[1]
;
Alarcón Guamán, Jonathan
[1]
Loja, Ecuador
Esta revisión narrativa tiene como objetivo presentar una visión actualizada de la literatura sobre los mecanismos de virulencia de Staphylococcus.sp asociada a infecciones de piel y tejidos blandos. A través de la búsqueda en bases de datos electrónicas: PubMed, BVS y Web of Science, obteniéndose 411 artículos, 15 artículos cumplieron con el objetivo de estudio. Encontrándose, que los mecanismos de virulencia, de mayor relevancia clínica fueron PVL, EsxA, EsxB, toxinas como spa, hla, fnbB, lukF-PV, clfA. Los genes como: gen mecA, gen que codifica PVL y TSST-1, SAgs, Agr-QS y genes Ica. Las proteínas que tuvieron relación con la adherencia de Staphylococcus, fueron Aap, SasG, SSL, AdsA, también Bap, SasC, FnBPA y FnBPB de S.aureus, y Aap, SSP1 y SSP2 de S. epidermidis. Concluyendo que el principal medio de protección a los Staphylococcus en infecciones de piel y tejidos blandos, es a través de evasión inmunitaria, supervivencia intracelular, prevención de apoptosis, la inhibición de la agregación plaquetaria, la desgranulación celular y el aumento de la producción de la citosina antiinflamatoria IL- 10.This narrative review aims to present an updated view of the literature on the virulence mechanisms of Staphylococcus.sp associated with skin and soft tissue infections. Through the search in electronic databases: PubMed, BVS and Web of Science, 411 articles were obtained, 15 articles fulfilled the objective of the study. It was found that the most clinically relevant virulence mechanisms were PVL, EsxA, EsxB, toxins such as spa, hla, fnbB, lukF-PV, clfA. Genes such as: mecA gene, gene encoding PVL and TSST-1, SAgs, Agr-QS and Ica genes. The proteins that were related to Staphylococcus adherence were Aap, SasG, SSL, AdsA, also Bap, SasC, FnBPA and FnBPB of S. aureus, and Aap, SSP1 and SSP2 of S. epidermidis. Concluding that the main means of protection to Staphylococcus in skin and soft tissue infections is through immune evasion, intracellular survival, prevention of apoptosis, inhibition of platelet aggregation, cell degranulation and increased production of the anti-inflammatory cytokine IL-10.Recibido: 06-04-2024Aprobado: 03-06-2024Publicado: 01-11-2024
This narrative review aims to present an updated view of the literature on the virulence mechanisms of Staphylococcus.sp associated with skin and soft tissue infections. Through the search in electronic databases: PubMed, BVS and Web of Science, 411 articles were obtained, 15 articles fulfilled the objective of the study. It was found that the most clinically relevant virulence mechanisms were PVL, EsxA, EsxB, toxins such as spa, hla, fnbB, lukF-PV, clfA. Genes such as: mecA gene, gene encoding PVL and TSST-1, SAgs, Agr-QS and Ica genes. The proteins that were related to Staphylococcus adherence were Aap, SasG, SSL, AdsA, also Bap, SasC, FnBPA and FnBPB of S. aureus, and Aap, SSP1 and SSP2 of S. epidermidis. Concluding that the main means of protection to Staphylococcus in skin and soft tissue infections is through immune evasion, intracellular survival, prevention of apoptosis, inhibition of platelet aggregation, cell degranulation and increased production of the anti-inflammatory cytokine IL-10.
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