Ornithine-A urea cycle metabolite enhances autophagy and controls Mycobacterium tuberculosis infection
Kupffer cells are more resistant to M. tuberculosis when compared with alveolar macrophages. Here the authors show that this distinction is caused by the presence of ornithine and imidazole in Kupffer cells and that these metabolites can drive autophagy and M. tuberculosis killing in alveolar macrop...
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2020-07-01
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Series: | Nature Communications |
Online Access: | https://doi.org/10.1038/s41467-020-17310-5 |
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doaj-f17c1a1cefad4df6a818b7dcf60e439b2021-07-18T11:44:04ZengNature Publishing GroupNature Communications2041-17232020-07-0111111510.1038/s41467-020-17310-5Ornithine-A urea cycle metabolite enhances autophagy and controls Mycobacterium tuberculosis infectionRamya Sivangala Thandi0Rajesh Kumar Radhakrishnan1Deepak Tripathi2Padmaja Paidipally3Abul K. Azad4Larry S. Schlesinger5Buka Samten6Sachin Mulik7Ramakrishna Vankayalapati8Department of Pulmonary Immunology, Center for Biomedical Research, University of Texas Health CenterDepartment of Pulmonary Immunology, Center for Biomedical Research, University of Texas Health CenterDepartment of Pulmonary Immunology, Center for Biomedical Research, University of Texas Health CenterDepartment of Pulmonary Immunology, Center for Biomedical Research, University of Texas Health CenterTexas Biomedical Research InstituteTexas Biomedical Research InstituteDepartment of Pulmonary Immunology, Center for Biomedical Research, University of Texas Health CenterDepartment of Pulmonary Immunology, Center for Biomedical Research, University of Texas Health CenterDepartment of Pulmonary Immunology, Center for Biomedical Research, University of Texas Health CenterKupffer cells are more resistant to M. tuberculosis when compared with alveolar macrophages. Here the authors show that this distinction is caused by the presence of ornithine and imidazole in Kupffer cells and that these metabolites can drive autophagy and M. tuberculosis killing in alveolar macrophages when given intranasally to infected mice.https://doi.org/10.1038/s41467-020-17310-5 |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Ramya Sivangala Thandi Rajesh Kumar Radhakrishnan Deepak Tripathi Padmaja Paidipally Abul K. Azad Larry S. Schlesinger Buka Samten Sachin Mulik Ramakrishna Vankayalapati |
spellingShingle |
Ramya Sivangala Thandi Rajesh Kumar Radhakrishnan Deepak Tripathi Padmaja Paidipally Abul K. Azad Larry S. Schlesinger Buka Samten Sachin Mulik Ramakrishna Vankayalapati Ornithine-A urea cycle metabolite enhances autophagy and controls Mycobacterium tuberculosis infection Nature Communications |
author_facet |
Ramya Sivangala Thandi Rajesh Kumar Radhakrishnan Deepak Tripathi Padmaja Paidipally Abul K. Azad Larry S. Schlesinger Buka Samten Sachin Mulik Ramakrishna Vankayalapati |
author_sort |
Ramya Sivangala Thandi |
title |
Ornithine-A urea cycle metabolite enhances autophagy and controls Mycobacterium tuberculosis infection |
title_short |
Ornithine-A urea cycle metabolite enhances autophagy and controls Mycobacterium tuberculosis infection |
title_full |
Ornithine-A urea cycle metabolite enhances autophagy and controls Mycobacterium tuberculosis infection |
title_fullStr |
Ornithine-A urea cycle metabolite enhances autophagy and controls Mycobacterium tuberculosis infection |
title_full_unstemmed |
Ornithine-A urea cycle metabolite enhances autophagy and controls Mycobacterium tuberculosis infection |
title_sort |
ornithine-a urea cycle metabolite enhances autophagy and controls mycobacterium tuberculosis infection |
publisher |
Nature Publishing Group |
series |
Nature Communications |
issn |
2041-1723 |
publishDate |
2020-07-01 |
description |
Kupffer cells are more resistant to M. tuberculosis when compared with alveolar macrophages. Here the authors show that this distinction is caused by the presence of ornithine and imidazole in Kupffer cells and that these metabolites can drive autophagy and M. tuberculosis killing in alveolar macrophages when given intranasally to infected mice. |
url |
https://doi.org/10.1038/s41467-020-17310-5 |
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