Quantifying donor-to-donor variation in macrophage responses to the human fungal pathogen Cryptococcus neoformans

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@article{38df3e1821434dfe8078baf088e4c678,
title = "Quantifying donor-to-donor variation in macrophage responses to the human fungal pathogen Cryptococcus neoformans",
abstract = "Cryptococcosis remains the leading cause of fungal meningitis worldwide, caused primarily by the pathogen Cryptococcus neoformans. Symptomatic cryptococcal infections typically affect immunocompromised patients. However, environmental exposure to cryptococcal spores is ubiquitous and most healthy individuals are thought to harbor infections from early childhood onwards that are either resolved, or become latent. Since macrophages are a key host cell for cryptococcal infection, we sought to quantify the extent of individual variation in this early phagocyte response within a small cohort of healthy volunteers with no reported immunocompromising conditions. We show that rates of both intracellular fungal proliferation and non-lytic expulsion (vomocytosis) are remarkably variable between individuals. However, we demonstrate that neither gender, in vitro host inflammatory cytokine profiles, nor polymorphisms in several key immune genes are responsible for this variation. Thus the data we present serve to quantify the natural variation in macrophage responses to this important human pathogen and will hopefully provide a useful “benchmark” for the research community.",
author = "Mariam Garelnabi and Ewa Bielska and Robin May and Leanne Taylor-Smith and Rebecca Hall and Daniel Stones",
year = "2018",
month = mar,
day = "29",
doi = "10.1371/journal.pone.0194615",
language = "English",
volume = "13",
journal = "PLoSONE",
issn = "1932-6203",
publisher = "Public Library of Science (PLOS)",
number = "3",

}

RIS

TY - JOUR

T1 - Quantifying donor-to-donor variation in macrophage responses to the human fungal pathogen Cryptococcus neoformans

AU - Garelnabi, Mariam

AU - Bielska, Ewa

AU - May, Robin

AU - Taylor-Smith, Leanne

AU - Hall, Rebecca

AU - Stones, Daniel

PY - 2018/3/29

Y1 - 2018/3/29

N2 - Cryptococcosis remains the leading cause of fungal meningitis worldwide, caused primarily by the pathogen Cryptococcus neoformans. Symptomatic cryptococcal infections typically affect immunocompromised patients. However, environmental exposure to cryptococcal spores is ubiquitous and most healthy individuals are thought to harbor infections from early childhood onwards that are either resolved, or become latent. Since macrophages are a key host cell for cryptococcal infection, we sought to quantify the extent of individual variation in this early phagocyte response within a small cohort of healthy volunteers with no reported immunocompromising conditions. We show that rates of both intracellular fungal proliferation and non-lytic expulsion (vomocytosis) are remarkably variable between individuals. However, we demonstrate that neither gender, in vitro host inflammatory cytokine profiles, nor polymorphisms in several key immune genes are responsible for this variation. Thus the data we present serve to quantify the natural variation in macrophage responses to this important human pathogen and will hopefully provide a useful “benchmark” for the research community.

AB - Cryptococcosis remains the leading cause of fungal meningitis worldwide, caused primarily by the pathogen Cryptococcus neoformans. Symptomatic cryptococcal infections typically affect immunocompromised patients. However, environmental exposure to cryptococcal spores is ubiquitous and most healthy individuals are thought to harbor infections from early childhood onwards that are either resolved, or become latent. Since macrophages are a key host cell for cryptococcal infection, we sought to quantify the extent of individual variation in this early phagocyte response within a small cohort of healthy volunteers with no reported immunocompromising conditions. We show that rates of both intracellular fungal proliferation and non-lytic expulsion (vomocytosis) are remarkably variable between individuals. However, we demonstrate that neither gender, in vitro host inflammatory cytokine profiles, nor polymorphisms in several key immune genes are responsible for this variation. Thus the data we present serve to quantify the natural variation in macrophage responses to this important human pathogen and will hopefully provide a useful “benchmark” for the research community.

U2 - 10.1371/journal.pone.0194615

DO - 10.1371/journal.pone.0194615

M3 - Article

VL - 13

JO - PLoSONE

JF - PLoSONE

SN - 1932-6203

IS - 3

M1 - e0194615

ER -