Revista da Sociedade Brasileira de Medicina Tropical ()

Association between polymorphisms in the genes encoding toll-like receptors and dectin-1 and susceptibility to invasive aspergillosis: a systematic review

  • Daiane de Oliveira Cunha,
  • Jacqueline Andréia Bernardes Leão-Cordeiro,
  • Hellen da Silva Cintra de Paula,
  • Fábio Silvestre Ataides,
  • Vera Aparecida Saddi,
  • Cesar Augusto Sam Tiago Vilanova-Costa,
  • Antonio Márcio Teodoro Cordeiro Silva

DOI
https://doi.org/10.1590/0037-8682-0314-2018
Journal volume & issue
Vol. 51, no. 6
pp. 725 – 730

Abstract

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Abstract Invasive aspergillosis is a common fungal infection in immunocompromised individuals. Some studies have shown that toll-like receptor and dectin-1 genetic polymorphisms may alter signaling pathways, thus increasing an individual’s susceptibility to invasive aspergillosis. We investigated the pertinent literature to determine whether polymorphisms in the genes encoding toll-like receptors and dectin-1 increase the susceptibility to invasive aspergillosis. This study systematically reviewed the literature using the databases PubMed/PMC, Scopus, and Web of Science using the keywords invasive aspergillosis, polymorphism, Toll-like, and Dectin-1. From the initial search, 415 studies were found and according to our inclusion and exclusion criteria, eight studies were selected. Several studies described single-nucleotide polymorphisms (SNPs) that are associated with a greater susceptibility to invasive aspergillosis. These SNPs were found in the genes that encode toll-like receptors 1, 3, 4, and 5 and the gene that encodes dectin-1; upon activation, both cellular receptors initiate a signaling cascade that can result in the production of cytokines and chemokines. Thus, our literature review uncovered a significant association between polymorphisms in the genes that encode toll-like receptors and dectin-1 and invasive aspergillosis. More studies should be performed to better understand the relationship between toll-like receptor and dectin-1 genetic polymorphisms and invasive aspergillosis susceptibility.

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