Limits...
Increased nuclear suppressor of cytokine signaling 1 in asthmatic bronchial epithelium suppresses rhinovirus induction of innate interferons.

Gielen V, Sykes A, Zhu J, Chan B, Macintyre J, Regamey N, Kieninger E, Gupta A, Shoemark A, Bossley C, Davies J, Saglani S, Walker P, Nicholson SE, Dalpke AH, Kon OM, Bush A, Johnston SL, Edwards MR - J. Allergy Clin. Immunol. (2015)

Bottom Line: SOCS1 levels were also correlated with asthma-related clinical outcomes.Suppression of virus-induced interferon levels was dependent on SOCS1 nuclear translocation but independent of proteasomal degradation of transcription factors.Nuclear SOCS1 levels were also increased in BECs from asthmatic patients.

View Article: PubMed Central - PubMed

Affiliation: Airway Disease Infection Section, National Heart and Lung Institute, Imperial College London, London, United Kingdom; MRC & Asthma UK Centre in Allergic Mechanisms of Asthma, London, United Kingdom; Centre for Respiratory Infection, Imperial College London, London, United Kingdom.

Show MeSH

Related in: MedlinePlus

SOCS1 overexpression increased RV1B-, IL-1β– and TNF-α–induced CXCL8 promoter activation. BEAS-2B cells were seeded and transfected with SOCS1 or the empty vector control pORF and infected with RV1B or treated with 10 ng/mL IL-1β or TNF-α. SOCS1 overexpression increased RV1B-induced (A), IL-1β–induced (B), and TNF-α–induced (C) CXCL8 promoter activation at 24 hours. Values are presented as means ± SEMs (n = 4 experiments). *P < .05 and ***P < .001, 1-way ANOVA with the Bonferroni multiple comparison test. ns, Not significant.
© Copyright Policy - CC BY
Related In: Results  -  Collection

License
getmorefigures.php?uid=PMC4541718&req=5

dfig4: SOCS1 overexpression increased RV1B-, IL-1β– and TNF-α–induced CXCL8 promoter activation. BEAS-2B cells were seeded and transfected with SOCS1 or the empty vector control pORF and infected with RV1B or treated with 10 ng/mL IL-1β or TNF-α. SOCS1 overexpression increased RV1B-induced (A), IL-1β–induced (B), and TNF-α–induced (C) CXCL8 promoter activation at 24 hours. Values are presented as means ± SEMs (n = 4 experiments). *P < .05 and ***P < .001, 1-way ANOVA with the Bonferroni multiple comparison test. ns, Not significant.

Mentions: Overexpression of SOCS1 also completely suppressed rhinovirus-induced IFN-β and IFN-λ1 promoter activation in primary human BECs (Fig 3, A). In contrast, overexpression of SOCS1 in BEAS-2B cells significantly increased rhinovirus-, IL-1β–, and TNF-α–induced CXCL8 promoter activation (around 20- to 25-fold; see Fig E4 in this article's Online Repository at www.jacionline.org).


Increased nuclear suppressor of cytokine signaling 1 in asthmatic bronchial epithelium suppresses rhinovirus induction of innate interferons.

Gielen V, Sykes A, Zhu J, Chan B, Macintyre J, Regamey N, Kieninger E, Gupta A, Shoemark A, Bossley C, Davies J, Saglani S, Walker P, Nicholson SE, Dalpke AH, Kon OM, Bush A, Johnston SL, Edwards MR - J. Allergy Clin. Immunol. (2015)

SOCS1 overexpression increased RV1B-, IL-1β– and TNF-α–induced CXCL8 promoter activation. BEAS-2B cells were seeded and transfected with SOCS1 or the empty vector control pORF and infected with RV1B or treated with 10 ng/mL IL-1β or TNF-α. SOCS1 overexpression increased RV1B-induced (A), IL-1β–induced (B), and TNF-α–induced (C) CXCL8 promoter activation at 24 hours. Values are presented as means ± SEMs (n = 4 experiments). *P < .05 and ***P < .001, 1-way ANOVA with the Bonferroni multiple comparison test. ns, Not significant.
© Copyright Policy - CC BY
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4541718&req=5

dfig4: SOCS1 overexpression increased RV1B-, IL-1β– and TNF-α–induced CXCL8 promoter activation. BEAS-2B cells were seeded and transfected with SOCS1 or the empty vector control pORF and infected with RV1B or treated with 10 ng/mL IL-1β or TNF-α. SOCS1 overexpression increased RV1B-induced (A), IL-1β–induced (B), and TNF-α–induced (C) CXCL8 promoter activation at 24 hours. Values are presented as means ± SEMs (n = 4 experiments). *P < .05 and ***P < .001, 1-way ANOVA with the Bonferroni multiple comparison test. ns, Not significant.
Mentions: Overexpression of SOCS1 also completely suppressed rhinovirus-induced IFN-β and IFN-λ1 promoter activation in primary human BECs (Fig 3, A). In contrast, overexpression of SOCS1 in BEAS-2B cells significantly increased rhinovirus-, IL-1β–, and TNF-α–induced CXCL8 promoter activation (around 20- to 25-fold; see Fig E4 in this article's Online Repository at www.jacionline.org).

Bottom Line: SOCS1 levels were also correlated with asthma-related clinical outcomes.Suppression of virus-induced interferon levels was dependent on SOCS1 nuclear translocation but independent of proteasomal degradation of transcription factors.Nuclear SOCS1 levels were also increased in BECs from asthmatic patients.

View Article: PubMed Central - PubMed

Affiliation: Airway Disease Infection Section, National Heart and Lung Institute, Imperial College London, London, United Kingdom; MRC & Asthma UK Centre in Allergic Mechanisms of Asthma, London, United Kingdom; Centre for Respiratory Infection, Imperial College London, London, United Kingdom.

Show MeSH
Related in: MedlinePlus