High angular resolution ALMA images of dust and molecules in the SN 1987A ejecta

We present high angular resolution (~80 mas) ALMA continuum images of the SN 1987A system, together with CO J = 2 $\to$ 1, J = 6 $\to$ 5, and SiO J = 5 $\to$ 4 to J = 7 $\to$ 6 images, which clearly resolve the ejecta (dust continuum and molecules) and ring (synchrotron continuum) components. Dust in the ejecta is asymmetric and clumpy, and overall the dust fills the spatial void seen in Hα images, filling that region with material from heavier elements. The dust clumps generally fill the space where CO J = 6 $\to$ 5 is fainter, tentatively indicating that these dust clumps and CO are locationally and chemically linked. In these regions, carbonaceous dust grains might have formed after dissociation of CO. The dust grains would have cooled by radiation, and subsequent collisions of grains with gas would also cool the gas, suppressing the CO J = 6 $\to$ 5 intensity. The data show a dust peak spatially coincident with the molecular hole seen in previous ALMA CO J = 2 $\to$ 1 and SiO J = 5 $\to$ 4 images. That dust peak, combined with CO and SiO line spectra, suggests that the dust and gas could be at higher temperatures than the surrounding material, though higher density cannot be totally excluded. One of the possibilities is that a compact source provides additional heat at that location. Fits to the far-infrared–millimeter spectral energy distribution give ejecta dust temperatures of 18–23 K. We revise the ejecta dust mass to M dust = 0.2–0.4 ${M}_{\odot }$ for carbon or silicate grains, or a maximum of <0.7 ${M}_{\odot }$ for a mixture of grain species, using the predicted nucleosynthesis yields as an upper limit

Author Correction: Early endosome autoantigen 1 regulates IL-1β release upon caspase-1 activation independently of gasdermin D membrane permeabilization

International audienceBackground: Inflammasome-activated IL-1β plays a major role in lung neutrophilic inflammation induced by inhaled silica. However, the exact mechanisms that contribute to the initial production of precursor IL-1β (pro-IL-1β) are still unclear. Here, we assessed the implication of alarmins (IL-1α, IL-33 and HMGB1) in the lung response to silica particles and found that IL-1α is a master cytokine that regulates IL-1β expression. Methods: Pro-and mature IL-1β as well as alarmins were assessed by ELISA, Western Blot or qRT-PCR in macrophage cultures and in mouse lung following nano-and micrometric silica exposure. Implication of these immune mediators in the establishment of lung inflammatory responses to silica was investigated in knockout mice or after antibody blockade by evaluating pulmonary neutrophil counts, CXCR2 expression and degree of histological injury. Results: We found that the early release of IL-1α and IL-33, but not HMGB1 in alveolar space preceded the lung expression of pro-IL-1β and neutrophilic inflammation in silica-treated mice. In vitro, the production of pro-IL-1β by alveolar macrophages was significantly induced by recombinant IL-1α but not by IL-33. Neutralization or deletion of IL-1α reduced IL-1β production and neutrophil accumulation after silica in mice. Finally, IL-1α released by J774 macrophages after in vitro exposure to a range of micro-and nanoparticles of silica was correlated with the degree of lung inflammation induced in vivo by these particles. Conclusions: We demonstrated that in response to silica exposure, IL-1α is rapidly released from pre-existing stocks in alveolar macrophages and promotes subsequent lung inflammation through the stimulation of IL-1β production. Moreover, we demonstrated that in vitro IL-1α release from macrophages can be used to predict the acute inflammogenic activity of silica micro-and nanoparticles