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
|
| Â |
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.
