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. 2015 Feb 5;16(1):12. doi: 10.1186/s12931-015-0179-5

Table 2.

Anti-inflammatory effects of roflumilast N-oxide and dexamethasone in human bronchial epithelial cells

A) HBEC; Non-smokers HBEC; Smokers HBEC; COPD
Stimulus Treatment Maximal % inhibition -logIC 50 Maximal % inhibition -logIC 50 Maximal % inhibition -logIC 50
Poly (I:C) 10 μg/mL RNO 58.8 ± 1.4 8.28 ± 0.43 56.6 ± 2.8 8.14 ± 0.21 50.5 ± 1.5 8.28 ± 0.17
DEX 59.2 ± 1.2 8.75 ± 0.21 24.5 ± 7.9* 8.62 ± 0.31 21.6 ± 2.8* 7.84 ± 1.7*#
B) BEAS2B BEAS2B + CSE
Treatment Maximal % inhibition -logIC 50 Maximal % inhibition -logIC 50
Poly (I:C) 10 μg/mL RNO 44.5 ± 1.5 8.07 ± 0.15 44.9 ± 4.7 8.08 ± 0.23
DEX 42.6 ± 2.9 8.06 ± 0.10 27.9 ± 6.7 7.77 ± 0.28

Inhibition of IL-8 release from (A) human primary bronchial epithelial cells (HBECs) from non-smokers (n = 4), smokers (n = 4) and chronic obstructive pulmonary disease patients (COPD; n = 5) or (B) BEAS2B cells exposed with or without cigarette smoke extract (CSE 1%). (A) Cells were incubated with Roflumilast N-oxide (RNO; 0.1 nM- 1 μM) or Dexamethasone (DEX; 0.1 nM- 1 μM) for 1 hour and stimulated with Poly (I:C) 10 μg/ml (TLR3 agonist) for 24 hours. (B) Cells were incubated with or without CSE 1% for 1 hour, followed by incubation with RNO or DEX for 1 hour and stimulated with Poly (I:C) 10 μg/ml for 24 hours. Values are mean ± SEM of 3–5 independent experiments run in triplicate. IC50 values for half-maximum inhibition were calculated by nonlinear regression analysis.*P < 0.05 vs RNO group; # P < 0.05 vs non-smoker and smoker group; P < 0.05 vs non-CSE treated group.