Hyphal growth of phagocytosed Fusarium oxysporum causes cell lysis and death of murine macrophages.

Katja Schäfer,Antonio Di Pietro,Neil A R Gow,Lars P Erwig,Judith M Bain

doi:10.1371/journal.pone.0101999

Katja Schäfer, Antonio Di Pietro + Show 3 more

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https://doi.org/10.1371/journal.pone.0101999

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Journal: PloS one	Publication Date: Jul 15, 2014
Citations: 44	License type: CC BY 4.0

Affiliation: University of Córdoba, University of Aberdeen

Abstract

Fusarium oxysporum is an important plant pathogen and an opportunistic pathogen of humans. Here we investigated phagocytosis of F. oxysporum by J774.1 murine cell line macrophages using live cell video microscopy. Macrophages avidly migrated towards F. oxysporum germlings and were rapidly engulfed after cell-cell contact was established. F. oxysporum germlings continued hyphal growth after engulfment by macrophages, leading to associated macrophage lysis and escape. Macrophage killing depended on the multiplicity of infection. After engulfment, F. oxysporum inhibited macrophages from completing mitosis, resulting in large daughter cells fused together by means of a F. oxysporum hypha. These results shed new light on the initial stages of Fusarium infection and the innate immune response of the mammalian host.

Highlights

Fusarium species cause devastating diseases on a wide variety of economically important crops worldwide [1]
Aspergillus conidia that escape from alveolar macrophages (AMs) can germinate, but are attacked by polymorphonuclear neutrophils (PMNs) which kill the hyphae through production of reactive oxygen species and degranulation [26,27,28]
Our results demonstrate that murine macrophages efficiently migrate towards and internalize F. oxysporum germlings

Summary

Introduction

Fusarium species cause devastating diseases on a wide variety of economically important crops worldwide [1]. Fusaria can cause a broad spectrum of diseases in humans, ranging from superficial or localized infections in immunocompetent hosts to lethal disseminated fusariosis in immunocompromised patients [2]. Lycopersici can cause disseminated infection in immunosupressed mice, making this the first fungal model for studying fungal pathogenicity across different host kingdoms [3,4]. Analysis of knockout mutants in the mouse model revealed striking similarities of infection mechanisms with other well-established human pathogens [3,5,6,7,8]. The mammalian immune response against human fungal pathogens relies mainly on phagocytosis of the fungus by cells of the innate immune system [9,10]. In C. albicans, phagocyte killing is associated with hyphal growth within the macrophage [12,13]. C. albicans yeast cells are engulfed preferentially compared to hyphal cells [13,17]

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