Effect of allergen provocation on inflammatory cell profile and endothelin‐like immunoreactivity in guinea‐pig airways

Andersson, Sven; Zackrisson, C.; Behrens, K; Hemsén, Anette; Forsberg, K.; Lindén, Magdalena; Lundberg, Jan M.

doi:10.1111/j.1398-9995.1995.tb01159.x

Cited by 22 publications

(13 citation statements)

References 25 publications

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“…In agreement with this, we have also recently detected increased levels of ET-l-LI in BALF from guinea pigs that developed bronchoconstriction after allergen challenge but not in animals where bronchoconstriction was induced by carbachol [19].…”

Section: Discussionsupporting

confidence: 70%

Release of Endothelin-1 into Rat Airways following Sephadex-Induced Inflammation; Modulation by Enzyme Inhibitors and Budesonide

Andersson

Hemsén²,

Zackrisson³

et al. 1996

Respiration

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The intratracheal (i.t.) instillation of Sephadex beads into the rat induced inflammation and a 30-fold increase in the endothelin-1-like immunoreactivity (ET-1-LI) of broncho-alveolar lavage fluid. The levels were highest 24 h after the instillation and had declined significantly after 48 h. At a dose of 1 mg kg^-1 i.t., the glucocorticosteroid budesonide almost abolished this response. Phosphoramidon, which inhibits neutral endopeptidase, an enzyme reported to degrade ET-1 and also to inhibit the endothelin-converting enzyme, potentiated the Sephadex-induced rise in ET-1-LI. Chymostatin and heparin, which are reported to reduce the formation of ET-1, did not affect the increase in ET-l-LI. The present model represents a very reactive system for analyzing the changes in ET-1 levels during inflammation.

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Section: Discussionsupporting

confidence: 70%

Release of Endothelin-1 into Rat Airways following Sephadex-Induced Inflammation; Modulation by Enzyme Inhibitors and Budesonide

Andersson

Hemsén²,

Zackrisson³

et al. 1996

Respiration

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“…When compared with control mice treated with rat IgG (4.4 ± 0.8 x 105 eosinophils/ml), antigen-induced eosinophilia was slightly inhibited by 25 µg of anti-ET antibody (2.5 ± 0.4 X 105 eosinophils/ml) and markedly inhibited with 50 pg of antibody (1.3 ± 0.3 x 105 eosinophils/ml) ( Figure 3). It has previously been reported that ET-like immunoreactivity was increased after allergen provocation is sensitized guineapig airways (19). Taken together, these observations suggest the involvement of endogenous ET in the development of lung granulocyte infiltration after allergen provocation.…”

Section: Resultsmentioning

confidence: 53%

Endothelin receptor antagonists inhibit antigen-induced lung inflammation in mice.

Fujitani¹,

Trifilieff²,

Tsuyuki³

et al. 1997

Am J Respir Crit Care Med

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In this study, we have examined the effect of endothelin (ET) receptor antagonists on lung granulocyte inflammation after antigen challenge in sensitized mice. The antagonists used were BQ-123, an ETA antagonist, BQ-788, an ETB antagonist, and SB209670, an ET(A&B) antagonist. Thirty minutes prior exposure to aerosolized ovalbumin, ET antagonists (50 pmol/mouse) were administered directly into the lungs of sensitized Balb/c mice via the intranasal route. BQ-123 and SB209670 significantly decreased eosinophil number in the bronchoalveolar lavage fluid by 47 and 68%, respectively. Both compounds also inhibited neutrophil infiltration into the lungs. In contrast, BQ-788 did not affect granulocyte infiltration. A similar inhibition of lung eosinophilia was also obtained with an anti-ET antibody applied via the intranasal route. BQ-123 and SB209670, but not BQ-788, significantly increased the production of interferon-gamma (Th1 cytokine) from purified lung Thy1.2+ cells without affecting interleukin-4 and interleukin-5 (Th2 cytokines) secretion. Furthermore, neutralizing antibody against interferon-gamma prevented the inhibitory effect of the ETA antagonist. Taken together, these results suggest an important pathophysiologic role for ET in the development of lung inflammation in asthma and highlight the potential of ET antagonists for the treatment of the disease.

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“…These methods are commonly employed and are fully described elsewhere. 32,33 Percent inhibition of inflammatory cell infiltration into the airways was calculated according to the following equation:…”

Section: Aerodynamic Characterizationmentioning

confidence: 99%

Rehydrated sterically stabilized phospholipid nanomicelles of budesonide for nebulization: physicochemical characterization and in vitro, in vivo evaluations

Sahib¹,

Darwis²,

Peh³

et al. 2011

IJN

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Background: Inhaled corticosteroids provide unique systems for local treatment of asthma or chronic obstructive pulmonary disease. However, the use of poorly soluble drugs for nebulization has been inadequate, and many patients rely on large doses to achieve optimal control of their disease. Theoretically, nanotechnology with a sustained-release formulation may provide a favorable therapeutic index. The aim of this study was to determine the feasibility of using sterically stabilized phospholipid nanomicelles of budesonide for pulmonary delivery via nebulization. Methods: PEG 5000 -DSPE polymeric micelles containing budesonide (BUD-SSMs) were prepared by the coprecipitation and reconstitution method, and the physicochemical and pharmacodynamic characteristics of BUD-SSMs were investigated. Results: The optimal concentration of solubilized budesonide at 5 mM PEG 5000 -DSPE was 605.71 ± 6.38 µg/mL, with a single-sized peak population determined by photon correlation spectroscopy and a particle size distribution of 21.51 ± 1.5 nm. The zeta potential of BUD-SSMs was −28.43 ± 1.98 mV. The percent entrapment efficiency, percent yield, and percent drug loading of the lyophilized formulations were 100.13% ± 1.09%, 97.98% ± 1.95%, and 2.01% ± 0.02%, respectively. Budesonide was found to be amorphous by differential scanning calorimetry, and had no chemical interaction with PEGylated polymer according to Fourier transform infrared spectroscopy. Transmission electron microscopic images of BUD-SSMs revealed spherical nanoparticles. BUD-SSMs exhibited prolonged dissolution behavior compared with Pulmicort Respules ® (P , 0.05). Aerodynamic characteristics indicated significantly higher deposition in the lungs compared with Pulmicort Respules ® . The mass median aerodynamic, geometric standard deviation, percent emitted dose, and the fine particle fraction were 2.83 ± 0.08 µm, 2.33 ± 0.04 µm, 59.13% ± 0.19%, and 52.31% ± 0.25%, respectively. Intratracheal administration of BUD-SSMs 23 hours before challenge (1 mg/kg) in an asthmatic/chronic obstructive pulmonary disease rat model led to a significant reduction in inflammatory cell counts (76.94 ± 5.11) in bronchoalveolar lavage fluid compared with administration of Pulmicort Respules ® (25.06 ± 6.91). Conclusion:The BUD-SSMs system might be advantageous for asthma or chronic obstructive pulmonary disease and other inflammatory airway diseases.

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Effect of allergen provocation on inflammatory cell profile and endothelin‐like immunoreactivity in guinea‐pig airways

Cited by 22 publications

References 25 publications

Release of Endothelin-1 into Rat Airways following Sephadex-Induced Inflammation; Modulation by Enzyme Inhibitors and Budesonide

Release of Endothelin-1 into Rat Airways following Sephadex-Induced Inflammation; Modulation by Enzyme Inhibitors and Budesonide

Endothelin receptor antagonists inhibit antigen-induced lung inflammation in mice.

Rehydrated sterically stabilized phospholipid nanomicelles of budesonide for nebulization: physicochemical characterization and in vitro, in vivo evaluations

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