Feldner J, Bredt W, Kahane I: Influence of cell shape and surface charge on attachment of Mycoplasma pneumoniae to glass surfaces. J Bacteriol 1983,153(1):1–5.PubMed 53. Vilei EM, Frey J: Genetic and biochemical characterization of glycerol uptake in Mycoplasma mycoides subsp. mycoides SC: its impact on H(2)O(2) production and virulence. Clin Diagn Lab Immunol 2001,8(1):85–92.PubMed selleck chemicals llc 54. Das K, De la Garza G, Maffi S,

Saikolappan S, Dhandayuthapani S: Methionine sulfoxide reductase A (MsrA) deficient Mycoplasma genitalium shows decreased interactions with host cells. PLoS One 2012,7(4):e36247.PubMedCrossRef 55. Dhandayuthapani S, Mudd M, Deretic V: Interactions of OxyR with the promoter region of the oxyR and ahpC genes from Mycobacterium leprae and Mycobacterium tuberculosis . J Bacteriol 1997,179(7):2401–2409.PubMed EMD 1214063 56. Dhandayuthapani S, Blaylock MW, Bebear CM, Rasmussen WG, Baseman JB: Peptide methionine sulfoxide reductase (MsrA) is a virulence determinant in Mycoplasma genitalium . J Bacteriol 2001,183(19):5645–5650.PubMedCrossRef 57. Gaydos C, Maldeis NE, Hardick A, Hardick J, Quinn TC: Mycoplasma genitalium as a contributor

to the multiple etiologies of cervicitis in women attending sexually transmitted disease clinics. Sex Transm Dis 2009,36(10):598–606.PubMedCrossRef 58. Nourooz-Zadeh J, Tajaddini-Sarmadi J, Wolff SP: Measurement of plasma hydroperoxide concentrations by the ferrous oxidation-xylenol orange assay in conjunction with triphenylphosphine.

Anal Biochem 1994,220(2):403–409.PubMedCrossRef 59. Saikolappan S, Das K, Sasindran SJ, Jagannath C, Dhandayuthapani S: OsmC proteins of Mycobacterium tuberculosis and Mycobacterium smegmatis protect against organic hydroperoxide stress. Tuberculosis (Edinb) 2011,91(Suppl 1):S119–127.CrossRef Competing interests The authors have no competing interests to declare. Authors’ contributions SD designed 5-FU manufacturer the study; MAM performed the overexpression of MG207 and phosphatase assay; KD performed all experiments involving microscopes, M. genitalium viability assays and glycerol utilization assays; SS performed the Southern blot and FOX assay, LAM helped in designing some experiments and writing the manuscript; KD analyzed the data and created the figures; SD wrote the manuscript. All authors have read and approved the manuscript.”
“Background Alveolar macrophages (MØ) represent the host’s first line of defense against Mycobacterium tuberculosis (Mtb). Phagocytosed Mtb bacilli are subjected to degradation via oxygen-dependent and -independent mechanisms. In the oxygen-dependent mechanism, MØ produce a variety of powerful mediators such as reactive oxygen species (ROS) and reactive nitrogen intermediates (RNI) that kill bacteria [1, 2]. The first step in the activation of innate host defenses against Mtb is the recognition of the pathogen. Host receptors involved in bacterial recognition and phagocytosis include complement receptors and pattern recognition receptors.