϫ/ϫ Micementioning

confidence: 99%

Lyn-Deficient Mice Develop Severe, Persistent Asthma: Lyn Is a Critical Negative Regulator of Th2 Immunity

Beavitt

Harder

Kemp

et al. 2005

The Journal of Immunology

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The etiology of asthma, a chronic inflammatory disorder of the airways, remains obscure, although T cells appear to be central disease mediators. Lyn tyrosine kinase has been implicated as both a facilitator and inhibitor of signaling pathways that play a role in allergic inflammation, although its role in asthma is unclear because Lyn is not expressed in T cells. We show in the present study that Lyn−/− mice develop a severe, persistent inflammatory asthma-like syndrome with lung eosinophilia, mast cell hyperdegranulation, intensified bronchospasm, hyper IgE, and Th2-polarizing dendritic cells. Dendritic cells from Lyn−/− mice have a more immature phenotype, exhibit defective inhibitory signaling pathways, produce less IL-12, and can transfer disease when adoptively transferred into wild-type recipients. Our results show that Lyn regulates the intensity and duration of multiple asthmatic traits and indicate that Lyn is an important negative regulator of Th2 immune responses.

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“…This difficulty has been overcome recently in sedated infants aged from 1 mo to 2 yrs by employing the Hering-Breuer inflation reflex and hyperventilation to induce a short apneic interval (11), during which low-frequency (0.5-20 Hz) Z rs (11)(12)(13)(14)(15)(16)(17) is measured. The use of sedation is generally contraindicated for lung function tests in healthy, spontaneously breathing infants Ͻ44 wk postconceptional age (18).…”

mentioning

confidence: 99%