Comparative effects of inhaled budesonide and the NO-donating budesonide derivative, NCX 1020, against leukocyte influx and airway hyperreactivity following lipopolysaccharide challenge

Nevin, Barra J.; Broadley, Kenneth J.

doi:10.1016/j.pupt.2004.04.002

Cited by 19 publications

(15 citation statements)

References 33 publications

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“…Because determinations of pulmonary function by noninvasive versus invasive methods are still very controversial [30, 31], we extended our findings by showing that murine tracheal rings exposed to LPS display an enhanced response to MCh. In a murine model of asthma, it was shown that noninvasive in vivo determination of airway reactivity to methacholine correlated with smooth muscle contraction of tracheal rings [32]. The responses of tracheal rings are well established with a clear role of TNF in modulating hyperreactivity, as reviewed by Amrani et al [33].…”

Section: Discussionmentioning

confidence: 99%

Enhancement of Methacholine-Evoked Tracheal Contraction Induced by Bacterial Lipopolysaccharides Depends on Epithelium and Tumor Necrosis Factor

et al. 2012

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Inhaled bacterial lipopolysaccharides (LPSs) induce an acute tumour necrosis factor-alpha (TNF-α-) dependent inflammatory response in the murine airways mediated by Toll-like receptor 4 (TLR4) via the myeloid differentiation MyD88 adaptor protein pathway. However, the contractile response of the bronchial smooth muscle and the role of endogenous TNFα in this process have been elusive. We determined the in vivo respiratory pattern of C57BL/6 mice after intranasal LPS administration with or without the presence of increasing doses of methacholine (MCh). We found that LPS administration altered the basal and MCh-evoked respiratory pattern that peaked at 90 min and decreased thereafter in the next 48 h, reaching basal levels 7 days later. We investigated in controlled ex vivo condition the isometric contraction of isolated tracheal rings in response to MCh cholinergic stimulation. We observed that preincubation of the tracheal rings with LPS for 90 min enhanced the subsequent MCh-induced contractile response (hyperreactivity), which was prevented by prior neutralization of TNFα with a specific antibody. Furthermore, hyperreactivity induced by LPS depended on an intact epithelium, whereas hyperreactivity induced by TNFα was well maintained in the absence of epithelium. Finally, the enhanced contractile response to MCh induced by LPS when compared with control mice was not observed in tracheal rings from TLR4- or TNF- or TNF-receptor-deficient mice. We conclude that bacterial endotoxin-mediated hyperreactivity of isolated tracheal rings to MCh depends upon TLR4 integrity that signals the activation of epithelium, which release endogenous TNFα.

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Section: Discussionmentioning

confidence: 99%

Enhancement of Methacholine-Evoked Tracheal Contraction Induced by Bacterial Lipopolysaccharides Depends on Epithelium and Tumor Necrosis Factor

et al. 2012

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“…A higher concentration of histamine (3 mM) causes a substantial bronchoconstriction in this model. Control experiments have shown that there is no loss of responsiveness on repeating this challenge 24 h after a saline exposure [25].…”

Section: Airway Reactivity To Histamine and Cell Countsmentioning

confidence: 98%

Optimisation of the sensitisation conditions for an ovalbumin challenge model of asthma

Smith

Broadley

2007

International Immunopharmacology

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“…This may, however, be rather due to altered neutrophil than eosinophil functions or survival [221,222]. Interestingly, a recent report showed that NO-releasing budesonide was more potent than budesonide in the inhibition of LPS-induced airway hyperreactivity and leukocyte activation in a guinea-pig model of lung inflammation [223].…”

Section: No and Eosinophilsmentioning

confidence: 99%

Nitric Oxide Production and Signaling in Inflammation

Korhonen

Lahti²,

Kankaanranta³

et al. 2005

CDTIA

839

609

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Nitric oxide (NO) is recognized as a mediator and regulator of inflammatory responses. It possesses cytotoxic properties that are aimed against pathogenic microbes, but it can also have damaging effects on host tissues. NO reacts with soluble guanylate cyclase to form cyclic guanosine monophosphate (cGMP), which mediates many of the effects of NO. NO can also interact with molecular oxygen and superoxide anion to produce reactive nitrogen species that can modify various cellular functions. These indirect effects of NO have a significant role in inflammation, where NO is produced in high amounts by inducible nitric oxide synthase (iNOS) and reactive oxygen species are synthesized by activated inflammatory cells. The present review deals with NO production and signaling in inflammation, especially in relation to human neutrophils and eosinophils.

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Comparative effects of inhaled budesonide and the NO-donating budesonide derivative, NCX 1020, against leukocyte influx and airway hyperreactivity following lipopolysaccharide challenge

Cited by 19 publications

References 33 publications

Enhancement of Methacholine-Evoked Tracheal Contraction Induced by Bacterial Lipopolysaccharides Depends on Epithelium and Tumor Necrosis Factor

Enhancement of Methacholine-Evoked Tracheal Contraction Induced by Bacterial Lipopolysaccharides Depends on Epithelium and Tumor Necrosis Factor

Optimisation of the sensitisation conditions for an ovalbumin challenge model of asthma

Nitric Oxide Production and Signaling in Inflammation

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