Common virulence factors between Histoplasma and Paracoccidioides: Recognition of Hsp60 and Enolase by CR3 and plasmin receptors in host cells
ABSTRACT: Over the last two decades, the incidence of Invasive Fungal Infections (IFIs) globally has risen, posing a considerable challenge despite available antifungal therapies. Addressing this, the World Health Organization (WHO) prioritized research on specific fungi, notably Histoplasma spp. an...
- Autores:
-
Rodríguez Echeverri, Carolina
González Marín, Ángel Augusto
de Matos Silva, Samanta
Soares Mendes Giannini, María José
Fusco Almeida, Ana Marisa
- Tipo de recurso:
- Review article
- Fecha de publicación:
- 2024
- Institución:
- Universidad de Antioquia
- Repositorio:
- Repositorio UdeA
- Idioma:
- eng
- OAI Identifier:
- oai:bibliotecadigital.udea.edu.co:10495/41683
- Acceso en línea:
- https://hdl.handle.net/10495/41683
- Palabra clave:
- Hongos
Fungi
Paracoccidioides
Histoplasma
Chaperonina 60
Chaperonin 60
Antígeno de Macrófago-1
Macrophage-1 Antigen
Fosfopiruvato Hidratasa
Phosphopyruvate Hydratase
Inmunidad Innata
Immunity, Innate
https://id.nlm.nih.gov/mesh/D005658
https://id.nlm.nih.gov/mesh/D010228
https://id.nlm.nih.gov/mesh/D006658
https://id.nlm.nih.gov/mesh/D018834
https://id.nlm.nih.gov/mesh/D016177
https://id.nlm.nih.gov/mesh/D010751
https://id.nlm.nih.gov/mesh/D007113
- Rights
- openAccess
- License
- http://creativecommons.org/licenses/by-nc-nd/2.5/co/
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| dc.title.spa.fl_str_mv |
Common virulence factors between Histoplasma and Paracoccidioides: Recognition of Hsp60 and Enolase by CR3 and plasmin receptors in host cells |
| title |
Common virulence factors between Histoplasma and Paracoccidioides: Recognition of Hsp60 and Enolase by CR3 and plasmin receptors in host cells |
| spellingShingle |
Common virulence factors between Histoplasma and Paracoccidioides: Recognition of Hsp60 and Enolase by CR3 and plasmin receptors in host cells Hongos Fungi Paracoccidioides Histoplasma Chaperonina 60 Chaperonin 60 Antígeno de Macrófago-1 Macrophage-1 Antigen Fosfopiruvato Hidratasa Phosphopyruvate Hydratase Inmunidad Innata Immunity, Innate https://id.nlm.nih.gov/mesh/D005658 https://id.nlm.nih.gov/mesh/D010228 https://id.nlm.nih.gov/mesh/D006658 https://id.nlm.nih.gov/mesh/D018834 https://id.nlm.nih.gov/mesh/D016177 https://id.nlm.nih.gov/mesh/D010751 https://id.nlm.nih.gov/mesh/D007113 |
| title_short |
Common virulence factors between Histoplasma and Paracoccidioides: Recognition of Hsp60 and Enolase by CR3 and plasmin receptors in host cells |
| title_full |
Common virulence factors between Histoplasma and Paracoccidioides: Recognition of Hsp60 and Enolase by CR3 and plasmin receptors in host cells |
| title_fullStr |
Common virulence factors between Histoplasma and Paracoccidioides: Recognition of Hsp60 and Enolase by CR3 and plasmin receptors in host cells |
| title_full_unstemmed |
Common virulence factors between Histoplasma and Paracoccidioides: Recognition of Hsp60 and Enolase by CR3 and plasmin receptors in host cells |
| title_sort |
Common virulence factors between Histoplasma and Paracoccidioides: Recognition of Hsp60 and Enolase by CR3 and plasmin receptors in host cells |
| dc.creator.fl_str_mv |
Rodríguez Echeverri, Carolina González Marín, Ángel Augusto de Matos Silva, Samanta Soares Mendes Giannini, María José Fusco Almeida, Ana Marisa |
| dc.contributor.author.none.fl_str_mv |
Rodríguez Echeverri, Carolina González Marín, Ángel Augusto de Matos Silva, Samanta Soares Mendes Giannini, María José Fusco Almeida, Ana Marisa |
| dc.contributor.researchgroup.spa.fl_str_mv |
Grupo de Investigación en Microbiología Básica y Aplicada-Microba |
| dc.subject.decs.none.fl_str_mv |
Hongos Fungi Paracoccidioides Histoplasma Chaperonina 60 Chaperonin 60 Antígeno de Macrófago-1 Macrophage-1 Antigen Fosfopiruvato Hidratasa Phosphopyruvate Hydratase Inmunidad Innata Immunity, Innate |
| topic |
Hongos Fungi Paracoccidioides Histoplasma Chaperonina 60 Chaperonin 60 Antígeno de Macrófago-1 Macrophage-1 Antigen Fosfopiruvato Hidratasa Phosphopyruvate Hydratase Inmunidad Innata Immunity, Innate https://id.nlm.nih.gov/mesh/D005658 https://id.nlm.nih.gov/mesh/D010228 https://id.nlm.nih.gov/mesh/D006658 https://id.nlm.nih.gov/mesh/D018834 https://id.nlm.nih.gov/mesh/D016177 https://id.nlm.nih.gov/mesh/D010751 https://id.nlm.nih.gov/mesh/D007113 |
| dc.subject.meshuri.none.fl_str_mv |
https://id.nlm.nih.gov/mesh/D005658 https://id.nlm.nih.gov/mesh/D010228 https://id.nlm.nih.gov/mesh/D006658 https://id.nlm.nih.gov/mesh/D018834 https://id.nlm.nih.gov/mesh/D016177 https://id.nlm.nih.gov/mesh/D010751 https://id.nlm.nih.gov/mesh/D007113 |
| description |
ABSTRACT: Over the last two decades, the incidence of Invasive Fungal Infections (IFIs) globally has risen, posing a considerable challenge despite available antifungal therapies. Addressing this, the World Health Organization (WHO) prioritized research on specific fungi, notably Histoplasma spp. and Paracoccidioides spp. These dimorphic fungi have a mycelial life cycle in soil and a yeast phase associated with tissues of mammalian hosts. Inhalation of conidia and mycelial fragments initiates the infection, crucially transforming into the yeast form within the host, influenced by factors like temperature, host immunity, and hormonal status. Survival and multiplication within alveolar macrophages are crucial for disease progression, where innate immune responses play a pivotal role in overcoming physical barriers. The transition to pathogenic yeast, triggered by increased temperature, involves yeast phase-specific gene expression, closely linked to infection establishment and pathogenicity. Cell adhesion mechanisms during host-pathogen interactions are intricately linked to fungal virulence, which is critical for tissue colonization and disease development. Yeast replication within macrophages leads to their rupture, aiding pathogen dissemination. Immune cells, especially macrophages, dendritic cells, and neutrophils, are key players during infection control, with macrophages crucial for defense, tissue integrity, and pathogen elimination. Recognition of common virulence molecules such as heat- shock protein-60 (Hsp60) and enolase by pattern recognition receptors (PRRs), mainly via the complement receptor 3 (CR3) and plasmin receptor pathways, respectively, could be pivotal in host-pathogen interactions for Histoplasma spp. and Paracoccidioides spp., influencing adhesion, phagocytosis, and inflammatory regulation. This review provides a comprehensive overview of the dynamic of these two IFIs between host and pathogen. Further research into these fungi's virulence factors promises insights into pathogenic mechanisms, potentially guiding the development of effective treatment strategies. |
| publishDate |
2024 |
| dc.date.accessioned.none.fl_str_mv |
2024-09-02T19:39:26Z |
| dc.date.available.none.fl_str_mv |
2024-09-02T19:39:26Z |
| dc.date.issued.none.fl_str_mv |
2024 |
| dc.type.spa.fl_str_mv |
Artículo de revisión |
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de Matos Silva S, Echeverri CR, Mendes-Giannini MJS, Fusco-Almeida AM, Gonzalez A. Common virulence factors between Histoplasma and Paracoccidioides: Recognition of Hsp60 and Enolase by CR3 and plasmin receptors in host cells. Curr Res Microb Sci. 2024 Jun 8;7:100246. doi: 10.1016/j.crmicr.2024.100246. |
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https://hdl.handle.net/10495/41683 |
| dc.identifier.doi.none.fl_str_mv |
10.1016/j.crmicr.2024.100246 |
| dc.identifier.eissn.none.fl_str_mv |
2666-5174 |
| identifier_str_mv |
de Matos Silva S, Echeverri CR, Mendes-Giannini MJS, Fusco-Almeida AM, Gonzalez A. Common virulence factors between Histoplasma and Paracoccidioides: Recognition of Hsp60 and Enolase by CR3 and plasmin receptors in host cells. Curr Res Microb Sci. 2024 Jun 8;7:100246. doi: 10.1016/j.crmicr.2024.100246. 10.1016/j.crmicr.2024.100246 2666-5174 |
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https://hdl.handle.net/10495/41683 |
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eng |
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eng |
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Curr. Res. Microb. Sci. |
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Current Research in Microbial Sciences |
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Rodríguez Echeverri, CarolinaGonzález Marín, Ángel Augustode Matos Silva, SamantaSoares Mendes Giannini, María JoséFusco Almeida, Ana MarisaGrupo de Investigación en Microbiología Básica y Aplicada-Microba2024-09-02T19:39:26Z2024-09-02T19:39:26Z2024de Matos Silva S, Echeverri CR, Mendes-Giannini MJS, Fusco-Almeida AM, Gonzalez A. Common virulence factors between Histoplasma and Paracoccidioides: Recognition of Hsp60 and Enolase by CR3 and plasmin receptors in host cells. Curr Res Microb Sci. 2024 Jun 8;7:100246. doi: 10.1016/j.crmicr.2024.100246.https://hdl.handle.net/10495/4168310.1016/j.crmicr.2024.1002462666-5174ABSTRACT: Over the last two decades, the incidence of Invasive Fungal Infections (IFIs) globally has risen, posing a considerable challenge despite available antifungal therapies. Addressing this, the World Health Organization (WHO) prioritized research on specific fungi, notably Histoplasma spp. and Paracoccidioides spp. These dimorphic fungi have a mycelial life cycle in soil and a yeast phase associated with tissues of mammalian hosts. Inhalation of conidia and mycelial fragments initiates the infection, crucially transforming into the yeast form within the host, influenced by factors like temperature, host immunity, and hormonal status. Survival and multiplication within alveolar macrophages are crucial for disease progression, where innate immune responses play a pivotal role in overcoming physical barriers. The transition to pathogenic yeast, triggered by increased temperature, involves yeast phase-specific gene expression, closely linked to infection establishment and pathogenicity. Cell adhesion mechanisms during host-pathogen interactions are intricately linked to fungal virulence, which is critical for tissue colonization and disease development. Yeast replication within macrophages leads to their rupture, aiding pathogen dissemination. Immune cells, especially macrophages, dendritic cells, and neutrophils, are key players during infection control, with macrophages crucial for defense, tissue integrity, and pathogen elimination. Recognition of common virulence molecules such as heat- shock protein-60 (Hsp60) and enolase by pattern recognition receptors (PRRs), mainly via the complement receptor 3 (CR3) and plasmin receptor pathways, respectively, could be pivotal in host-pathogen interactions for Histoplasma spp. and Paracoccidioides spp., influencing adhesion, phagocytosis, and inflammatory regulation. This review provides a comprehensive overview of the dynamic of these two IFIs between host and pathogen. Further research into these fungi's virulence factors promises insights into pathogenic mechanisms, potentially guiding the development of effective treatment strategies.Fundação de Amparo à Pesquisa do Estado de São PauloCoordenação de Aperfeicoamento de Pessoal de Nível SuperiorCOL012613111 páginasapplication/pdfengElsevierÁmsterdam, Países Bajoshttp://creativecommons.org/licenses/by-nc-nd/2.5/co/https://creativecommons.org/licenses/by-nc-nd/4.0/info:eu-repo/semantics/openAccesshttp://purl.org/coar/access_right/c_abf2Common virulence factors between Histoplasma and Paracoccidioides: Recognition of Hsp60 and Enolase by CR3 and plasmin receptors in host cellsArtículo de revisiónhttp://purl.org/coar/resource_type/c_dcae04bchttp://purl.org/coar/resource_type/c_2df8fbb1https://purl.org/redcol/resource_type/ARTREVhttp://purl.org/coar/version/c_970fb48d4fbd8a85info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionHongosFungiParacoccidioidesHistoplasmaChaperonina 60Chaperonin 60Antígeno de Macrófago-1Macrophage-1 AntigenFosfopiruvato HidratasaPhosphopyruvate HydrataseInmunidad InnataImmunity, Innatehttps://id.nlm.nih.gov/mesh/D005658https://id.nlm.nih.gov/mesh/D010228https://id.nlm.nih.gov/mesh/D006658https://id.nlm.nih.gov/mesh/D018834https://id.nlm.nih.gov/mesh/D016177https://id.nlm.nih.gov/mesh/D010751https://id.nlm.nih.gov/mesh/D007113Curr. Res. Microb. 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