Int J Food Microbiol 2006, 108:125–129.PubMedCrossRef 30. Liao LF, Lien CF, Lin JL: FTIR study of adsorption and photoreactions of acetic acid on TiO2. Phys Chem Chem Phys 2001, 3:831–837.CrossRef 31. Jackson M, Ramjiawan B, Hewko M, Mantsch

HH: Infrared microscopic functional group mapping and spectral clustering analysis of hypercholesterolemic rabbit liver. Cell Mol Biol 1998, 44:89–98.PubMed 32. Nichols PD, Henson JM, Guckert JB, Nivens DE, White DC: FTIR methods microbial ecology: Analysis of bacteria, bacteria-polymer mixtures and biofilms. J Microbiol Meth 1985, 4:79–94.CrossRef 33. Szalontai B, Nishiyama Y, Gombos Z, Murata N: Membrane dynamics as seen by Fourier transform RAAS inhibitor infrared spectroscopy in a cyanobacterium, Synechocystis PCC 6803. The effects of lipid unsaturation and the protein-tolipid ratio. Biochim Biophys Acta 2000, 1509:409–419.PubMedCrossRef 34. Haris PI, Severcan F: FTIR spectroscopic characterization of protein structure in aqueous and non-aqueous media. J Mol Catal B Enzym 1999, 7:207–221.CrossRef Competing interests None declared. Authors’ contributions Wang YL and Li B designed the experiments and wrote selleck chemicals the paper. Liu BP, Zhou Q, Wu GX and Ibrahim M performed the experiments. Xie GL, Li HY and Sun GC coordinated the project. All authors

have read and approved the manuscript.”
“Background Cystic fibrosis (CF), an inherited disorder caused by mutations in the gene that encodes the cystic fibrosis Resveratrol transmembrane conductance regulator, affects approximately 30,000 Americans, primarily those of Northern European origin [1, 2]. These mutations cause a deficiency in chloride secretion with ensuing accumulation of thick, stagnant mucus within the lung alveoli of the patients [1–4]. Nutrients in the thick mucus facilitate the colonization of various bacterial pathogens, including Pseudomonas aeruginosa, Staphylococcus aureus, and Haemophilus influenzae[3, 5]. Colonization by these pathogens elicits a strong host inflammatory response which leads to destruction of the lung

tissue and, ultimately, death from respiratory failure [1, 6, 7]. P. aeruginosa is one of the significant pathogens in chronic lung infections of CF patients [1, 8]. Among the different factors that contribute to the virulence of P. aeruginosa is its ability to form a biofilm, a community within which bacteria are attached to a substratum or to each other [9]. Within the biofilm, the bacteria are surrounded by extracellular polymeric substance (EPS), which protects them from the effects of the host immune system and from diverse antibiotics [10–12]. Biofilm development occurs in stages that require specific bacterial factors at each stage. For example, during the initial (attachment) stage of biofilm formation, bacteria depend on both the flagellum-mediated swimming motility and the VX-689 price pili-mediated twitching motility [13]. A number of P.