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A Gram-type-negative, obligately anaerobic, selenate-respiring bacterium, strain S4 T , was isolated from activated sludge of a wastewater treatment plant in New Jersey after enrichment with 10 mM selenate as the sole electron acceptor. In addition to its selenate-respiring capability, strain S4T also respired arsenate with acetate as carbon source and electron donor. Fermentative growth was not observed. The optimum growth temperature was 37 6C and optimum pH was pH 7. Phylogenetic analysis of the 16S rRNA gene sequence revealed that strain S4 T is a novel member of the family Deferribacteraceae, with the type strain of Denitrovibrio acetiphilus as its closest cultivated relative, with 91.5 % sequence similarity. The cellular fatty acid profile was composed predominantly of straight-chain fatty acids C 14 : 0 , C 15 : 0 , C 16 : 0 , C 17 : 0 and C 18 : 0 , which distinguishes this organism from its closest relatives. The DNA G+C content was 47.7 mol%. Together, these findings support the conclusion that strain S4 T represents a novel genus and species, for which the name Seleniivibrio woodruffii gen. nov., sp. nov. is proposed. The type strain of Seleniivibrio woodruffii is S4 T (5DSM 24984 T

Epidemiological studies demonstrate a link between exposure to indoor air pollution and cigarette smoke and risk of development of Tuberculosis (TB). The role of ambient air pollution PM in human antimycobacterial immunity has not been studied. We examined the effects of PM (<2.5 and <10 μm diameter, from Mexico City) on Mycobacterium tuberculosis (M.tb)-induced expression of mRNA and protein of human β-defensin 2 and 3 (HBD-2,3, antimicrobial peptides), IL-8 and MCP-1 by qRT-PCR and ELISA, respectively. In addition, cell-mediated growth control of M.tb was measured by colony forming units (CFU) assay. Respiratory alveolar type II epithelial (A549) cells were exposed for 18 hours to PM at 0.1, 1, 10 and 50 μg/mL followed by M.tb exposure at a multiplicity of infection of 10 (MOI 10) for an additional 18 hours. We observed that PM exposure decreased the expression of HBD-2 and HBD-3 (p<0.05), while IL-8 and MCP-1 expression remained unaltered in M.tb-infected A549 cells. Decreased antimicrobial peptide expression was not due to decreased cell viability upon PM exposure (shown by MTS and LDH assay). Interestingly, A549 cells exposed to PM exhibited a decreased capability to control M.tb growth (p<0.05, CFU assays). We conclude that PM inhibits the gene expression and protein production of antimicrobial peptides in A549 cells, thus enhancing intracellular growth of M.tb that could potentially increase the susceptibility to M.tb infection.