Publication

The novel compound Sul-121 inhibits airway inflammation and hyperresponsiveness in experimental models of chronic obstructive pulmonary disease

Han, B., Poppinga, W. J., Zuo, H., Zuidhof, A. B., Bos, I. S. T., Smit, M., Vogelaar, P., Krenning, G., Henning, R. H., Maarsingh, H., Halayko, A. J., van Vliet, B., Stienstra, S., van der Graaf, A. C., Meurs, H. & Schmidt, M., 27-May-2016, In : Scientific Reports. 6, p. 1-13 13 p., 26928.

Research output: Contribution to journalArticleAcademicpeer-review

APA

Han, B., Poppinga, W. J., Zuo, H., Zuidhof, A. B., Bos, I. S. T., Smit, M., ... Schmidt, M. (2016). The novel compound Sul-121 inhibits airway inflammation and hyperresponsiveness in experimental models of chronic obstructive pulmonary disease. Scientific Reports, 6, 1-13. [26928]. https://doi.org/10.1038/srep26928

Author

Han, Bing ; Poppinga, Wilfred J. ; Zuo, Haoxiao ; Zuidhof, Annet B. ; Bos, I. Sophie T. ; Smit, Marieke ; Vogelaar, Pieter ; Krenning, Guido ; Henning, Robert H. ; Maarsingh, Harm ; Halayko, Andrew J. ; van Vliet, Bernard ; Stienstra, Stef ; van der Graaf, Adrianus Cornelis ; Meurs, Herman ; Schmidt, Martina. / The novel compound Sul-121 inhibits airway inflammation and hyperresponsiveness in experimental models of chronic obstructive pulmonary disease. In: Scientific Reports. 2016 ; Vol. 6. pp. 1-13.

Harvard

Han, B, Poppinga, WJ, Zuo, H, Zuidhof, AB, Bos, IST, Smit, M, Vogelaar, P, Krenning, G, Henning, RH, Maarsingh, H, Halayko, AJ, van Vliet, B, Stienstra, S, van der Graaf, AC, Meurs, H & Schmidt, M 2016, 'The novel compound Sul-121 inhibits airway inflammation and hyperresponsiveness in experimental models of chronic obstructive pulmonary disease', Scientific Reports, vol. 6, 26928, pp. 1-13. https://doi.org/10.1038/srep26928

Standard

The novel compound Sul-121 inhibits airway inflammation and hyperresponsiveness in experimental models of chronic obstructive pulmonary disease. / Han, Bing; Poppinga, Wilfred J.; Zuo, Haoxiao; Zuidhof, Annet B.; Bos, I. Sophie T.; Smit, Marieke; Vogelaar, Pieter; Krenning, Guido; Henning, Robert H.; Maarsingh, Harm; Halayko, Andrew J.; van Vliet, Bernard; Stienstra, Stef; van der Graaf, Adrianus Cornelis; Meurs, Herman; Schmidt, Martina.

In: Scientific Reports, Vol. 6, 26928, 27.05.2016, p. 1-13.

Research output: Contribution to journalArticleAcademicpeer-review

Vancouver

Han B, Poppinga WJ, Zuo H, Zuidhof AB, Bos IST, Smit M et al. The novel compound Sul-121 inhibits airway inflammation and hyperresponsiveness in experimental models of chronic obstructive pulmonary disease. Scientific Reports. 2016 May 27;6:1-13. 26928. https://doi.org/10.1038/srep26928


BibTeX

@article{61abb5cd6a134fdb92df5f063ebb7418,
title = "The novel compound Sul-121 inhibits airway inflammation and hyperresponsiveness in experimental models of chronic obstructive pulmonary disease",
abstract = "COPD is characterized by persistent airflow limitation, neutrophilia and oxidative stress from endogenous and exogenous insults. Current COPD therapy involving anticholinergics, beta(2)-adrenoceptor agonists and/or corticosteroids, do not specifically target oxidative stress, nor do they reduce chronic pulmonary inflammation and disease progression in all patients. Here, we explore the effects of Sul-121, a novel compound with anti-oxidative capacity, on hyperresponsiveness (AHR) and inflammation in experimental models of COPD. Using a guinea pig model of lipopolysaccharide (LPS)-induced neutrophilia, we demonstrated that Sul-121 inhalation dose-dependently prevented LPS-induced airway neutrophilia (up to similar to 60{\%}) and AHR (up to similar to 90{\%}). Non-cartilaginous airways neutrophilia was inversely correlated with blood H2S, and LPS-induced attenuation of blood H2S (similar to 60{\%}) was prevented by Sul-121. Concomitantly, Sul-121 prevented LPS-induced production of the oxidative stress marker, malondialdehyde by similar to 80{\%}. In immortalized human airway smooth muscle (ASM) cells, Sul-121 dose-dependently prevented cigarette smoke extract-induced IL-8 release parallel with inhibition of nuclear translocation of the NF-kappa B subunit, p65 (each similar to 90{\%}). Sul-121 also diminished cellular reactive oxygen species production in ASM cells, and inhibited nuclear translocation of the anti-oxidative response regulator, Nrf2. Our data show that Sul-121 effectively inhibits airway inflammation and AHR in experimental COPD models, prospectively through inhibition of oxidative stress.",
keywords = "GUINEA-PIG MODEL, SMOOTH-MUSCLE-CELLS, ACUTE LUNG INJURY, NF-KAPPA-B, OXIDATIVE STRESS, HYDROGEN-SULFIDE, CIGARETTE-SMOKE, EPITHELIAL BARRIER, REDOX REGULATION, GENE-TRANSCRIPTION",
author = "Bing Han and Poppinga, {Wilfred J.} and Haoxiao Zuo and Zuidhof, {Annet B.} and Bos, {I. Sophie T.} and Marieke Smit and Pieter Vogelaar and Guido Krenning and Henning, {Robert H.} and Harm Maarsingh and Halayko, {Andrew J.} and {van Vliet}, Bernard and Stef Stienstra and {van der Graaf}, {Adrianus Cornelis} and Herman Meurs and Martina Schmidt",
year = "2016",
month = "5",
day = "27",
doi = "10.1038/srep26928",
language = "English",
volume = "6",
pages = "1--13",
journal = "Scientific Reports",
issn = "2045-2322",
publisher = "Nature Publishing Group",

}

RIS

TY - JOUR

T1 - The novel compound Sul-121 inhibits airway inflammation and hyperresponsiveness in experimental models of chronic obstructive pulmonary disease

AU - Han, Bing

AU - Poppinga, Wilfred J.

AU - Zuo, Haoxiao

AU - Zuidhof, Annet B.

AU - Bos, I. Sophie T.

AU - Smit, Marieke

AU - Vogelaar, Pieter

AU - Krenning, Guido

AU - Henning, Robert H.

AU - Maarsingh, Harm

AU - Halayko, Andrew J.

AU - van Vliet, Bernard

AU - Stienstra, Stef

AU - van der Graaf, Adrianus Cornelis

AU - Meurs, Herman

AU - Schmidt, Martina

PY - 2016/5/27

Y1 - 2016/5/27

N2 - COPD is characterized by persistent airflow limitation, neutrophilia and oxidative stress from endogenous and exogenous insults. Current COPD therapy involving anticholinergics, beta(2)-adrenoceptor agonists and/or corticosteroids, do not specifically target oxidative stress, nor do they reduce chronic pulmonary inflammation and disease progression in all patients. Here, we explore the effects of Sul-121, a novel compound with anti-oxidative capacity, on hyperresponsiveness (AHR) and inflammation in experimental models of COPD. Using a guinea pig model of lipopolysaccharide (LPS)-induced neutrophilia, we demonstrated that Sul-121 inhalation dose-dependently prevented LPS-induced airway neutrophilia (up to similar to 60%) and AHR (up to similar to 90%). Non-cartilaginous airways neutrophilia was inversely correlated with blood H2S, and LPS-induced attenuation of blood H2S (similar to 60%) was prevented by Sul-121. Concomitantly, Sul-121 prevented LPS-induced production of the oxidative stress marker, malondialdehyde by similar to 80%. In immortalized human airway smooth muscle (ASM) cells, Sul-121 dose-dependently prevented cigarette smoke extract-induced IL-8 release parallel with inhibition of nuclear translocation of the NF-kappa B subunit, p65 (each similar to 90%). Sul-121 also diminished cellular reactive oxygen species production in ASM cells, and inhibited nuclear translocation of the anti-oxidative response regulator, Nrf2. Our data show that Sul-121 effectively inhibits airway inflammation and AHR in experimental COPD models, prospectively through inhibition of oxidative stress.

AB - COPD is characterized by persistent airflow limitation, neutrophilia and oxidative stress from endogenous and exogenous insults. Current COPD therapy involving anticholinergics, beta(2)-adrenoceptor agonists and/or corticosteroids, do not specifically target oxidative stress, nor do they reduce chronic pulmonary inflammation and disease progression in all patients. Here, we explore the effects of Sul-121, a novel compound with anti-oxidative capacity, on hyperresponsiveness (AHR) and inflammation in experimental models of COPD. Using a guinea pig model of lipopolysaccharide (LPS)-induced neutrophilia, we demonstrated that Sul-121 inhalation dose-dependently prevented LPS-induced airway neutrophilia (up to similar to 60%) and AHR (up to similar to 90%). Non-cartilaginous airways neutrophilia was inversely correlated with blood H2S, and LPS-induced attenuation of blood H2S (similar to 60%) was prevented by Sul-121. Concomitantly, Sul-121 prevented LPS-induced production of the oxidative stress marker, malondialdehyde by similar to 80%. In immortalized human airway smooth muscle (ASM) cells, Sul-121 dose-dependently prevented cigarette smoke extract-induced IL-8 release parallel with inhibition of nuclear translocation of the NF-kappa B subunit, p65 (each similar to 90%). Sul-121 also diminished cellular reactive oxygen species production in ASM cells, and inhibited nuclear translocation of the anti-oxidative response regulator, Nrf2. Our data show that Sul-121 effectively inhibits airway inflammation and AHR in experimental COPD models, prospectively through inhibition of oxidative stress.

KW - GUINEA-PIG MODEL

KW - SMOOTH-MUSCLE-CELLS

KW - ACUTE LUNG INJURY

KW - NF-KAPPA-B

KW - OXIDATIVE STRESS

KW - HYDROGEN-SULFIDE

KW - CIGARETTE-SMOKE

KW - EPITHELIAL BARRIER

KW - REDOX REGULATION

KW - GENE-TRANSCRIPTION

U2 - 10.1038/srep26928

DO - 10.1038/srep26928

M3 - Article

VL - 6

SP - 1

EP - 13

JO - Scientific Reports

JF - Scientific Reports

SN - 2045-2322

M1 - 26928

ER -

ID: 32897241