Meth Cell Sci 1998, 20: 223–231.CrossRef 39. Guggenheim B, Gmür R, Galicia JC, Stathopoulou P, Benakanakere MR, Meier A, Thurnheer T, Kinane D: In vitro modeling of host-parasite interactions: the ‘subgingival’ biofilm challenge of primary human epithelial cells. BMC Microbiol 2009, 9: 280.PubMedCrossRef p53 activator 40. Amann RI, Navitoclax concentration Binder BJ, Olson RJ, Chisholm SW, Devereux R, Stahl DA: Combination of 16S rRNA-targeted oligonucleotide probes with flow cytometry for analyzing mixed microbial populations. Appl Environ Microbiol 1990, 56: 1919–1925.PubMed Authors’ contributions BQ and HLS carried out and read FISH analyses. VZ and

TT contributed to probe design and editing of the manuscript. EG and BG designed and carried out the in situ study and participated in editing selleck chemical the manuscript. RG designed the project and the probes, analyzed FISH experiments and wrote the manuscript. All authors read and approved the final manuscript. The authors declare no conflict of interest.”
“Background Staphylococcus aureus is an opportunistic pathogen that causes a wide range of diseases in both immunologically normal and compromised hosts. The natural habitat of S. aureus is the nasal cavity of warm-blooded animals. Over the past ~50 years, S. aureus has undergone genetic changes that have resulted

in antibiotic-resistant strains [1, 2]. Importantly, the methicillin-resistant strains (MRSA) are now the Org 27569 most common cause of nosocomial S. aureus infections and are spreading throughout communities [3]. Staphylococcus aureus has a number of characteristics that allow it

to survive host bactericidal factors and environmental stresses, including drastic changes in osmotic pressure [4–6]. Osmoprotectants such as choline, glycine betaine, and proline accumulate in cells in response to osmotic stress [7–11]. Multiple genes, including the branched-chain amino acid transporter gene brnQ [12] and the arsenic operon regulatory gene arsR [13], cooperatively participate in salt tolerance. In addition, a very large cell wall protein, Ebh, is involved in tolerance to transient hyperosmotic pressure [14]. In general strategy, the phospholipid composition of bacteria changes in response to growth phase or environmental stressors such as osmolality [15], pH [16, 17], temperature, and the presence of organic solvents [18, 19]. In the 1970s, the molecular mechanism of staphylococcal salt resistance was studied, focusing on a phospholipid, cardiolipin (CL) [20]. CL possesses four acyl groups and carries two negative charges [21]. In stationary phase, 30% of the S. aureus cell membrane is composed of CL [22]. It has been reported that CL can stabilize liposomes during osmotic stress [23] and that it is required for the growth of Escherichia coli and Bacillus subtilis under high-salt conditions [24, 25].