Comparative Genomics of Host-Symbiont and Free-Living Oceanobacillus Species.

Survival in a given environment requires specific functions, so genomic variation is anticipated within in individual taxonomic groups that exhibit a large diversity in lifestyles. In this study, we sequence and assemble the genome of Oceanobacillus faecalis strain HM6, a resident of the human gut. Using the genus Oceanobacillus and the HM6 draft genome sequence, we explore the functional requirements for survival in a symbiotic arrangement within the human gut, in contrast to free living in the environment. Comparative genomics of seven available Oceanobacillus complete genomes highlight a genomically heterogeneous group. Our analysis did not find strict phylogenetic separation between free-living and host-symbiont Oceanobacillus members. By comparing functional gene content between host-associated and free-living species, we identified candidate genes that are potentially involved in symbiotic lifestyles, including phosphotransferase genes, transporters and two component response regulators. This study summarizes genomic and phylogenetic differences in the Oceanobacillus genus. Additionally, we highlight functions that may be key for survival in the human gut community.

Expression profiling of lymph nodes in tuberculosis patients reveal inflammatory milieu at site of infection.

Extrapulmonary manifestations constitute 15 to 20% of tuberculosis cases, with lymph node tuberculosis (LNTB) as the most common form of infection. However, diagnosis and treatment advances are hindered by lack of understanding of LNTB biology. To identify host response, Mycobacterium tuberculosis infected lymph nodes from LNTB patients were studied by means of transcriptomics and quantitative proteomics analyses. The selected targets obtained by comparative analyses were validated by quantitative PCR and immunohistochemistry. This approach provided expression data for 8,728 transcripts and 102 proteins, differentially regulated in the infected human lymph node. Enhanced inflammation with upregulation of T-helper1-related genes, combined with marked dysregulation of matrix metalloproteinases, indicates tissue damage due to high immunoactivity at infected niche. This expression signature was accompanied by significant upregulation of an immunoregulatory gene, leukotriene A4 hydrolase, at both transcript and protein levels. Comparative transcriptional analyses revealed LNTB-specific perturbations. In contrast to pulmonary TB-associated increase in lipid metabolism, genes involved in fatty-acid metabolism were found to be downregulated in LNTB suggesting differential lipid metabolic signature. This study investigates the tissue molecular signature of LNTB patients for the first time and presents findings that indicate the possible mechanism of disease pathology through dysregulation of inflammatory and tissue-repair processes.