Identification of synthetic peptides that inhibit lipopolysaccharide (LPS) binding to myeloid differentiation protein-2 (MD-2).

Many studies have suggested that the synergic effect of myeloid differential protein-2 (MD-2) on bacterial lipopolysaccharide (LPS) stimulation of toll-like receptor 4 (TLR4) may be a critical step during the LPS-TLR4 response signaling pathway. We performed a bioinformatic analysis on the MD-2 protein and identified the amino acid sequence NH2-FSKGKYKCV-COOH (K128-132) as a possible key sequence involved in the binding between MD-2 and LPS. We then screened a random phage display peptide library using this sequence as bait in order to identify antagonistic peptides.

[Cloning and identification of NF-kappaB p50 Rel homology domain and detection of its autonomous reporter gene activity].

Aim: To clone NF-kappaB p50 Rel homology domain (RHD) gene and construct the "bait" vector in yeast two-hybrid system, and detect the yeast cell toxicity and autonomous reporter gene activity of target gene.

Methods: Total RNA was extracted from human peripheral blood mononuclear cells and NF-kappaB p50 RHD gene was amplified by RT-PCR, and cloned into pGBKT7. The recombinant plasmid was transformed into yeast AH109.

[Changes in human leukocyte antigen-DR expression on monocytes and its value of prediction on infection complication in trauma patients].

Objective: To observe the changes of human leukocyte antigen DR (HLA-DR) expression in monocytes of trauma patients and its value of prediction on infection complications.

Methods: Fifty-four trauma patients were divided into three groups according to severity of injury: severe trauma group injury severity score (ISS) >or=25, moderate trauma group (16or=16) were divided into three groups according to infection or not: no infection group, localized infection group and systemic infection group.

[Effect of severe thoracic trauma combined with endotoxin challenge on phagocytosis function of alveolar macrophages and pulmonary interstitial macrophages].

Objective: To observe the difference of phagocytosis between alveolar macrophages and pulmonary interstitial macrophages, and to investigate their responses to severe thoracic trauma with or without lipopolysaccharide (LPS) challenge.

Methods: A rat model of severe thoracic trauma was reproduced by thoracic impact machine. The alveolar macrophages and interstitial macrophages were isolated before injury and at 2, 4, 8, 16, 24 hours after injury respectively.