Summary of the different types of gene expression in response to treatment of different stimulations
| Gene type | TGF-β | LXA4 + TGF-β | BALF | LXA4 + BALF |
| Type I collagen | 323.35±168.07* | 14.87±7.53# | 9.47±3.78* | 5.69±2.77+ |
| Type IV collagen | 27.04±14.46* | 5.81±2.55# | 13.48±3.67* | 1.94±0.98++ |
| N-cadherin | 7.93±0.3** | 1.95±0.37## | 8.51±2.73* | 0.67±0.31++ |
| α-SMA | 22.36±2.93** | 7.24±0.62## | 4.01±1.05* | 1.34±0.62++ |
Data are presented as mean±sem fold change in gene expression over control. Lipoxin A4 (LXA4) reduces primary human lung fibroblast (HLF) collagen production, N-cadherin, SLUG and α-smooth muscle actin (α-SMA) induced by transforming growth factor β (TGF-β) and bronchoalveolar lavage fluid (BALF) from patients with acute respiratory distress syndrome (ARDS). Gene expression of type I collagen, type IV collagen, α-SMA and N-cadherin were increased in HLF induced by TGF-β relative to control group. LXA4 significantly inhibited gene expression of type I collagen, type IV collagen, N-cadherin and α-SMA in HLF induced by TGF-β compared to TGF-β group. Gene expression of type I collagen, type IV collagen, SLUG and α-SMA and were increased in HLF induced by ARDS bronchoalveolar lavage fluid (BALF) relative to control group. LXA4 significantly inhibited gene expression of type I collagen, type IV collagen, α-SMA and SLUG in HLF induced by BALF from patients with ARDS (compared to BALF group). Data are mean±sem of three independent experiments. *: p<0.05; and **: p<0.01 relative to control group, respectively; #: p<0.05, ##: p<0.01 compared with TGF-β group, respectively; +: p<0.05; and ++: p<0.01 compared with the bronchoalveolar lavage fluid (BALF) group, respectively.