Anti-inflammatory actions of aspirin-triggered resolvin D1 (AT-RvD1) in
bronchial epithelial cells stimulated by cigarette smoke extract
Smoking causes several diseases such as chronic obstructive pulmonary
disease (COPD). Aspirin-triggered-resolvin D1 (AT-RvD1) is a lipid
mediator produced during the resolution of inflammation and demonstrates
anti-inflammatory and pro-resolution effects in several inflammatory
experimental models including in the airways. Here we evaluated the role
of AT-RvD1 (100nM) in bronchial epithelial cells (BEAS-2B) stimulated by
cigarette smoke extract (CSE; 1%; 1 cigarette) for 24h. CSE induced the
productions of IL-1β, TNF-α, IL-10, IL-4 and IFN-γ as well as the
activations of NF-κB and STAT3 and the expression of ALX/FPR2 receptor.
AT-RvD1 reduced the IL-1β and TNF-α production and increased the
production of IFN-γ, while the production of IL-4 and IL-10 were not
altered, in the cells stimulated by CSE when compared to CSE group.
These effects were reversed BOC2, an antagonist of ALX/FPR2 receptor for
AT-RvD1. In addition, AT-RvD1 reduced the phosphorylation of NF-κB and
STAT3 when compared to CSE-stimulated BEAS-2B cells. No alteration of
ALX/FPR2 expression was observed by AT-RvD1 when compared to CSE group.
In the human monocytic leukemia cell line, the relative number of copies
of IL-1β and IL-4 was significantly higher in CSE + AT-RvD1 group
compared CSE group, however, the expression of M1 cytokine is more
pronounced than M2 profile. AT-RvD1 could be an important target for the
reduction of inflammation in the airways associated with smoking.