From grazing resistance to pathogenesis: the coincidental evolution of virulence factors.

To many pathogenic bacteria, human hosts are an evolutionary dead end. This begs the question what evolutionary forces have shaped their virulence traits. Why are these bacteria so virulent? The coincidental evolution hypothesis suggests that such virulence factors result from adaptation to other ec...

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Autores principales:	Sandrine Adiba, Clément Nizak, Minus van Baalen, Erick Denamur, Frantz Depaulis
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2010
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/8238f6a365134b139d0e6f21c83673dd
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spelling	oai:doaj.org-article:8238f6a365134b139d0e6f21c83673dd2021-11-18T06:36:11ZFrom grazing resistance to pathogenesis: the coincidental evolution of virulence factors.1932-620310.1371/journal.pone.0011882https://doaj.org/article/8238f6a365134b139d0e6f21c83673dd2010-08-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/20711443/pdf/?tool=EBIhttps://doaj.org/toc/1932-6203To many pathogenic bacteria, human hosts are an evolutionary dead end. This begs the question what evolutionary forces have shaped their virulence traits. Why are these bacteria so virulent? The coincidental evolution hypothesis suggests that such virulence factors result from adaptation to other ecological niches. In particular, virulence traits in bacteria might result from selective pressure exerted by protozoan predator. Thus, grazing resistance may be an evolutionarily exaptation for bacterial pathogenicity. This hypothesis was tested by subjecting a well characterized collection of 31 Escherichia coli strains (human commensal or extra-intestinal pathogenic) to grazing by the social haploid amoeba Dictyostelium discoideum. We then assessed how resistance to grazing correlates with some bacterial traits, such as the presence of virulence genes. Whatever the relative population size (bacteria/amoeba) for a non-pathogenic bacteria strain, D. discoideum was able to phagocytise, digest and grow. In contrast, a pathogenic bacterium strain killed D. discoideum above a certain bacteria/amoeba population size. A plating assay was then carried out using the E. coli collection faced to the grazing of D. discoideum. E. coli strains carrying virulence genes such as iroN, irp2, fyuA involved in iron uptake, belonging to the B2 phylogenetic group and being virulent in a mouse model of septicaemia were resistant to the grazing from D. discoideum. Experimental proof of the key role of the irp gene in the grazing resistance was evidenced with a mutant strain lacking this gene. Such determinant of virulence may well be originally selected and (or) further maintained for their role in natural habitat: resistance to digestion by free-living protozoa, rather than for virulence per se.Sandrine AdibaClément NizakMinus van BaalenErick DenamurFrantz DepaulisPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 5, Iss 8, p e11882 (2010)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Sandrine Adiba Clément Nizak Minus van Baalen Erick Denamur Frantz Depaulis From grazing resistance to pathogenesis: the coincidental evolution of virulence factors.
description	To many pathogenic bacteria, human hosts are an evolutionary dead end. This begs the question what evolutionary forces have shaped their virulence traits. Why are these bacteria so virulent? The coincidental evolution hypothesis suggests that such virulence factors result from adaptation to other ecological niches. In particular, virulence traits in bacteria might result from selective pressure exerted by protozoan predator. Thus, grazing resistance may be an evolutionarily exaptation for bacterial pathogenicity. This hypothesis was tested by subjecting a well characterized collection of 31 Escherichia coli strains (human commensal or extra-intestinal pathogenic) to grazing by the social haploid amoeba Dictyostelium discoideum. We then assessed how resistance to grazing correlates with some bacterial traits, such as the presence of virulence genes. Whatever the relative population size (bacteria/amoeba) for a non-pathogenic bacteria strain, D. discoideum was able to phagocytise, digest and grow. In contrast, a pathogenic bacterium strain killed D. discoideum above a certain bacteria/amoeba population size. A plating assay was then carried out using the E. coli collection faced to the grazing of D. discoideum. E. coli strains carrying virulence genes such as iroN, irp2, fyuA involved in iron uptake, belonging to the B2 phylogenetic group and being virulent in a mouse model of septicaemia were resistant to the grazing from D. discoideum. Experimental proof of the key role of the irp gene in the grazing resistance was evidenced with a mutant strain lacking this gene. Such determinant of virulence may well be originally selected and (or) further maintained for their role in natural habitat: resistance to digestion by free-living protozoa, rather than for virulence per se.
format	article
author	Sandrine Adiba Clément Nizak Minus van Baalen Erick Denamur Frantz Depaulis
author_facet	Sandrine Adiba Clément Nizak Minus van Baalen Erick Denamur Frantz Depaulis
author_sort	Sandrine Adiba
title	From grazing resistance to pathogenesis: the coincidental evolution of virulence factors.
title_short	From grazing resistance to pathogenesis: the coincidental evolution of virulence factors.
title_full	From grazing resistance to pathogenesis: the coincidental evolution of virulence factors.
title_fullStr	From grazing resistance to pathogenesis: the coincidental evolution of virulence factors.
title_full_unstemmed	From grazing resistance to pathogenesis: the coincidental evolution of virulence factors.
title_sort	from grazing resistance to pathogenesis: the coincidental evolution of virulence factors.
publisher	Public Library of Science (PLoS)
publishDate	2010
url	https://doaj.org/article/8238f6a365134b139d0e6f21c83673dd
work_keys_str_mv	AT sandrineadiba fromgrazingresistancetopathogenesisthecoincidentalevolutionofvirulencefactors AT clementnizak fromgrazingresistancetopathogenesisthecoincidentalevolutionofvirulencefactors AT minusvanbaalen fromgrazingresistancetopathogenesisthecoincidentalevolutionofvirulencefactors AT erickdenamur fromgrazingresistancetopathogenesisthecoincidentalevolutionofvirulencefactors AT frantzdepaulis fromgrazingresistancetopathogenesisthecoincidentalevolutionofvirulencefactors
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From grazing resistance to pathogenesis: the coincidental evolution of virulence factors.

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