1. Nitric oxide inhibits IFN regulatory factor 1 and nuclear factor-κB pathways in rhinovirus- infected epithelial cells 
Rommy Koetzler, MD, MSc, Raza S. Zaheer, BSc, Robert Newton, PhD, David Proud, PhD 
Journal of Allergy and Clinical Immunology 
Volume 124, Issue 3, Pages (September 2009)
DOI: /j.jaci
Copyright © 2009 American Academy of Allergy, Asthma & Immunology Terms and Conditions

2. Fig 1
Selective inhibitors of IKKβ inhibit HRV-16–induced production of CXCL10 from airway epithelial cells. Both PS-1145 (A) and ML120B (B) inhibit, in a concentration-dependent manner, HRV-induced production of CXCL10 from BEAS-2B epithelial cells (n = 6). PS-1145 (C) and ML120B (D), at a concentration of 10 μmol/L, also inhibit HRV-16–induced CXCL10 production from primary cultures of HBEs (n = 3). ∗Statistical significance compared with HRV-16 alone.
Journal of Allergy and Clinical Immunology  , DOI: ( /j.jaci )
Copyright © 2009 American Academy of Allergy, Asthma & Immunology Terms and Conditions

3. Fig 2
PAPA NONOate inhibits NF-κB DNA binding and IκBα phosphorylation. Preincubation of rh p50 for 90 minutes with 500 μmol/L of PAPA NONOate inhibited its ability to bind to either the κB1 (A) or κB2 (B) recognition sequences from the CXCL10 promoter. PAPA NONOate also prevented the HRV-16–induced phosphorylation of IκBα observed 3 hours after infection of BEAS-2B (C) or HBEs (D). All experiments are representative of n ≥ 3.
Journal of Allergy and Clinical Immunology  , DOI: ( /j.jaci )
Copyright © 2009 American Academy of Allergy, Asthma & Immunology Terms and Conditions

4. Fig 3
PAPA NONOate inhibits IRF-1 DNA binding and HRV-16–induced IRF-1 expression. A, Preincubation of rhIRF-1 for 90 minutes with 500 μmol/L of PAPA NONOate inhibits its ability to bind to the ISRE recognition sequence in the CXCL10 promoter (representative of n = 3). B, PAPA NONOate inhibits HRV-16–induced epithelial increases in IRF-1 mRNA in BEAS-2B cells (n = 9). ∗Statistical significance compared to HRV-16 alone. C, PAPA NONOate also inhibits HRV-16–induced expression of IRF-1 protein (representative of n = 3).
Journal of Allergy and Clinical Immunology  , DOI: ( /j.jaci )
Copyright © 2009 American Academy of Allergy, Asthma & Immunology Terms and Conditions

5. Fig 4
Reduction of HRV-16–induced epithelial expression of IRF-1 by selective inhibitors of IKKβ. Both PS-1145 (A; n = 6) and ML120B (B; n = 3) inhibit HRV-16–induced increases in IRF-1 mRNA in BEAS-2B cells. Asterisk indicates statistical significance compared to HRV-16 alone. (C) PS-1145 and ML120B partially inhibit HRV-16–induced expression of IRF-1 protein (representative of n = 3).
Journal of Allergy and Clinical Immunology  , DOI: ( /j.jaci )
Copyright © 2009 American Academy of Allergy, Asthma & Immunology Terms and Conditions

6. Fig 5
Reduced nuclear translocation and binding of IRF-1 in HRV-16–infected epithelial cells treated with selective inhibitors of IKKβ. A, Both PS-1145 and ML120B inhibited HRV-16–induced nuclear translocation and binding of IRF-1 in BEAS-2B cells (representative of n = 3). B, Neither inhibitor directly affected binding of rhIRF-1 to the ISRE recognition sequence from the CXCL10 promoter (representative of n = 3).
Journal of Allergy and Clinical Immunology  , DOI: ( /j.jaci )
Copyright © 2009 American Academy of Allergy, Asthma & Immunology Terms and Conditions