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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.

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SOCS3 mRNA and protein were induced in BECs by rhinovirus and polyI:C. Primary human BECs were infected with RV1B, RV16, or polyI:C (1 μg/mL), and total RNA and total protein were harvested over time. RV1B (A), RV16 (B), and polyI:C (C) all induced SOCS3 mRNA and protein in a time-dependent manner. Values are presented as means ± SEMs (n = 4 experiments). **P < .01 versus medium treatment, 2-way ANOVA.
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dfig2: SOCS3 mRNA and protein were induced in BECs by rhinovirus and polyI:C. Primary human BECs were infected with RV1B, RV16, or polyI:C (1 μg/mL), and total RNA and total protein were harvested over time. RV1B (A), RV16 (B), and polyI:C (C) all induced SOCS3 mRNA and protein in a time-dependent manner. Values are presented as means ± SEMs (n = 4 experiments). **P < .01 versus medium treatment, 2-way ANOVA.

Mentions: We next investigated the ability of the proinflammatory cytokines TNF-α and IL-1β, rhinovirus infection, and polyinosinic-polycytidylic acid (polyI:C; as a mimic of other viral infections) to induce SOCS expression in BECs. We found that TNF-α and IL-1β both induced SOCS1 (Fig 1, B) but not any other SOCS family member, whereas both SOCS1 (Fig 1, C) and SOCS3 (see Fig E2 in this article's Online Repository at www.jacionline.org) were induced by RV1B (representative of minor group rhinoviruses), RV16 (major group), and polyI:C. RV1B and RV16 did not induce SOCS2, SOCS4 through SOCS6, or CISH in BECs. The induction of SOCS1 by RV1B and RV16 was susceptible to UV irradiation and through filtering out virus with a 30-kDa molecular weight filter and was dose dependent (see Fig E1). These data indicate that SOCS1 is induced by proinflammatory cytokines and rhinovirus infection in primary human BECs.


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)

SOCS3 mRNA and protein were induced in BECs by rhinovirus and polyI:C. Primary human BECs were infected with RV1B, RV16, or polyI:C (1 μg/mL), and total RNA and total protein were harvested over time. RV1B (A), RV16 (B), and polyI:C (C) all induced SOCS3 mRNA and protein in a time-dependent manner. Values are presented as means ± SEMs (n = 4 experiments). **P < .01 versus medium treatment, 2-way ANOVA.
© Copyright Policy - CC BY
Related In: Results  -  Collection

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

dfig2: SOCS3 mRNA and protein were induced in BECs by rhinovirus and polyI:C. Primary human BECs were infected with RV1B, RV16, or polyI:C (1 μg/mL), and total RNA and total protein were harvested over time. RV1B (A), RV16 (B), and polyI:C (C) all induced SOCS3 mRNA and protein in a time-dependent manner. Values are presented as means ± SEMs (n = 4 experiments). **P < .01 versus medium treatment, 2-way ANOVA.
Mentions: We next investigated the ability of the proinflammatory cytokines TNF-α and IL-1β, rhinovirus infection, and polyinosinic-polycytidylic acid (polyI:C; as a mimic of other viral infections) to induce SOCS expression in BECs. We found that TNF-α and IL-1β both induced SOCS1 (Fig 1, B) but not any other SOCS family member, whereas both SOCS1 (Fig 1, C) and SOCS3 (see Fig E2 in this article's Online Repository at www.jacionline.org) were induced by RV1B (representative of minor group rhinoviruses), RV16 (major group), and polyI:C. RV1B and RV16 did not induce SOCS2, SOCS4 through SOCS6, or CISH in BECs. The induction of SOCS1 by RV1B and RV16 was susceptible to UV irradiation and through filtering out virus with a 30-kDa molecular weight filter and was dose dependent (see Fig E1). These data indicate that SOCS1 is induced by proinflammatory cytokines and rhinovirus infection in primary human BECs.

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