HST/NICMOS observations of the GLIMPSE9 stellar cluster

We present HST/NICMOS photometry, and low-resolution K-band spectra of the GLIMPSE9 stellar cluster. The newly obtained color-magnitude diagram shows a cluster sequence with H-Ks =1 mag, indicating an interstellar extinction Aks=1.6\pm0.2 mag. The spectra of the three brightest stars show deep CO band-heads, which indicate red supergiants with spectral type M1-M2. Two 09-B2 supergiants are also identified, which yield a spectrophotometric distance of 4.2\pm0.4 kpc. Presuming that the population is coeval, we derive an age between 15 and 27 Myr, and a total cluster mass of 1600\pm400 Msun, integrated down to 1 Msun. In the vicinity of GLIMPSE9 are several HII regions and SNRs, all of which (including GLIMPSE 9) are probably associated with a giant molecular cloud (GMC) in the inner galaxy. GLIMPSE9 probably represents one episode of massive star formation in this GMC. We have identified several other candidate stellar clusters of the same complex.Comment: 13 pages, 14 figures. accepted for publication in ApJ. A version with high-resolution figures can be found at the following location ftp://ftp.rssd.esa.int/pub/mmessine/ms.pdf New version with updated reference

Phosphoethanolamine Transferase LptA in Haemophilus ducreyi Modifies Lipid A and Contributes to Human Defensin Resistance In Vitro

Haemophilus ducreyi resists the cytotoxic effects of human antimicrobial peptides (APs), including α-defensins, β-defensins, and the cathelicidin LL-37. Resistance to LL-37, mediated by the sensitive to antimicrobial peptide (Sap) transporter, is required for H. ducreyi virulence in humans. Cationic APs are attracted to the negatively charged bacterial cell surface. In other gram-negative bacteria, modification of lipopolysaccharide or lipooligosaccharide (LOS) by the addition of positively charged moieties, such as phosphoethanolamine (PEA), confers AP resistance by means of electrostatic repulsion. H. ducreyi LOS has PEA modifications at two sites, and we identified three genes (lptA, ptdA, and ptdB) in H. ducreyi with homology to a family of bacterial PEA transferases. We generated non-polar, unmarked mutants with deletions in one, two, or all three putative PEA transferase genes. The triple mutant was significantly more susceptible to both α- and β-defensins; complementation of all three genes restored parental levels of AP resistance. Deletion of all three PEA transferase genes also resulted in a significant increase in the negativity of the mutant cell surface. Mass spectrometric analysis revealed that LptA was required for PEA modification of lipid A; PtdA and PtdB did not affect PEA modification of LOS. In human inoculation experiments, the triple mutant was as virulent as its parent strain. While this is the first identified mechanism of resistance to α-defensins in H. ducreyi, our in vivo data suggest that resistance to cathelicidin LL-37 may be more important than defensin resistance to H. ducreyi pathogenesis

Massive stars in the Cl 1813-178 Cluster. An episode of massive star formation in the W33 complex

Young massive (M >10^4 Msun) stellar clusters are a good laboratory to study the evolution of massive stars. Only a dozen of such clusters are known in the Galaxy. Here we report about a new young massive stellar cluster in the Milky Way. Near-infrared medium-resolution spectroscopy with UIST on the UKIRT telescope and NIRSPEC on the Keck telescope, and X-ray observations with the Chandra and XMM satellites, of the Cl 1813-178 cluster confirm a large number of massive stars. We detected 1 red supergiant, 2 Wolf-Rayet stars, 1 candidate luminous blue variable, 2 OIf, and 19 OB stars. Among the latter, twelve are likely supergiants, four giants, and the faintest three dwarf stars. We detected post-main sequence stars with masses between 25 and 100 Msun. A population with age of 4-4.5 Myr and a mass of ~10000 Msun can reproduce such a mixture of massive evolved stars. This massive stellar cluster is the first detection of a cluster in the W33 complex. Six supernova remnants and several other candidate clusters are found in the direction of the same complex.Comment: 11 Figures. Accepted for publication in Ap

Massive Stars In The W33 Giant Molecular Complex

Rich in H II regions, giant molecular clouds are natural laboratories to study massive stars and sequential star formation. The Galactic star-forming complex W33 is located at = ∼ ◦ l 12.8 and at a distance of 2.4 kpc and has a size of ≈10 pc and a total mass of ≈(0.8−8.0) × 105 M⊙. The integrated radio and IR luminosity of W33—when combined with the direct detection of methanol masers, the protostellar object W33A, and the protocluster embedded within the radio source W33 main—mark the region as a site of vigorous ongoing star formation. In order to assess the long-term star formation history, we performed an infrared spectroscopic search for massive stars, detecting for the first time 14 early-type stars, including one WN6 star and four O4–7 stars. The distribution of spectral types suggests that this population formed during the past ∼2–4 Myr, while the absence of red supergiants precludes extensive star formation at ages 6–30 Myr. This activity appears distributed throughout the region and does not appear to have yielded the dense stellar clusters that characterize other star-forming complexes such as Carina and G305. Instead, we anticipate that W33 will eventually evolve into a loose stellar aggregate, with Cyg OB2 serving as a useful, albeit richer and more massive, comparator. Given recent distance estimates, and despite a remarkably similar stellar population, the rich cluster Cl 1813–178 located on the northwest edge of W33 does not appear to be physically associated with W33

LptA contributes to modification of lipid A with PEA.

<p>Negative-ion MALDI-MS spectra of <i>O</i>-LOS from (A) 35000HP<i>ΔptdB</i>, (B) 35000HP<i>ΔptdA</i>, (C) 35000HP<i>ΔlptA</i>, and (D) 35000HP. The Fig shows zoomed images from representative spectra for each strain. The <i>O</i>-deacylated monophosphorylated lipid A (MPLA) was observed at <i>m/z</i> 951.46 or 951.45, this structure plus the addition of PEA was observed at <i>m/z</i> 1074.46 or 1074.47. The MPLA plus PEA was not observed in the 35000HP<i>ΔlptA</i> samples.</p

<i>H</i>. <i>ducreyi</i> PEA transferases confer resistance to α- and β-defensins.

<p>35000HP, 35000HPΔPEAT and 35000HPΔPEAT/pPEAT were tested for resistance to the (A) α-defensin HD-5 (B) β-defensin HBD-3, and (C) human cathelicidin LL-37. Asterisks indicate statistically significant differences from 35000HP (<i>P</i> < 0.05). Complementation with pPEAT restored parental levels of susceptibility to defensins. Data represent average ± standard error of six independent replicates, and statistical significance was determined by Student’s t-test.</p

Bacterial strains and plasmids used in study.

<p>^a StrepR, resistance to streptomycin; Cm^R, resistance to chloramphenicol; AmpR, resistance to ampicillin; KanR, resistance to kanamycin; SpecR, resistance to spectinomycin.</p><p>Bacterial strains and plasmids used in study.</p

Putative <i>H</i>. <i>ducreyi</i> PEA transferases.

<p>Putative <i>H</i>. <i>ducreyi</i> PEA transferases.</p

35000HPΔPEAT is fully virulent in vivo.

<p>^a Volunteers 441 and 442 were inoculated in the first iteration. Volunteers 444, 445, and 446 were inoculated in the second iteration. Volunteer 447 was inoculated in the third iteration. Volunteers 451 and 453 were inoculated in the fourth iteration.</p><p>^b M, Male; F, Female</p><p>^c P, 35000HP (parent); M, 35000HPΔPEAT (mutant)</p><p>^d Mutant-inoculated sites received estimated delivered doses of 56, 112, or 224 CFU.</p><p>^e Mutant-inoculated sites received estimated delivered doses of 40, 80, or 159 CFU.</p><p>35000HPΔPEAT is fully virulent in vivo.</p