Mol Microbiol 1999, 33:1254–1266 PubMedCrossRef Authors’ contribu

Mol Microbiol 1999, 33:1254–1266.PubMedCrossRef Authors’ contributions SM, and SS carried out the elastase assay and lasB reporter assay. HI carried out cross-streak experiments. TK constructed lasB promoter-gfp reporter strains. SM synthesized FRET-AGLA, elastase substrate. MH synthesized acyl-HSLs. JO and NG conceived of the study, and participated click here in its design and coordination and helped to draft

the manuscript. All authors read and approved the final manuscript.”
“Background The procalcitonin (PCT), the precursor for the hormone calcitonin (CT), is composed of 116-aminoacids and has a molecular weight selleck kinase inhibitor of 13 kDa. PCT was discovered by Moya et al. in 1975, but its molecular structure was elucidated nine years later [1, 2]. The primary structure of whole PCT includes some relevant polycationic motifs (2–3 bibasic aminoacids within

a sequence of four) [1]. In sepsis, the marked increase of PCT concentration in serum has been reported [1, 3]. The role of PCT as mediator of the sepsis cascade received much less attention. A pro-inflammatory activity of PCT in the pathogenesis of sepsis has been suggested based on immune-neutralization findings in two animal species [3]. An anti-inflammatory effect of PCT has been reported in very few studies [4–6], where the scarcity of the models/outcomes used does not lead to any firm conclusion. When human recombinant PCT was added to endotoxin-stimulated human whole blood, there was a marked decrease of the pro-inflammatory cytokine TNFα [5]. Interestingly, a reduction in IL-1β by administration of PCT was observed in the same animal model, the septic hamster, used for the first experiment of PCT immune-neutralization [6]. Lipopolysaccharide (LPS), the

principal component of the outer leaflet of the outer membrane of Gram-negative bacteria, is recognized as the most potent microbial mediator implicated BCKDHB in the pathogenesis of sepsis sequelae and septic shock. Lipid A, the hydrophobic anchor of LPS, produces most of the responses after its detection by Toll-like receptor 4 (TLR-4). Some LPS such as Salmonella typhimurium (S. typhimurium) LPS and Escherichia coli (E. coli) LPS, are well known endotoxins of rough and smooth chemotype [7]. Lipid A of S. typhimurium and E. coli LPS is a β1′-6-linked disaccharide of glucosamine, phosphorylated at the 1 and 4′ positions and acylated at the 2, 3, 2′, and 3′ positions with R-3-hydroxymyristate [8]. Therapeutic strategies for the treatment of septic shock in humans are currently focused on neutralization of the LPS molecule and its many deleterious effects [9].

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