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...

Full description

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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network_acronym_str UDEA2
network_name_str Repositorio UdeA
repository_id_str
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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dc.identifier.citation.spa.fl_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.
dc.identifier.uri.none.fl_str_mv 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
url https://hdl.handle.net/10495/41683
dc.language.iso.spa.fl_str_mv eng
language eng
dc.relation.ispartofjournalabbrev.spa.fl_str_mv Curr. Res. Microb. Sci.
dc.relation.citationendpage.spa.fl_str_mv 11
dc.relation.citationstartpage.spa.fl_str_mv 1
dc.relation.citationvolume.spa.fl_str_mv 7
dc.relation.ispartofjournal.spa.fl_str_mv Current Research in Microbial Sciences
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spelling 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. 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