Modulation of the complement system by human beta-defensin 2.

摘要: Objective: Human β-defensin (HBD) and the complement system are two important innate immune mechanisms active against a broad range of burn wound pathogens. However, excessive or uncontrolled activation, following thermal injury, contributes to tissue damage. Previous studies from our laboratory suggested decreased expression HBD-2 in wounds its absence blister fluid. Prior have demonstrated that human neutrophil peptide can bind C1q component prevent activation. The objective this study was determine whether HBD-1 also modulate activity. Methods: binding efficiency determined by utilizing dot blot hybridization. effect on activation classical alternative pathways CH50 AP50 assays. In addition, ability inhibit activity predicted comparison with known inhibitor 2J DNAStar computer modeling study. Results: strong, whereas weak. inhibits pathway significantly without affecting pathway. revealed structural homology inhibitory sequences HBD-2. Conclusion: replacement missing defensin, natural system, may dual protective role not only as an antimicrobial agent but providing protection system.