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Commercial strain‐derived clinical Saccharomyces cerevisiae can evolve new phenotypes without higher pathogenicity
Author(s) -
Pfliegler Walter P.,
Boros Enikő,
Pázmándi Kitti,
Jakab Ágnes,
Zsuga Imre,
Kovács Renátó,
Urbán Edit,
Antunovics Zsuzsa,
Bácsi Attila,
Sipiczki Matthias,
Majoros László,
Pócsi István
Publication year - 2017
Publication title -
molecular nutrition and food research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.495
H-Index - 131
eISSN - 1613-4133
pISSN - 1613-4125
DOI - 10.1002/mnfr.201601099
Subject(s) - virulence , biology , pathogenicity , phenotype , microbiology and biotechnology , pathogenicity island , saccharomyces cerevisiae , probiotic , strain (injury) , host (biology) , colonization , genetics , gene , bacteria , anatomy
Scope Saccharomyces cerevisiae is one of the most important microbes in food industry, but there is growing evidence on its potential pathogenicity as well. Its status as a member of human mycobiome is still not fully understood. Methods and results In this study, we characterize clinical S. cerevisiae isolates from Hungarian hospitals along with commercial baking and probiotic strains, and determine their phenotypic parameters, virulence factors, interactions with human macrophages, and pathogenicity. Four of the clinical isolates could be traced back to commercial strains based on genetic fingerprinting. Our observations indicate that the commercial‐derived clinical isolates have evolved new phenotypes and show similar, or in two cases, significantly decreased pathogenicity. Furthermore, immunological experiments revealed that the variability in human primary macrophage activation after coincubation with yeasts is largely donor and not isolate dependent. Conclusion Isolates in this study offer an interesting insight into the potential microevolution of probiotic and food strains in human hosts. These commensal yeasts display various changes in their phenotypes, indicating that the colonization of the host does not necessarily impose a selective pressure toward higher virulence/pathogenicity.