Thus, lipopolysaccharide-induced activation of monocytes from patients with sepsis may occur through direct binding of lipopolysaccharide to the CD11-CD18 complex or other lipopolysaccharide receptors, whereas binding of the lipopolysaccharide-lipopolysaccharide-binding protein complex to the CD14 receptor may not play a pivotal role in sepsis.
Unraveling of the mechanism of transcriptional activation of the LBP gene, involving three known transcription factors, may contribute to our understanding of the acute-phase response and the pathophysiology of sepsis and septic shock.
The presence of LBP genotypes with the less frequent Gly98 allele was found to be associated with sepsis (p < .02) in male patients, but not in females.
The lipopolysaccharide-binding protein is an acute-phase protein that plays a dominant role in the genesis of sepsis by initiating signal transduction pathways leading to the activation of the inflammatory host response.
In these patients, median (interquartile range) LBP (41.8 [41.1] µg/dL vs. 26.2 [25] µg/dL), CRP (240 [205] mg/L vs. 160 [148] mg/dL) and PCT (5.19 [13.68] µg/L vs. 0.39 [1.09] µg/L) were significantly higher than in patients classified as not having sepsis ( P < 0.001 for all three biomarkers).
Furthermore, meta-analysis of four studies (including the present study) confirmed that rs2232618 within LBP increased the risk of sepsis (OR = 1.75, <i>P</i> < 0.001 for the dominant model; OR = 6.08, <i>P</i> = 0.003 for the recessive model; OR = 2.72, <i>P</i> < 0.001 for the allelic model).