Microbiology 2003, 149:1095–1102 PubMedCrossRef 41 Daims H, Luck

Microbiology 2003, 149:1095–1102.PubMedCrossRef 41. Daims H, Lucker S, Wagner M: daime, a novel image analysis program for microbial ecology and biofilm research. Environ Microbiol 2006, 8:200–213.PubMedCrossRef 42. ten Cate JM: Biofilms, a new approach to the microbiology of dental plaque. Odontology 2006, 94:1–9.PubMedCrossRef 43. Listgarten MA: Structure of the microbial flora associated with periodontal health and disease in man. A light and electron microscopic study. J Periodontol 1976, 47:1–18.PubMedCrossRef 44. Marchesi JR, Sato T, Weightman AJ, Martin TA, Fry JC, Hiom SJ, Dymock D, Wade WG: Design and evaluation of useful bacterium-specific

PCR primers that amplify genes coding for bacterial 16S rRNA. Appl Environ Microbiol 1998, 64:795–799.PubMed 45. Rickard AH, Gilbert P, High NJ, Kolenbrander PE, Handley PS: Bacterial coaggregation: an integral process PARP cancer in the development of multi-species biofilms. Trends Microbiol 2003, 11:94–100.PubMedCrossRef Authors’ contributions SS assisted in designing the study, designed and Q-VD-Oph research buy optimized the oligonucleotide probe FIAL, participated in patient sample preparation, carried out dot blot and fluorescence in situ hybridizations,

evaluated the data and drafted the manuscript. BR collected patient samples DMXAA cell line for dot blot hybridization, performed statistical analysis and helped to draft the manuscript. ALG provided the initial idea and participated in designing the study. AP participated in patient sample preparation, dot

blot hybridizations and FISH probe optimization. JH provided the gingival biopsy, participated in patient sample preparation and FISH experiments. MB assisted in probe design and dot blot hybridizations. AF developed the periodontal carriers and collected subgingival biofilms for FISH experiments. UBG was involved in designing the study and supervised the work. AM designed and supervised the study and the experiments, analysed the data and participated in writing. All authors read and approved the final manuscript.”
“Background Iron is required by a wide variety of intracellular bacterial pathogens to achieve full virulence. Deprivation of iron in-vivo and in-vitro severely reduces the pathogenicity of Mycobacterium tuberculosis, Coxiella why burnettii, Legionella pneumophila, and Salmonella typhimurium [1–4]. Attempts to withhold iron by sequestering free iron during infection is a major defense strategy used by many species [5]. Inflammatory signaling cascades during infection lead to a reduction in available free iron and sequestration of iron in the reticuloendothelial system (RES) [6]. On the other hand, iron is needed by host cells for cellular functions and first line defense mechanisms [7]. Iron homeostasis also affects macrophage and lymphocyte effector pathways of the innate and adaptive immune response [6, 8].

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