Transcriptional profiles of lung macrophage subsets in Mycobacterium Tuberculosis infection
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ABSTRACT:
PROVIDER: PRJNA428925 | ENA |
REPOSITORIES: ENA
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Project description:Mycobacterium tuberculosis (Mtb) infects multiple lung myeloid cell subsets and persists despite innate and adaptive immune responses. However, the mechanisms allowing Mtb to evade elimination by these subsets are not fully understood. Here, we determined that four weeks post infection, after development of adaptive immune responses, CD11clo monocyte-derived lung cells termed MNC1 (mononuclear cell subset 1), harbor more live Mtb compared to alveolar macrophages (AM), neutrophils, and less permissive CD11chi MNC2. Bulk RNA-seq analysis for these subsets identified that lysosome biogenesis pathway is underexpressed in MNC1. Functional assays confirmed that Mtb-permissive MNC1 are deficient in lysosome content, lysosomal acidification, and lysosomal activity compared to AM, and have less nuclear TFEB, a master regulator of lysosome biogenesis. Mtb infection does not alter lysosome deficiency in MNC1. Instead, Mtb recruits MNC1 and MNC2 to the lungs for its spread from AM to these subsets, which depend on Mtb ESX-1 secretion system. Furthermore, nilotinib-mediated TFEB activation enhances lysosome function of primary macrophages in vitro, and MNC1 and MNC2 in vivo, improving control of Mtb infection. Our results suggest that Mtb exploits lysosome-poor monocyte-derived lung cells for persistence; targeting lysosome biogenesis may be an effective approach to host-directed therapy for tuberculosis, enabling permissive lung cells to restrict and kill Mtb through autophagy and other mechanisms.
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2019-10-08 | PXD011958 | Pride
Project description:Resident macrophages are highly abundant in the bladder, playing key roles in directing immunity to uropathogens. Yet, whether they are heterogeneous, where they come from, and precisely how they respond to infection remain largely unknown. We identified two macrophage subsets in mouse bladders with distinct localization, protein expression, and transcriptomes. Using a model of urinary tract infection, we validated our transcriptomics analyses finding that one macrophage subset phagocytosed more bacteria and polarized to a more anti-inflammatory profile, whereas the other subset died rapidly after infection. After resolution of infection, tissue-resident macrophage subsets were partially replaced by monocyte-derived cells with distinct transcriptional profiles. Elimination of these macrophages led to a type 1 biased immune response to challenge infection. Our study brings considerably more knowledge about the biology of bladder resident macrophages and their response to primary and recurrent infection, which may have broader implications for macrophage subsets in other mucosal tissues.
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