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Biology subjects

Planas, A. M.

Publications and source records attributed to Planas, A. M..

3 recordsLinked to original sources

Intravital pH Imaging using the sensor ApHID Reveals Incomplete Lysosomal Acidification in Resident Meningeal Phagocytes.

Tracking lysosomes and quantifying their pH in the living, intact brain has been challenging owing to the lack of suitable in vivo tools. Here we report the use of dextran polymers labeled with the pH sensor ApHID to visualize and quantify lysosomal pH in mouse brain resident phagocytes. ApHID-dextrans delivered systemically are rapidly endocytosed by phagocytes in the meninges -mainly dural and subdural macrophages- and accumulate in lysosomal compartments. Intravital pH imaging revealed a striking heterogeneity in lysosomal acidification, with only ~5% of meningeal phagocytes reaching pH values below 5.0, in marked contrast with measurements in macrophage cell cultures. Photothrombotic ischemic lesions induced progressive lysosomal acidification in local phagocytes, while acute chloroquine treatment led to rapid alkalinization. Our methodology enables direct, quantitative pH measurements without genetic manipulations, and unveils a previously unappreciated heterogeneity in lysosomal acidification among brain-resident myeloid cells.

neuroscience↗

Defensive lipid droplets are PUFA reservoirs driving bacterial clearance and inflammation

Lipid droplets (LDs) rapidly form in infected cells to participate in the defence against microbes. Here, we investigate the involvement of LD lipids in these immune responses. Comparative shotgun and targeted lipidomics demonstrate that in vivo host LDs accumulate polyunsaturated fatty acids (PUFAs). PUFAs arrive at cells from the bloodstream to be further metabolised into complex PUFAs accrued by LD-triglycerides and -phospholipids. Host lipid metabolism is transcriptionally controlled by rapid, transient, and intricate immune programs initiated by pathogen-associated molecular patterns and relayed by cytokines such as interferons (type I and II), interleukins (IL-1{beta}), and tumour necrosis factor. When this lipid and signalling environment is reproduced in cultured macrophages, newly formed LDs accumulate defensive proteins, coordinate the synthesis of complex PUFAs, and become PUFA reservoirs and suppliers. Among LD-PUFAs, the {omega}-6 arachidonic acid is the most actively metabolised during the initial phases of innate immunity. Released from LDs by adipose triglyceride lipase, arachidonic acid is used by macrophages for prostaglandin synthesis, bacterial phagocytosis, and elimination of microbes. Graphical Abstract O_FIG O_LINKSMALLFIG WIDTH=163 HEIGHT=200 SRC="FIGDIR/small/711356v2_ufig1.gif" ALT="Figure 1"> View larger version (107K): org.highwire.dtl.DTLVardef@14d65eorg.highwire.dtl.DTLVardef@5ecc1org.highwire.dtl.DTLVardef@fa99e5org.highwire.dtl.DTLVardef@8d9632_HPS_FORMAT_FIGEXP M_FIG C_FIG

cell biology↗

Age-dependent lipid droplet-rich microglia worsen stroke outcome in old mice

Microglial cells of the aged brain manifest signs of dysfunction that could contribute to the worse neurological outcome of stroke in the elderly. Treatment with colony-stimulating factor-1 receptor antagonists enable transient microglia depletion that can be followed by microglia repopulation after interruption of the treatment, causing no known harm to mice. Using this strategy, we aimed to restore microglia function and ameliorate stroke outcome in aged mice. Cerebral ischemia/reperfusion induces strong innate immune responses in microglia highlighted by prominent type I interferon signaling, together with cellular metabolic perturbances and lipid droplet biogenesis in young mice. In aged mice, a subset of microglia accumulates lipid droplets under steady state and displays exacerbated innate immune responses after stroke. Microglia renewal in old mice reduces the lipid droplet content, prevents the ischemia-induced exaggerated type I interferon response, and improves the neurological outcome of stroke. This study shows that age-dependent lipid droplet-enriched microglia contribute to impair stroke outcome in old mice.

neuroscience↗