LPS-Binding-Protein (LBP), a class I acute phase protein, is capable of enhancing inflammatory cytokine production in response to LPS. It also functions as a bacterial opsonin and potentiates the bacterial killing effect of antimicrobial peptides such as BPI. We have previously found evidence of LBP production within burn wounds and have observed that topical application of recombinant LBP in infected burn wounds leads to enhanced bacterial killing. We therefore hypothesized that bacterial killing within infected burn wounds would be significantly augmented by local topical gene therapy expressing LBP.

Female inbred LBP-knockout (LBPko) mice and matched C57b wild-type (C57BL6) mice received a 25% body surface partial thickness burn. Mice were randomized to receive intradermal injection of adenoviral constructs expressing either rat LBP or beta-galactosidase (control). Seventy-two hours after wound inoculation with P.aeruginosa wounds were harvested for quantitative bacterial cultures.

In both LBPko and C57BL6 treatment with LBP-adenovirus resulted in significantly lower bacterial counts than animals treated with the control adenovirus (p<.04).

Local gene therapy-driven over-expression of LBP can suppress bacterial infection within burn wounds. These findings confirm LBP’s importance in host immune defense against Gram-negative infection and the notion of local gene therapy for the treatment of burn wound infections.