Mouse alveolar
macrophages and human THP-1 macrophages are more
responsive to inflammatory stimuli when Ces1d and CES1 expression
are ablated. (A) Alveolar macrophages from WT and Ces1d−/− mice (male and female) were isolated and pooled to obtain enough
cells, which were then treated with LPS. The levels of PGE2, the most abundant prostaglandin in lung tissues, were determined
in culture supernatants and normalized on cell protein content, left.
The extent of murine Il6 and Tnfa mRNA expression was also determined,
right. (B) Human THP-1 macrophages with ablated CES1 expression were
treated with either LPS (left) or TNFα/IFNγ (right), and
their inflammatory responses were compared to control THP-1 macrophages
(no CES1 knockdown). The expression levels of human IL1b, IL6, TNFa,
and CCL3 (MIP-1α) mRNA are shown. Data are expressed as mean
± SD (n = 3–4 replicate wells), and the
results are representative of two independent experiments (alveolar
macrophages) or three independent experiments (THP-1 macrophages).
Two-way ANOVA assessed significant differences between groups. #p < 0.05, ##p < 0.01, ###p < 0.001, **p < 0.01, and ***p < 0.001; comparisons are indicated. In panel B, ***p < 0.001 for TNFα/IFNγ treatment vs corresponding
untreated controls.