Targeting quorum sensing with sodium salicylate modulates immune responses and .

Introduction: Chronic infections are a major clinical challenge in hard-to-heal wounds and implanted devices. is a common causative pathogen that produces numerous virulence factors. Due to the increasing problem of antibiotic resistance, new alternative treatment strategies are needed.

Role of sodium salicylate in quorum sensing, virulence, biofilm formation and antimicrobial susceptibility.

The widespread threat of antibiotic resistance requires new treatment options. Disrupting bacterial communication, quorum sensing (QS), has the potential to reduce pathogenesis by decreasing bacterial virulence. The aim of this study was to investigate the influence of sodium salicylate (NaSa) on QS, virulence production and biofilm formation.

Sodium Salicylate Influences the Biofilm Structure and Susceptibility Towards Silver.

Hard-to-heal wounds are typically infected with biofilm-producing microorganisms, such as which strongly contribute to delayed healing. Due to the global challenge of antimicrobial resistance, alternative treatment strategies are needed. Here, we investigated whether inhibition of quorum sensing (QS) by sodium salicylate in different strains (QS-competent, QS-mutant, and chronic wound strains) influences biofilm formation and tolerance to silver.

A pulsed current electric field alters protein expression creating a wound healing phenotype in human skin cells.

Pulsed current (PC) electric field (EF) devices promote healing in chronic wounds but the underpinning mechanisms are largely unknown. The gap between clinical evidence and mechanistic understanding limits device uptake in clinics. Migration, proliferation and gene/protein expression profiles were investigated in the presence/absence of PCEF, in skin: keratinocytes (NHK); dermal fibroblasts (HDF); dermal microvascular endothelial cells (HDMEC) and macrophages (THP-1).

Sodium salicylate interferes with quorum-sensing-regulated virulence in chronic wound isolates of in simulated wound fluid.

An important factor for delayed healing of chronic wounds is the presence of bacteria. Quorum sensing (QS), a cell density-dependent signalling system, controls the production of many virulence factors and biofilm formation in . Inhibition by sodium salicylate (NaSa) of QS-regulated virulence expression was evaluated in QS-characterized clinical wound isolates of cultured in serum-containing medium.

Amelogenins modulate cytokine expression in LPS-challenged cultured human macrophages.

Amelogenins are enamel matrix proteins with a proven ability to restore tissues in patients with advanced periodontitis and chronic skin wounds. To explore the mechanisms of action of amelogenins in wound inflammation, the in vitro effect on the expression of selected cell mediators involved in inflammation and tissue repair from human monocyte-derived macrophages was studied. Macrophages were treated with amelogenins in serum-enriched medium with simultaneous lipopolysaccharide (LPS) stimulation, for 6, 24 and 72 h, and the conditioned culture medium was analysed for 28 different cytokines.

Enamel matrix derivative stimulates expression and secretion of resistin in mesenchymal cells.

In this study we wanted to identify the effect of enamel matrix derivative (EMD) on adipocytokines, so-called adipokines. Primary human cells of mesenchymal origin (osteoblasts, periodontal ligament cells, mesenchymal stem cells, and pulp cells) and hematopoietic origin (monocytes) were incubated with EMD. The levels of adipokines in cell culture medium were quantified using the Lincoplex human adipocyte panel (Luminex) and by real-time PCR of mRNA isolated from cell lysates.

Amelogenin is phagocytized and induces changes in integrin configuration, gene expression and proliferation of cultured normal human dermal fibroblasts.

Fibroblasts are central in wound healing by expressing important mediators and producing and remodelling extracellular matrix (ECM) components. This study aimed at elucidating possible mechanisms of action of the ECM protein amelogenin on normal human dermal fibroblasts (NHDF). Amelogenin at 100 and 1000 microg/ml increased binding of NHDF via several integrins, including alphavbeta3, alphavbeta5 and alpha5beta1.