Galaxy And Mass Assembly (GAMA)

The GAMA survey aims to deliver 250,000 optical spectra (3--7Ang resolution) over 250 sq. degrees to spectroscopic limits of r_{AB} <19.8 and K_{AB}<17.0 mag. Complementary imaging will be provided by GALEX, VST, UKIRT, VISTA, HERSCHEL and ASKAP to comparable flux levels leading to a definitive multi-wavelength galaxy database. The data will be used to study all aspects of cosmic structures on 1kpc to 1Mpc scales spanning all environments and out to a redshift limit of z ~ 0.4. Key science drivers include the measurement of: the halo mass function via group velocity dispersions; the stellar, HI, and baryonic mass functions; galaxy component mass-size relations; the recent merger and star-formation rates by mass, types and environment. Detailed modeling of the spectra, broad SEDs, and spatial distributions should provide individual star formation histories, ages, bulge-disc decompositions and stellar bulge, stellar disc, dust disc, neutral HI gas and total dynamical masses for a significant subset of the sample (~100k) spanning both the giant and dwarf galaxy populations. The survey commenced March 2008 with 50k spectra obtained in 21 clear nights using the Anglo Australian Observatory's new multi-fibre-fed bench-mounted dual-beam spectroscopic system (AAOmega).Comment: Invited talk at IAU 254 (The Galaxy Disk in Cosmological Context, Copenhagen), 6 pages, 5 figures, high quality PDF version available at http://www.eso.org/~jliske/gama

Galaxy And Mass Assembly (GAMA): trends in galaxy colours, morphology, and stellar populations with large-scale structure, group, and pair environments

We explore trends in galaxy properties with Mpc-scale structures using catalogues of environment and large-scale structure from the Galaxy And Mass Assembly (GAMA) survey. Existing GAMA catalogues of large-scale structure, group, and pair membership allow us to construct galaxy stellar mass functions for different environmental types. To avoid simply extracting the known underlying correlations between galaxy properties and stellar mass, we create a mass matched sample of galaxies with stellar masses within 9.5 ≤ log M*/h−2 M⊙ ≤ 11 for each environmental population. Using these samples, we show that mass normalized galaxies in different large-scale environments have similar energy outputs, u − r colours, luminosities, and morphologies. Extending our analysis to group and pair environments, we show that galaxies that are not in groups or pairs exhibit similar characteristics to each other regardless of broader environment. For our mass controlled sample, we fail to see a strong dependence of Sérsic index or galaxy luminosity on halo mass, but do find that it correlates very strongly with colour. Repeating our analysis for galaxies that have not been mass controlled introduces and amplifies trends in the properties of galaxies in pairs, groups, and large-scale structure, indicating that stellar mass is the most important predictor of the galaxy properties we examine, as opposed to environmental classifications

Galaxy And Mass Assembly (GAMA) : trends in galaxy colours, morphology, and stellar populations with large-scale structure, group, and pair environments

We explore trends in galaxy properties with Mpc-scale structures using catalogues of environment and large-scale structure from the Galaxy And Mass Assembly (GAMA) survey. Existing GAMA catalogues of large-scale structure, group, and pair membership allow us to construct galaxy stellar mass functions for different environmental types. To avoid simply extracting the known underlying correlations between galaxy properties and stellar mass, we create a mass matched sample of galaxies with stellar masses within 9.5 ≤ log M*/h−2 M⊙ ≤ 11 for each environmental population. Using these samples, we show that mass normalized galaxies in different large-scale environments have similar energy outputs, u − r colours, luminosities, and morphologies. Extending our analysis to group and pair environments, we show that galaxies that are not in groups or pairs exhibit similar characteristics to each other regardless of broader environment. For our mass controlled sample, we fail to see a strong dependence of Sérsic index or galaxy luminosity on halo mass, but do find that it correlates very strongly with colour. Repeating our analysis for galaxies that have not been mass controlled introduces and amplifies trends in the properties of galaxies in pairs, groups, and large-scale structure, indicating that stellar mass is the most important predictor of the galaxy properties we examine, as opposed to environmental classifications.Publisher PDFPeer reviewe

The Staphylococcus aureus superantigen SElX is a bifunctional toxin that inhibits neutrophil function:SElX Inhibits Neutrophil Function

Bacterial superantigens (SAgs) cause Vβ-dependent T-cell proliferation leading to immune dysregulation associated with the pathogenesis of life-threatening infections such as toxic shock syndrome, and necrotizing pneumonia. Previously, we demonstrated that staphylococcal enterotoxin-like toxin X (SElX) from Staphylococcus aureus is a classical superantigen that exhibits T-cell activation in a Vβ-specific manner, and contributes to the pathogenesis of necrotizing pneumonia. Here, we discovered that SElX can also bind to neutrophils from human and other mammalian species and disrupt IgG-mediated phagocytosis. Site-directed mutagenesis of the conserved sialic acid-binding motif of SElX abolished neutrophil binding and phagocytic killing, and revealed multiple glycosylated neutrophil receptors for SElX binding. Furthermore, the neutrophil binding-deficient mutant of SElX retained its capacity for T-cell activation demonstrating that SElX exhibits mechanistically independent activities on distinct cell populations associated with acquired and innate immunity, respectively. Finally, we demonstrated that the neutrophil-binding activity rather than superantigenicity is responsible for the SElX-dependent virulence observed in a necrotizing pneumonia rabbit model of infection. Taken together, we report the first example of a SAg, that can manipulate both the innate and adaptive arms of the human immune system during S. aureus pathogenesis

Manipulation of Innate and Adaptive Immunity by Staphylococcal Superantigens

Staphylococcal superantigens (SAgs) constitute a family of potent exotoxins secreted by Staphylococcus aureus and other select staphylococcal species. SAgs function to cross-link major histocompatibility complex (MHC) class II molecules with T cell receptors (TCRs) to stimulate the uncontrolled activation of T lymphocytes, potentially leading to severe human illnesses such as toxic shock syndrome. The ubiquity of SAgs in clinical S. aureus isolates suggests that they likely make an important contribution to the evolutionary fitness of S. aureus. Although the apparent redundancy of SAgs in S. aureus has not been explained, the high level of sequence diversity within this toxin family may allow for SAgs to recognize an assorted range of TCR and MHC class II molecules, as well as aid in the avoidance of humoral immunity. Herein, we outline the major diseases associated with the staphylococcal SAgs and how a dysregulated immune system may contribute to pathology. We then highlight recent research that considers the importance of SAgs in the pathogenesis of S. aureus infections, demonstrating that SAgs are more than simply an immunological diversion. We suggest that SAgs can act as targeted modulators that drive the immune response away from an effective response, and thus aid in S. aureus persistence

The Streptococcus pyogenes hyaluronic acid capsule promotes experimental nasal and skin infection by preventing neutrophil-mediated clearance.

Streptococcus pyogenes is a globally prominent human-specific pathogen responsible for an enormous burden of human illnesses, including >600 million pharyngeal and >100 million skin infections each year. Despite intensive efforts that focus on invasive indications, much remains unknown about this bacterium in its natural state during colonization of the nasopharynx and skin. Using acute experimental infection models in HLA-transgenic mice, we evaluated how the hyaluronic acid (HA) capsule contributes to S. pyogenes MGAS8232 infection within these limited biological niches. Herein, we demonstrate that HA capsule expression promotes bacterial burden in murine nasal turbinates and skin lesions by resisting neutrophil-mediated killing. HA capsule production is encoded by the hasABC operon and compared to wildtype S. pyogenes infections, mice infected with a ΔhasA mutant exhibited over a 1000-fold CFU reduction at 48-hours post-nasal challenge, and a 10,000-fold CFU reduction from skin lesions 72-hours post-skin challenge. HA capsule expression contributed substantially to skin lesion size development following subdermal inoculations. In the absence of capsule expression, S. pyogenes revealed drastically impeded growth in whole human blood and increased susceptibility to killing by isolated neutrophils ex vivo, highlighting its important role in resisting phagocytosis. Furthermore, we establish that neutrophil depletion in mice recovered the reduced burden by the ΔhasA mutant in both the nasopharynx and skin. Together, this work confirms that the HA capsule is a key virulence determinant during acute infections by S. pyogenes and demonstrates that its predominant function is to protect S. pyogenes against neutrophil-mediated killing

Early clearance of the HA capsule-deficient mutant from murine nasal turbinates is due to enhanced susceptibility to neutrophil-mediated killing.

(A) Schematic outline for in vivo depletion of neutrophils with injections of 250 μg (500 μg total) of αLy6G or isotype control rat IgG2a 24 h prior to and 24 h post-intranasal challenge with 108 CFUs of S. pyogenes wildtype or ΔhasA mutant strains. (B) Representative flow cytometric analyses of nasal and blood innate immune cells from the neutrophil depletion experiments at 48 h. Flow plots show live cells that were negative for CD4, CD45R and CD19, and gates were set on Ly6G+ and F4/80- cells for neutrophils, and Ly6G- and F4/80+ for macrophage populations. Percentage of innate immune cell populations from either nasal cell extracts (C) or blood (D) for the indicated treatment groups as percentage of live cells. Data points represent individual mice and the bars represent the mean. Significance was determined by Mann-Whitney test (*, P (E) Neutrophil effects on S. pyogenes survival in the nasopharynx. Data points represent CFUs from cNTs of individual mice 24 and 48 h post-infection. Horizontal bars represent the geometric mean. The horizontal dotted line indicates limit of detection. Significance was determined by two-way ANOVA with Tukey’s multiple comparisons (*, P P P Biorender.com.</p

Cytokine response in nasal turbinates of B6_HLA mice during streptococcal infection.

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The <i>S</i>. <i>pyogenes</i> HA capsule inhibits host cell invasion but promotes survival from neutrophil-mediated killing.

Binding of S. pyogenes to wells pre-coated with 1 μg of human ECM components (A) fibronectin and (B) collagen type IV. (C) Adhesion of S. pyogenes to D562 pharyngeal epithelial cells. Confluent cell monolayers were cultured with S. pyogenes (MOI of 100) for 2 h at 37°C + 5% CO2. Cells were washed with PBS and lysed with Triton X-100 for enumerating remaining adherent bacteria. (D) Internalization of S. pyogenes into D562 cells. Confluent D562 cells were cultured with S. pyogenes (MOI of 100) for 2 h at 37°C + 5% CO2 followed by 1 h in media supplemented with 100 μg mL-1 of gentamycin. Bars represent mean CFUs ± SEM and each dot represents a biological replicate. Statistical differences were evaluated by unpaired t-test (A–C) (**, P P D) one-way ANOVA (*, P P (E) Whole human blood survival assay. Heparinized blood from human donors were inoculated with ~103 CFUs of S. pyogenes MGAS8232 at 37°C with rotation for 3 h. Data points represent geometric mean CFUs ± SD at each timepoint (n ≥ 3). Statistical significance was determined using one-way ANOVA with Friedman test (***, P (F) Neutrophil survival assay. Neutrophils were isolated from human blood by density centrifugation and inoculated with opsonized S. pyogenes at a MOI of 10. Surviving bacteria were enumerated after 60 mins at 37°C with rotation and calculated as the difference between survival in the no neutrophil control and in the presence of neutrophils. Each data point represents S. pyogenes CFUs from an individual donor. Data shown are the means of percent survival ± SD. Statistical analyses were performed using one-way ANOVA with Kruskal-Wallis test (*, P < 0.05).</p