Steroids and extracellular signal-regulated kinase 1/2 activity suppress activating transcription factor 3 expression in patients with severe asthma

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Presentation transcript:

Steroids and extracellular signal-regulated kinase 1/2 activity suppress activating transcription factor 3 expression in patients with severe asthma Lucie Roussel, PhD, Stephanie Robins, BSc, Amanda Schachter, BSc, Julie Bérubé, MSc, Qutayba Hamid, MD, PhD, Simon Rousseau, PhD Journal of Allergy and Clinical Immunology Volume 127, Issue 6, Pages 1632-1634 (June 2011) DOI: 10.1016/j.jaci.2011.03.034 Copyright © 2011 American Academy of Allergy, Asthma & Immunology Terms and Conditions

Fig 1 ATF3 expression is lost in patients with severe asthma compared to mild asthmatics. A, ATF3 mRNA abundance (PCR primers: ATF3 reverse, 5′- TTT CTT TCT CGT CGC CTC TTT T -3′; ATF3 forward, 5′- AAG TGA GTG CTT CTG CCA TC -3′). ∗P < .05, patients with mild asthma compared with control subjects. #P < .05, patients with severe asthma compared with patients with mild asthma (ANOVA followed by Bonferroni multiple comparison test). GAPDH, Glyceraldehyde 3-phosphate dehydrogenase. B, ATF3 localization. End, Endothelial cells; Ep, epithelial cells; I, inflammatory cells; SM, smooth muscle cells. Panels are ×200 magnifications, and the insert is the isotype control. C, Percentages of neutrophils and eosinophils in WBCs of sputum from patients with severe asthma determined as published in Hastie et al.1 D, Use and dosage of oral and inhaled glucocorticoids in patients with mild (M) and severe (S) asthma. N/A, Not applicable. Journal of Allergy and Clinical Immunology 2011 127, 1632-1634DOI: (10.1016/j.jaci.2011.03.034) Copyright © 2011 American Academy of Allergy, Asthma & Immunology Terms and Conditions

Fig 2 Steroids and ERK1/ERK2 activity suppress TNF-α–driven ATF3 expression. Airway smooth muscle cells (A), human microvascular endothelial cells (HMEC-1; B), and airway epithelial cells (Beas-2B; C) were left untreated or pretreated with 100 nmol/L dexamethasone (DEX), 2 μmol/L PD184352, or 0.1 μmol/L BIRB0796 for 1 hour before exposure to 10 ng/mL TNF-α for 8 hours. ATF3 mRNA levels were measured as in Fig 1. ∗P < .05, TNF-α treated compared with unstimulated. #P < .05, dexamethasone or PD184352 treated compared with TNF-α treated. GAPDH, Glyceraldehyde 3-phosphate dehydrogenase. Journal of Allergy and Clinical Immunology 2011 127, 1632-1634DOI: (10.1016/j.jaci.2011.03.034) Copyright © 2011 American Academy of Allergy, Asthma & Immunology Terms and Conditions

Fig 3 TLR3 and TLR9 agonists are the most potent inducers of ATF3 expression in epithelial cells. Beas-2B cells were left untreated or pretreated with 100 nmol/L dexamethasone and incubated 24 hours in the absence or presence of Pam3CSK4 (1 μg/mL), heat-killed Listeria monocytogenes (HKLM; 108 cells/mL), Poly I:C (10 μg/mL), Escherichia coli K12 LPS (100 ng/mL), Salmonella typhimurium flagellin (100 ng/mL), FSL-1 (1 μg/mL, a synthetic diacylated lipoprotein), imiquimod (1 μg/mL), ssRNA40 (1 μg/mL), or ODN2006 (2 μmol/L). The TLR activated is indicated in brackets. ATF3 mRNA levels were measured as in Fig 1. ∗P < .05, TLR agonist treated compared with unstimulated. #P < .05, dexamethasone compared with respective TLR agonist. GAPDH, Glyceraldehyde 3-phosphate dehydrogenase. Journal of Allergy and Clinical Immunology 2011 127, 1632-1634DOI: (10.1016/j.jaci.2011.03.034) Copyright © 2011 American Academy of Allergy, Asthma & Immunology Terms and Conditions