Journal of Fungi

3 pages, 174 KiB

Open AccessEditorial

Special Issue: Mucosal Fungal Infections

by Jonathan P. Richardson and Julian R. Naglik

J. Fungi 2018, 4(2), 43; https://doi.org/10.3390/jof4020043 - 26 Mar 2018

Cited by 7 | Viewed by 3635

The past four decades have seen a staggering escalation in the number of invasive fungal infections worldwide.[...] Full article

(This article belongs to the Special Issue Mucosal Fungal Infections)

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Open AccessReview

The Human Mucosal Mycobiome and Fungal Community Interactions

by Elizabeth A. Witherden, Saeed Shoaie, Rebecca A. Hall and David L. Moyes

J. Fungi 2017, 3(4), 56; https://doi.org/10.3390/jof3040056 - 07 Oct 2017

Cited by 38 | Viewed by 9278

Abstract

With the advent of high-throughput sequencing techniques, the astonishing extent and complexity of the microbial communities that reside within and upon us has begun to become clear. Moreover, with advances in computing and modelling methods, we are now beginning to grasp just how [...] Read more.

With the advent of high-throughput sequencing techniques, the astonishing extent and complexity of the microbial communities that reside within and upon us has begun to become clear. Moreover, with advances in computing and modelling methods, we are now beginning to grasp just how dynamic our interactions with these communities are. The diversity of both these communities and their interactions—both within the community and with us—are dependent on a multitude of factors, both microbial- and host-mediated. Importantly, it is becoming clear that shifts in the makeup of these communities, or their responses, are linked to different disease states. Although much of the work to define these interactions and links has been investigating bacterial communities, recently there has been significant growth in the body of knowledge, indicating that shifts in the host fungal communities (mycobiome) are also intimately linked to disease status. In this review, we will explore these associations, along with the interactions between fungal communities and their human and microbial habitat, and discuss the future applications of systems biology in determining their role in disease status. Full article

(This article belongs to the Special Issue Mucosal Fungal Infections)

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14 pages, 632 KiB

Open AccessReview

Candida–Epithelial Interactions

by Jonathan P. Richardson, Jemima Ho and Julian R. Naglik

J. Fungi 2018, 4(1), 22; https://doi.org/10.3390/jof4010022 - 08 Feb 2018

Cited by 63 | Viewed by 8311

Abstract

A plethora of intricate and dynamic molecular interactions occur between microbes and the epithelial cells that form the mucosal surfaces of the human body. Fungi, particularly species of Candida, are commensal members of our microbiota, continuously interacting with epithelial cells. Transient and [...] Read more.

A plethora of intricate and dynamic molecular interactions occur between microbes and the epithelial cells that form the mucosal surfaces of the human body. Fungi, particularly species of Candida, are commensal members of our microbiota, continuously interacting with epithelial cells. Transient and localised perturbations to the mucosal environment can facilitate the overgrowth of fungi, causing infection. This minireview will examine the direct and indirect mechanisms by which Candida species and epithelial cells interact with each other, and explore the factors involved in the central processes of adhesion, invasion, and destruction of host mucosal surfaces. Full article

(This article belongs to the Special Issue Mucosal Fungal Infections)

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Open AccessReview

Innate Immunity to Mucosal Candida Infections

by Akash Verma, Sarah L. Gaffen and Marc Swidergall

J. Fungi 2017, 3(4), 60; https://doi.org/10.3390/jof3040060 - 31 Oct 2017

Cited by 45 | Viewed by 10644

Abstract

Mucosal epithelial tissues are exposed to high numbers of microbes, including commensal fungi, and are able to distinguish between those that are avirulent and those that cause disease. Epithelial cells have evolved multiple mechanisms to defend against colonization and invasion by Candida species. [...] Read more.

Mucosal epithelial tissues are exposed to high numbers of microbes, including commensal fungi, and are able to distinguish between those that are avirulent and those that cause disease. Epithelial cells have evolved multiple mechanisms to defend against colonization and invasion by Candida species. The interplay between mucosal epithelial tissues and immune cells is key for control and clearance of fungal infections. Our understanding of the mucosal innate host defense system has expanded recently with new studies bringing to light the importance of epithelial cell responses, innate T cells, neutrophils, and other phagocytes during Candida infections. Epithelial tissues release cytokines, host defense peptides, and alarmins during Candida invasion that act in concert to limit fungal proliferation and recruit immune effector cells. The innate T cell/IL-17 axis and recruitment of neutrophils are of central importance in controlling mucosal fungal infections. Here, we review current knowledge of the innate immunity at sites of mucosal Candida infection, with a focus on infections caused by C. albicans. Full article

(This article belongs to the Special Issue Mucosal Fungal Infections)

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17 pages, 806 KiB

Open AccessReview

Anti-Aspergillus Activities of the Respiratory Epithelium in Health and Disease

by Margherita Bertuzzi, Gemma E. Hayes, Uju J. Icheoku, Norman Van Rhijn, David W. Denning, Nir Osherov and Elaine M. Bignell

J. Fungi 2018, 4(1), 8; https://doi.org/10.3390/jof4010008 - 08 Jan 2018

Cited by 44 | Viewed by 6612

Abstract

Respiratory epithelia fulfil multiple roles beyond that of gaseous exchange, also acting as primary custodians of lung sterility and inflammatory homeostasis. Inhaled fungal spores pose a continual antigenic, and potentially pathogenic, challenge to lung integrity against which the human respiratory mucosa has developed [...] Read more.

Respiratory epithelia fulfil multiple roles beyond that of gaseous exchange, also acting as primary custodians of lung sterility and inflammatory homeostasis. Inhaled fungal spores pose a continual antigenic, and potentially pathogenic, challenge to lung integrity against which the human respiratory mucosa has developed various tolerance and defence strategies. However, respiratory disease and immune dysfunction frequently render the human lung susceptible to fungal diseases, the most common of which are the aspergilloses, a group of syndromes caused by inhaled spores of Aspergillus fumigatus. Inhaled Aspergillus spores enter into a multiplicity of interactions with respiratory epithelia, the mechanistic bases of which are only just becoming recognized as important drivers of disease, as well as possible therapeutic targets. In this mini-review we examine current understanding of Aspergillus-epithelial interactions and, based upon the very latest developments in the field, we explore two apparently opposing schools of thought which view epithelial uptake of Aspergillus spores as either a curative or disease-exacerbating event. Full article

(This article belongs to the Special Issue Mucosal Fungal Infections)

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The Multifaceted Role of T-Helper Responses in Host Defense against Aspergillus fumigatus

by Intan M. W. Dewi, Frank L. Van de Veerdonk and Mark S. Gresnigt

J. Fungi 2017, 3(4), 55; https://doi.org/10.3390/jof3040055 - 04 Oct 2017

Cited by 42 | Viewed by 10015

Abstract

The ubiquitous opportunistic fungal pathogen Aspergillus fumigatus rarely causes infections in immunocompetent individuals. A healthy functional innate immune system plays a crucial role in preventing Aspergillus-infection. This pivotal role for the innate immune system makes it a main research focus in studying [...] Read more.

The ubiquitous opportunistic fungal pathogen Aspergillus fumigatus rarely causes infections in immunocompetent individuals. A healthy functional innate immune system plays a crucial role in preventing Aspergillus-infection. This pivotal role for the innate immune system makes it a main research focus in studying the pathogenesis of aspergillosis. Although sometimes overshadowed by the innate immune response, the adaptive immune response, and in particular T-helper responses, also represents a key player in host defense against Aspergillus. Virtually all T-helper subsets have been described to play a role during aspergillosis, with the Th1 response being crucial for fungal clearance. However; morbidity and mortality of aspergillosis can also be partly attributed to detrimental immune responses resulting from adaptive immune activation. Th2 responses benefit fungal persistence; and are the foundation of allergic forms of aspergillosis. The Th17 response has two sides; although crucial for granulocyte recruitment, it can be involved in detrimental immunopathology. Regulatory T-cells, the endogenous regulators of inflammatory responses, play a key role in controlling detrimental inflammatory responses during aspergillosis. The current knowledge of the adaptive immune response against A. fumigatus is summarized in this review. A better understanding on how T-helper responses facilitate clearance of Aspergillus-infection and control inflammation can be the fundamental basis for understanding the pathogenesis of aspergillosis and for the development of novel host-directed therapies. Full article

(This article belongs to the Special Issue Mucosal Fungal Infections)

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Open AccessReview

Cryptococcus–Epithelial Interactions

by Leanne M. Taylor-Smith

J. Fungi 2017, 3(4), 53; https://doi.org/10.3390/jof3040053 - 02 Oct 2017

Cited by 23 | Viewed by 7124

Abstract

The fungal pathogen, Cryptococcus neoformans, causes devastating levels of morbidity and mortality. Infections with this fungus tend to be predominantly in immunocompromised individuals, such as those with HIV. Infections initiate with inhalation of cryptococcal cells and entry of the pathogen into the [...] Read more.

The fungal pathogen, Cryptococcus neoformans, causes devastating levels of morbidity and mortality. Infections with this fungus tend to be predominantly in immunocompromised individuals, such as those with HIV. Infections initiate with inhalation of cryptococcal cells and entry of the pathogen into the lungs. The bronchial epithelial cells of the upper airway and the alveolar epithelial cells of the lower airway are likely to be the first host cells that Cryptococcus engage with. Thus the interaction of cryptococci and the respiratory epithelia will be the focus of this review. C. neoformans has been shown to adhere to respiratory epithelial cells, although if the role of the capsule is in aiding or hindering this adhesion is debatable. The epithelia are also able to react to cryptococci with the release of cytokines and chemokines to start the immune response to this invading pathogen. The activity of surfactant components that line this mucosal barrier towards Cryptococcus and the metabolic and transcriptional reaction of cryptococci when encountering epithelial cells will also be discussed. Full article

(This article belongs to the Special Issue Mucosal Fungal Infections)

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Open AccessReview

Adaptive Immunity to Cryptococcus neoformans Infections

by Liliane Mukaremera and Kirsten Nielsen

J. Fungi 2017, 3(4), 64; https://doi.org/10.3390/jof3040064 - 21 Nov 2017

Cited by 42 | Viewed by 12598

Abstract

The Cryptococcus neoformans/Cryptococcus gattii species complex is a group of fungal pathogens with different phenotypic and genotypic diversity that cause disease in immunocompromised patients as well as in healthy individuals. The immune response resulting from the interaction between Cryptococcus and the [...] Read more.

The Cryptococcus neoformans/Cryptococcus gattii species complex is a group of fungal pathogens with different phenotypic and genotypic diversity that cause disease in immunocompromised patients as well as in healthy individuals. The immune response resulting from the interaction between Cryptococcus and the host immune system is a key determinant of the disease outcome. The species C. neoformans causes the majority of human infections, and therefore almost all immunological studies focused on C. neoformans infections. Thus, this review presents current understanding on the role of adaptive immunity during C. neoformans infections both in humans and in animal models of disease. Full article

(This article belongs to the Special Issue Mucosal Fungal Infections)

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Open AccessReview

Innate and Adaptive Immunity to Mucorales

by Harlene Ghuman and Kerstin Voelz

J. Fungi 2017, 3(3), 48; https://doi.org/10.3390/jof3030048 - 05 Sep 2017

Cited by 60 | Viewed by 7478

Abstract

Mucormycosis is an invasive fungal infection characterised by rapid filamentous growth, which leads to angioinvasion, thrombosis, and tissue necrosis. The high mortality rates (50–100%) associated with mucormycosis are reflective of not only the aggressive nature of the infection and the poor therapeutics currently [...] Read more.

Mucormycosis is an invasive fungal infection characterised by rapid filamentous growth, which leads to angioinvasion, thrombosis, and tissue necrosis. The high mortality rates (50–100%) associated with mucormycosis are reflective of not only the aggressive nature of the infection and the poor therapeutics currently employed, but also the failure of the human immune system to successfully clear the infection. Immune effector interaction with Mucorales is influenced by the developmental stage of the mucormycete spore. In a healthy immune environment, resting spores are resistant to phagocytic killing. Contrarily, swollen spores and hyphae are susceptible to damage and degradation by macrophages and neutrophils. Under the effects of immune suppression, the recruitment and efficacy of macrophage and neutrophil activity against mucormycetes is considerably reduced. Following penetration of the endothelial lining, Mucorales encounter platelets. Platelets adhere to both mucormycete spores and hyphae, and exhibit germination suppression and hyphal damage capacity in vitro. Dendritic cells are activated in response to Mucorales hyphae only, and induce adaptive immunity. It is crucial to further knowledge regarding our immune system’s failure to eradicate resting spores under intact immunity and inhibit fungal growth under immunocompromised conditions, in order to understand mucormycosis pathogenicity and enhance therapeutic strategies for mucormycosis. Full article

(This article belongs to the Special Issue Mucosal Fungal Infections)

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