The Phagocyte Oxidase Controls Tolerance to Mycobacterium tuberculosis Infection [INFECTIOUS DISEASE AND HOST RESPONSE]
Olive, A. J., Smith, C. M., Kiritsy, M. C., Sassetti, C. M.
The American Association of Immunologists (AAI)
Published 2018
The American Association of Immunologists (AAI)
Published 2018
| Publication Date: |
2018-09-05
|
|---|---|
| Publisher: |
The American Association of Immunologists (AAI)
|
| Print ISSN: |
0022-1767
|
| Electronic ISSN: |
1550-6606
|
| Topics: |
Medicine
|
| Published by: |
| _version_ | 1836399043046014976 |
|---|---|
| autor | Olive, A. J., Smith, C. M., Kiritsy, M. C., Sassetti, C. M. |
| beschreibung | Protection from infectious disease relies on two distinct strategies: antimicrobial resistance directly inhibits pathogen growth, whereas infection tolerance protects from the negative impact of infection on host health. A single immune mediator can differentially contribute to these strategies in distinct contexts, confounding our understanding of protection to different pathogens. For example, the NADPH-dependent phagocyte oxidase (Phox) complex produces antimicrobial superoxide and protects from tuberculosis (TB) in humans. However, Phox-deficient mice display no sustained resistance defects to Mycobacterium tuberculosis , suggesting a more complicated role for NADPH Phox complex than strictly controlling bacterial growth. We examined the mechanisms by which Phox contributes to protection from TB and found that mice lacking the Cybb subunit of Phox suffered from a specific defect in tolerance, which was caused by unregulated Caspase-1 activation, IL-1β production, and neutrophil influx into the lung. These studies imply that a defect in tolerance alone is sufficient to compromise immunity to M. tuberculosis and highlight a central role for Phox and Caspase-1 in regulating TB disease progression. |
| citation_standardnr | 6327985 |
| datenlieferant | ipn_articles |
| feed_id | 333 |
| feed_publisher | The American Association of Immunologists (AAI) |
| feed_publisher_url | http://www.aai.org/ |
| insertion_date | 2018-09-05 |
| journaleissn | 1550-6606 |
| journalissn | 0022-1767 |
| publikationsjahr_anzeige | 2018 |
| publikationsjahr_facette | 2018 |
| publikationsjahr_intervall | 7984:2015-2019 |
| publikationsjahr_sort | 2018 |
| publisher | The American Association of Immunologists (AAI) |
| quelle | Journal of Immunology |
| relation | http://www.jimmunol.org/cgi/content/short/201/6/1705?rss=1 |
| search_space | articles |
| shingle_author_1 | Olive, A. J., Smith, C. M., Kiritsy, M. C., Sassetti, C. M. |
| shingle_author_2 | Olive, A. J., Smith, C. M., Kiritsy, M. C., Sassetti, C. M. |
| shingle_author_3 | Olive, A. J., Smith, C. M., Kiritsy, M. C., Sassetti, C. M. |
| shingle_author_4 | Olive, A. J., Smith, C. M., Kiritsy, M. C., Sassetti, C. M. |
| shingle_catch_all_1 | The Phagocyte Oxidase Controls Tolerance to Mycobacterium tuberculosis Infection [INFECTIOUS DISEASE AND HOST RESPONSE] Protection from infectious disease relies on two distinct strategies: antimicrobial resistance directly inhibits pathogen growth, whereas infection tolerance protects from the negative impact of infection on host health. A single immune mediator can differentially contribute to these strategies in distinct contexts, confounding our understanding of protection to different pathogens. For example, the NADPH-dependent phagocyte oxidase (Phox) complex produces antimicrobial superoxide and protects from tuberculosis (TB) in humans. However, Phox-deficient mice display no sustained resistance defects to Mycobacterium tuberculosis , suggesting a more complicated role for NADPH Phox complex than strictly controlling bacterial growth. We examined the mechanisms by which Phox contributes to protection from TB and found that mice lacking the Cybb subunit of Phox suffered from a specific defect in tolerance, which was caused by unregulated Caspase-1 activation, IL-1β production, and neutrophil influx into the lung. These studies imply that a defect in tolerance alone is sufficient to compromise immunity to M. tuberculosis and highlight a central role for Phox and Caspase-1 in regulating TB disease progression. Olive, A. J., Smith, C. M., Kiritsy, M. C., Sassetti, C. M. The American Association of Immunologists (AAI) 0022-1767 00221767 1550-6606 15506606 |
| shingle_catch_all_2 | The Phagocyte Oxidase Controls Tolerance to Mycobacterium tuberculosis Infection [INFECTIOUS DISEASE AND HOST RESPONSE] Protection from infectious disease relies on two distinct strategies: antimicrobial resistance directly inhibits pathogen growth, whereas infection tolerance protects from the negative impact of infection on host health. A single immune mediator can differentially contribute to these strategies in distinct contexts, confounding our understanding of protection to different pathogens. For example, the NADPH-dependent phagocyte oxidase (Phox) complex produces antimicrobial superoxide and protects from tuberculosis (TB) in humans. However, Phox-deficient mice display no sustained resistance defects to Mycobacterium tuberculosis , suggesting a more complicated role for NADPH Phox complex than strictly controlling bacterial growth. We examined the mechanisms by which Phox contributes to protection from TB and found that mice lacking the Cybb subunit of Phox suffered from a specific defect in tolerance, which was caused by unregulated Caspase-1 activation, IL-1β production, and neutrophil influx into the lung. These studies imply that a defect in tolerance alone is sufficient to compromise immunity to M. tuberculosis and highlight a central role for Phox and Caspase-1 in regulating TB disease progression. Olive, A. J., Smith, C. M., Kiritsy, M. C., Sassetti, C. M. The American Association of Immunologists (AAI) 0022-1767 00221767 1550-6606 15506606 |
| shingle_catch_all_3 | The Phagocyte Oxidase Controls Tolerance to Mycobacterium tuberculosis Infection [INFECTIOUS DISEASE AND HOST RESPONSE] Protection from infectious disease relies on two distinct strategies: antimicrobial resistance directly inhibits pathogen growth, whereas infection tolerance protects from the negative impact of infection on host health. A single immune mediator can differentially contribute to these strategies in distinct contexts, confounding our understanding of protection to different pathogens. For example, the NADPH-dependent phagocyte oxidase (Phox) complex produces antimicrobial superoxide and protects from tuberculosis (TB) in humans. However, Phox-deficient mice display no sustained resistance defects to Mycobacterium tuberculosis , suggesting a more complicated role for NADPH Phox complex than strictly controlling bacterial growth. We examined the mechanisms by which Phox contributes to protection from TB and found that mice lacking the Cybb subunit of Phox suffered from a specific defect in tolerance, which was caused by unregulated Caspase-1 activation, IL-1β production, and neutrophil influx into the lung. These studies imply that a defect in tolerance alone is sufficient to compromise immunity to M. tuberculosis and highlight a central role for Phox and Caspase-1 in regulating TB disease progression. Olive, A. J., Smith, C. M., Kiritsy, M. C., Sassetti, C. M. The American Association of Immunologists (AAI) 0022-1767 00221767 1550-6606 15506606 |
| shingle_catch_all_4 | The Phagocyte Oxidase Controls Tolerance to Mycobacterium tuberculosis Infection [INFECTIOUS DISEASE AND HOST RESPONSE] Protection from infectious disease relies on two distinct strategies: antimicrobial resistance directly inhibits pathogen growth, whereas infection tolerance protects from the negative impact of infection on host health. A single immune mediator can differentially contribute to these strategies in distinct contexts, confounding our understanding of protection to different pathogens. For example, the NADPH-dependent phagocyte oxidase (Phox) complex produces antimicrobial superoxide and protects from tuberculosis (TB) in humans. However, Phox-deficient mice display no sustained resistance defects to Mycobacterium tuberculosis , suggesting a more complicated role for NADPH Phox complex than strictly controlling bacterial growth. We examined the mechanisms by which Phox contributes to protection from TB and found that mice lacking the Cybb subunit of Phox suffered from a specific defect in tolerance, which was caused by unregulated Caspase-1 activation, IL-1β production, and neutrophil influx into the lung. These studies imply that a defect in tolerance alone is sufficient to compromise immunity to M. tuberculosis and highlight a central role for Phox and Caspase-1 in regulating TB disease progression. Olive, A. J., Smith, C. M., Kiritsy, M. C., Sassetti, C. M. The American Association of Immunologists (AAI) 0022-1767 00221767 1550-6606 15506606 |
| shingle_title_1 | The Phagocyte Oxidase Controls Tolerance to Mycobacterium tuberculosis Infection [INFECTIOUS DISEASE AND HOST RESPONSE] |
| shingle_title_2 | The Phagocyte Oxidase Controls Tolerance to Mycobacterium tuberculosis Infection [INFECTIOUS DISEASE AND HOST RESPONSE] |
| shingle_title_3 | The Phagocyte Oxidase Controls Tolerance to Mycobacterium tuberculosis Infection [INFECTIOUS DISEASE AND HOST RESPONSE] |
| shingle_title_4 | The Phagocyte Oxidase Controls Tolerance to Mycobacterium tuberculosis Infection [INFECTIOUS DISEASE AND HOST RESPONSE] |
| timestamp | 2025-06-30T23:36:41.736Z |
| titel | The Phagocyte Oxidase Controls Tolerance to Mycobacterium tuberculosis Infection [INFECTIOUS DISEASE AND HOST RESPONSE] |
| titel_suche | The Phagocyte Oxidase Controls Tolerance to Mycobacterium tuberculosis Infection [INFECTIOUS DISEASE AND HOST RESPONSE] |
| topic | WW-YZ |
| uid | ipn_articles_6327985 |