Figure 5.

Proteolysis of apolipoprotein A-I (apoA-I) impairs its ability to inhibit lipopolysaccharide (LPS)-induced inflammation in vivo and to neutralize endotoxin activity of LPS in vitro. Mice (6–8 per group) were randomized to receive vehicle (PBS), LPS (1 mg/kg), LPS (1 mg/kg) plus apoA-I (10 mg/kg), or LPS (1 mg/kg) plus chymase-treated apoA-I (10 mg/kg). After 3 h, serum was collected, and TNF-α (A) and IL-1β (B) concentrations were measured. Data are means±SD, *P<0.05. C, LPS (1 μg/mL) was mixed with untreated apoA-I and chymase-treated apoA-I (10 μg/mL) and endotoxin activity was measured with kinetic colorimetric limulus amebocyte lysate (LAL) assay. Data represent the means±SD from triplicate wells and are representative of 2 independent experiments.