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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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SOCS1 mRNA and protein were induced in primary BECs by viruses and cytokines important in asthma pathogenesis. A, The TH2 cytokines IL-4 and IL-13 both induced SOCS1 mRNA and protein in a time-dependent manner. B, The proinflammatory cytokines TNF-α and IL-1β also induced SOCS1 mRNA and protein in a time-dependent manner. C, RV1B, RV16, and 1 μg/mL polyI:C all induced SOCS1 mRNA and protein in a time-dependent manner. *P < .05 versus medium-treated cells.
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fig1: SOCS1 mRNA and protein were induced in primary BECs by viruses and cytokines important in asthma pathogenesis. A, The TH2 cytokines IL-4 and IL-13 both induced SOCS1 mRNA and protein in a time-dependent manner. B, The proinflammatory cytokines TNF-α and IL-1β also induced SOCS1 mRNA and protein in a time-dependent manner. C, RV1B, RV16, and 1 μg/mL polyI:C all induced SOCS1 mRNA and protein in a time-dependent manner. *P < .05 versus medium-treated cells.

Mentions: SOCS3 mRNA expression is increased in T cells in asthmatic patients,20 but upregulation of SOCS1 by IL-13 in airway smooth muscle cells from asthmatic patients is impaired.22 Thus whether SOCS proteins are upregulated in asthmatic patients is uncertain, and whether SOCS proteins are upregulated in cells that are infected by respiratory tract viruses is unknown. Therefore we first investigated the effects of the TH2 cytokines IL-4 and IL-13 on SOCS1 through SOCS6 and CISH mRNA and protein expression in BECs because these cytokines are strongly implicated in asthma pathogenesis.29,30 IL-4 and IL-13 both induced SOCS1 mRNA and protein expression (Fig 1, A). Densitometric analysis for the Western blots in Fig 1 are shown in Fig E1 in this article's Online Repository at www.jacionline.org. No other SOCS proteins/mRNAs were induced by IL-4 or IL-13, with the exception of CISH, which was significantly induced by both.


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 mRNA and protein were induced in primary BECs by viruses and cytokines important in asthma pathogenesis. A, The TH2 cytokines IL-4 and IL-13 both induced SOCS1 mRNA and protein in a time-dependent manner. B, The proinflammatory cytokines TNF-α and IL-1β also induced SOCS1 mRNA and protein in a time-dependent manner. C, RV1B, RV16, and 1 μg/mL polyI:C all induced SOCS1 mRNA and protein in a time-dependent manner. *P < .05 versus medium-treated cells.
© Copyright Policy - CC BY
Related In: Results  -  Collection

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

fig1: SOCS1 mRNA and protein were induced in primary BECs by viruses and cytokines important in asthma pathogenesis. A, The TH2 cytokines IL-4 and IL-13 both induced SOCS1 mRNA and protein in a time-dependent manner. B, The proinflammatory cytokines TNF-α and IL-1β also induced SOCS1 mRNA and protein in a time-dependent manner. C, RV1B, RV16, and 1 μg/mL polyI:C all induced SOCS1 mRNA and protein in a time-dependent manner. *P < .05 versus medium-treated cells.
Mentions: SOCS3 mRNA expression is increased in T cells in asthmatic patients,20 but upregulation of SOCS1 by IL-13 in airway smooth muscle cells from asthmatic patients is impaired.22 Thus whether SOCS proteins are upregulated in asthmatic patients is uncertain, and whether SOCS proteins are upregulated in cells that are infected by respiratory tract viruses is unknown. Therefore we first investigated the effects of the TH2 cytokines IL-4 and IL-13 on SOCS1 through SOCS6 and CISH mRNA and protein expression in BECs because these cytokines are strongly implicated in asthma pathogenesis.29,30 IL-4 and IL-13 both induced SOCS1 mRNA and protein expression (Fig 1, A). Densitometric analysis for the Western blots in Fig 1 are shown in Fig E1 in this article's Online Repository at www.jacionline.org. No other SOCS proteins/mRNAs were induced by IL-4 or IL-13, with the exception of CISH, which was significantly induced by both.

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