1 research outputs found
Supplementary Material for: Antibacterial Defense of Human Airway Epithelial Cells from Chronic Obstructive Pulmonary Disease Patients Induced by Acute Exposure to Nontypeable Haemophilus influenzae: Modulation by Cigarette Smoke
<p>Antimicrobial proteins and peptides (AMPs) are a central component of
the antibacterial activity of airway epithelial cells. It has been
proposed that a decrease in antibacterial lung defense contributes to an
increased susceptibility to microbial infection in smokers and patients
with chronic obstructive pulmonary disease (COPD). However, whether
reduced AMP expression in the epithelium contributes to this lower
defense is largely unknown. We investigated the bacterial killing
activity and expression of AMPs by air-liquid interface-cultured primary
bronchial epithelial cells from COPD patients and non-COPD (ex-)smokers
that were stimulated with nontypeable <i>Haemophilus influenzae </i>(NTHi).
In addition, the effect of cigarette smoke on AMP expression and the
activation of signaling pathways was determined. COPD cell cultures
displayed reduced antibacterial activity, whereas smoke exposure
suppressed the NTHi-induced expression of AMPs and further increased
IL-8 expression in COPD and non-COPD cultures. Moreover, smoke exposure
impaired NTHi-induced activation of NF-κB, but not MAP-kinase signaling.
Our findings demonstrate that the antibacterial activity of cultured
airway epithelial cells induced by acute bacterial exposure was reduced
in COPD and suppressed by cigarette smoke, whereas inflammatory
responses persisted. These findings help to explain the imbalance
between protective antibacterial and destructive inflammatory innate
immune responses in COPD.</p