Host-directed therapies targeting the tuberculosis granuloma stroma.
- Publisher:
- Oxford University Press (OUP)
- Publication Type:
- Journal Article
- Citation:
- Pathogens and disease, 2020, 78, (2)
- Issue Date:
- 2020-03
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Host-directed_therapies_target.pdf | 669.89 kB | Adobe PDF |
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Full metadata record
Field | Value | Language |
---|---|---|
dc.contributor.author |
Hortle, E https://orcid.org/0000-0001-9633-5638 |
|
dc.contributor.author | Oehlers, SH | |
dc.date.accessioned | 2021-05-26T03:00:32Z | |
dc.date.available | 2020-03-03 | |
dc.date.available | 2021-05-26T03:00:32Z | |
dc.date.issued | 2020-03 | |
dc.identifier.citation | Pathogens and disease, 2020, 78, (2) | |
dc.identifier.issn | 2049-632X | |
dc.identifier.issn | 2049-632X | |
dc.identifier.uri | http://hdl.handle.net/10453/149231 | |
dc.description.abstract | Mycobacteria have co-evolved with their hosts resulting in pathogens adept at intracellular survival. Pathogenic mycobacteria actively manipulate infected macrophages to drive granuloma formation while subverting host cell processes to create a permissive niche. Granuloma residency confers phenotypic antimicrobial resistance by physically excluding or neutralising antibiotics. Host-directed therapies (HDTs) combat infection by restoring protective immunity and reducing immunopathology independent of pathogen antimicrobial resistance status. This review covers innovative research that has discovered 'secondary' symptoms of infection in the granuloma stroma are actually primary drivers of infection and that relieving these stromal pathologies with HDTs benefits the host. Advances in our understanding of the relationship between tuberculosis and the host vasculature, haemostatic system and extracellular matrix reorganisation are discussed. Preclinical and clinical use of HDTs against these stromal targets are summarised. | |
dc.format | ||
dc.language | eng | |
dc.publisher | Oxford University Press (OUP) | |
dc.relation.ispartof | Pathogens and disease | |
dc.relation.isbasedon | 10.1093/femspd/ftaa015 | |
dc.rights | info:eu-repo/semantics/restrictedAccess | |
dc.subject | 1102 Cardiorespiratory Medicine and Haematology, 1107 Immunology, 1108 Medical Microbiology | |
dc.subject.classification | Microbiology | |
dc.subject.mesh | Animals | |
dc.subject.mesh | Biomarkers | |
dc.subject.mesh | Fibrosis | |
dc.subject.mesh | Granuloma | |
dc.subject.mesh | Hemostasis | |
dc.subject.mesh | Host-Pathogen Interactions | |
dc.subject.mesh | Humans | |
dc.subject.mesh | Molecular Targeted Therapy | |
dc.subject.mesh | Neovascularization, Pathologic | |
dc.subject.mesh | Permeability | |
dc.subject.mesh | Precision Medicine | |
dc.subject.mesh | Tuberculosis | |
dc.subject.mesh | Animals | |
dc.subject.mesh | Humans | |
dc.subject.mesh | Tuberculosis | |
dc.subject.mesh | Granuloma | |
dc.subject.mesh | Fibrosis | |
dc.subject.mesh | Neovascularization, Pathologic | |
dc.subject.mesh | Hemostasis | |
dc.subject.mesh | Permeability | |
dc.subject.mesh | Host-Pathogen Interactions | |
dc.subject.mesh | Molecular Targeted Therapy | |
dc.subject.mesh | Biomarkers | |
dc.subject.mesh | Precision Medicine | |
dc.subject.mesh | Animals | |
dc.subject.mesh | Biomarkers | |
dc.subject.mesh | Fibrosis | |
dc.subject.mesh | Granuloma | |
dc.subject.mesh | Hemostasis | |
dc.subject.mesh | Host-Pathogen Interactions | |
dc.subject.mesh | Humans | |
dc.subject.mesh | Molecular Targeted Therapy | |
dc.subject.mesh | Neovascularization, Pathologic | |
dc.subject.mesh | Permeability | |
dc.subject.mesh | Precision Medicine | |
dc.subject.mesh | Tuberculosis | |
dc.title | Host-directed therapies targeting the tuberculosis granuloma stroma. | |
dc.type | Journal Article | |
utslib.citation.volume | 78 | |
utslib.location.activity | United States | |
utslib.for | 1102 Cardiorespiratory Medicine and Haematology | |
utslib.for | 1107 Immunology | |
utslib.for | 1108 Medical Microbiology | |
pubs.organisational-group | /University of Technology Sydney | |
pubs.organisational-group | /University of Technology Sydney/Faculty of Science | |
pubs.organisational-group | /University of Technology Sydney/Faculty of Science/School of Life Sciences | |
utslib.copyright.status | in_progress | * |
pubs.consider-herdc | false | |
dc.date.updated | 2021-05-26T03:00:31Z | |
pubs.issue | 2 | |
pubs.publication-status | Published | |
pubs.volume | 78 | |
utslib.citation.issue | 2 |
Abstract:
Mycobacteria have co-evolved with their hosts resulting in pathogens adept at intracellular survival. Pathogenic mycobacteria actively manipulate infected macrophages to drive granuloma formation while subverting host cell processes to create a permissive niche. Granuloma residency confers phenotypic antimicrobial resistance by physically excluding or neutralising antibiotics. Host-directed therapies (HDTs) combat infection by restoring protective immunity and reducing immunopathology independent of pathogen antimicrobial resistance status. This review covers innovative research that has discovered 'secondary' symptoms of infection in the granuloma stroma are actually primary drivers of infection and that relieving these stromal pathologies with HDTs benefits the host. Advances in our understanding of the relationship between tuberculosis and the host vasculature, haemostatic system and extracellular matrix reorganisation are discussed. Preclinical and clinical use of HDTs against these stromal targets are summarised.
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