Special Issue "Host–Fungus Interactions"

A special issue of Journal of Fungi (ISSN 2309-608X).

Deadline for manuscript submissions: closed (31 July 2017) | Viewed by 35347

Special Issue Editor

Prof. Dr. Adilia Warris
E-Mail Website
Guest Editor
Aberdeen Fungal Group, MRC Centre for Medical Mycology, Institute of Medical Sciences, Foresterhill, AB25 2ZD Aberdeen, Scotland, UK
Interests: invasive aspergillosis; host–fungus interaction; paediatric mycology; chronic granulomatous disease; cystic fibrosis; Aspergillus fumigatus; Aspergillus nidulans

Special Issue Information

Dear Colleagues,

The clinical presentation of fungal disease is strongly determined by the underlying immune defect present. In particular, the increased recognition of monogenic disorders (e.g. primary immunodeficiencies) have provided us with valuable insights into human immunity to fungal infections over the last two decades. While the innate immune system plays a key role in the resistance to fungal disease, the interaction with the adaptive immune system plays a non-redundant role in the orchestration of the host response. Major scientific developments in a variety of techniques to explore immune pathways and individual components of the immune system in greater detail have uncovered novel aspects in the host–fungus interaction. Recognition of the differentiated interaction of the host with various morphologies of both yeast and moulds, as well as fungal species specific recognition followed by stimulation of the immune system, has further deciphered our understanding of unique host–fungus interactions. Exploration and understanding of those immunological pathways will ultimately lead to new directions in the development of immunotherapeutic strategies. The aim of this Special Issue is to focus on specific host–fungal interactions from both the bench- and the bed-side. Topics include, but are not limited to, phagocyte-fungus interactions, primary immunodeficiencies associated with an increase susceptibility to fungal disease, adaptive antifungal immunity, the role of specific receptors and pathways in the recognition of fungal pathogens, specific fungal morphologies shaping the immune response. Contributions of experts who are actively researching these topics are invited. In addition, manuscripts summarizing recent advances in the topic or introducing novel hypotheses are particularly welcome and colleagues are encouraged to submit their contributions to this Special Issue.

Prof. Dr. Adilia Warris
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Journal of Fungi is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2000 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • Host–fungus interaction
  • Primary immunodeficiency
  • Fungal disease
  • Moulds
  • Yeasts
  • Innate immunity
  • Adaptive immunity
  • Phagocytes

Published Papers (10 papers)

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Editorial

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Editorial
Special Issue: Host–Fungus Interactions
J. Fungi 2018, 4(1), 7; https://doi.org/10.3390/jof4010007 - 02 Jan 2018
Cited by 1 | Viewed by 1582
Abstract
The clinical presentation of fungal disease is strongly determined by the underlying immune defect present [...]
Full article
(This article belongs to the Special Issue Host–Fungus Interactions)

Research

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Article
Conserved Inhibition of Neutrophil Extracellular Trap Release by Clinical Candida albicans Biofilms
J. Fungi 2017, 3(3), 49; https://doi.org/10.3390/jof3030049 - 06 Sep 2017
Cited by 18 | Viewed by 2878
Abstract
Candida albicans biofilms are difficult to eradicate due to their resistance to host defenses and antifungal drugs. Although neutrophils are the primary responder to C. albicans during invasive candidiasis, biofilms resist killing by neutrophils. Prior investigation, with the commonly used laboratory strain SC5314, [...] Read more.
Candida albicans biofilms are difficult to eradicate due to their resistance to host defenses and antifungal drugs. Although neutrophils are the primary responder to C. albicans during invasive candidiasis, biofilms resist killing by neutrophils. Prior investigation, with the commonly used laboratory strain SC5314, linked this phenotype to the impaired release of neutrophil extracellular traps (NETs), which are structures of DNA, histones, and antimicrobial proteins involved in extracellular microbial killing. Considering the diversity of C. albicans biofilms, we examined the neutrophil response to a subset of clinical isolates forming biofilms with varying depths and architectures. Using fluorescent staining of DNA and scanning electron microscopy, we found that inhibition of NET release was conserved across the clinical isolates. However, the dampening of the production of reactive oxygen species (ROS) by neutrophils was strain-dependent, suggesting an uncoupling of ROS and NET inhibition. Our findings show that biofilms formed by clinical C. albicans isolates uniformly impair the release of NETs. Further investigation of this pathway may reveal novel approaches to augment immunity to C. albicans biofilm infections. Full article
(This article belongs to the Special Issue Host–Fungus Interactions)
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Article
Macrophage Migration Is Impaired within Candida albicans Biofilms
J. Fungi 2017, 3(3), 31; https://doi.org/10.3390/jof3030031 - 22 Jun 2017
Cited by 15 | Viewed by 3517
Abstract
Candida albicans is an opportunistic fungal pathogen that infects immunocompromised patients. Infection control requires phagocytosis by innate immune cells, including macrophages. Migration towards, and subsequent recognition of, C. albicans fungal cell wall components by macrophages is critical for phagocytosis. Using live-cell imaging of [...] Read more.
Candida albicans is an opportunistic fungal pathogen that infects immunocompromised patients. Infection control requires phagocytosis by innate immune cells, including macrophages. Migration towards, and subsequent recognition of, C. albicans fungal cell wall components by macrophages is critical for phagocytosis. Using live-cell imaging of phagocytosis, the macrophage cell line J774.1 showed enhanced movement in response to C. albicans cell wall mutants, particularly during the first 30 min, irrespective of the infection ratio. However, phagocyte migration was reduced up to 2-fold within a C. albicans biofilm compared to planktonic fungal cells. Biofilms formed from C. albicans glycosylation mutant cells also inhibited macrophage migration to a similar extent as wildtype Candida biofilms, suggesting that the physical structure of the biofilm, rather than polysaccharide matrix composition, may hamper phagocyte migration. These data illustrate differential macrophage migratory capacities, dependent upon the form of C. albicans encountered. Impaired migration of macrophages within a C. albicans biofilm may contribute to the recalcitrant nature of clinical infections in which biofilm formation occurs. Full article
(This article belongs to the Special Issue Host–Fungus Interactions)
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Article
Monocyte Phenotype and IFN-γ-Inducible Cytokine Responses Are Associated with Cryptococcal Immune Reconstitution Inflammatory Syndrome
J. Fungi 2017, 3(2), 28; https://doi.org/10.3390/jof3020028 - 02 Jun 2017
Cited by 11 | Viewed by 2952
Abstract
A third of adults with AIDS and cryptococcal meningitis (CM) develop immune reconstitution inflammatory syndrome (IRIS) after initiating antiretroviral therapy (ART), which is thought to result from exaggerated inflammatory antigen-specific T cell responses. The contribution of monocytes to the immunopathogenesis of cryptococcal IRIS [...] Read more.
A third of adults with AIDS and cryptococcal meningitis (CM) develop immune reconstitution inflammatory syndrome (IRIS) after initiating antiretroviral therapy (ART), which is thought to result from exaggerated inflammatory antigen-specific T cell responses. The contribution of monocytes to the immunopathogenesis of cryptococcal IRIS remains unclear. We compared monocyte subset frequencies and immune responses in HIV-infected Ugandans at time of CM diagnosis (IRIS-Baseline) for those who later developed CM-IRIS, controls who did not develop CM-IRIS (Control-Baseline) at CM-IRIS (IRIS-Event), and for controls at a time point matched for ART duration (Control-Event) to understand the association of monocyte distribution and immune responses with cryptococcal IRIS. At baseline, stimulation with IFN-γ ex vivo induced a higher frequency of TNF-α- and IL-6-producing monocytes among those who later developed IRIS. Among participants who developed IRIS, ex vivo IFN-γ stimulation induced higher frequencies of activated monocytes, IL-6+, TNF-α+ classical, and IL-6+ intermediate monocytes compared with controls. In conclusion, we have demonstrated that monocyte subset phenotype and cytokine responses prior to ART are associated with and may be predictive of CM-IRIS. Larger studies to further delineate innate immunological responses and the efficacy of immunomodulatory therapies during cryptococcal IRIS are warranted. Full article
(This article belongs to the Special Issue Host–Fungus Interactions)
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Article
Innate and Adaptive Immune Defects in Chronic Pulmonary Aspergillosis
J. Fungi 2017, 3(2), 26; https://doi.org/10.3390/jof3020026 - 29 May 2017
Cited by 197 | Viewed by 3588
Abstract
We evaluated the expression of biomarkers of innate and adaptive immune response in correlation with underlying conditions in 144 patients with chronic pulmonary aspergillosis (CPA). Patients with complete medical and radiological records, white cell counts, and a complete panel of CD3, CD4, CD8, [...] Read more.
We evaluated the expression of biomarkers of innate and adaptive immune response in correlation with underlying conditions in 144 patients with chronic pulmonary aspergillosis (CPA). Patients with complete medical and radiological records, white cell counts, and a complete panel of CD3, CD4, CD8, CD19, and CD56 lymphocyte subsets were included. Eighty-four (58%) patients had lymphopenia. Six (4%) patients had lymphopenia in all five CD variables. There were 62 (43%) patients with low CD56 and 62 (43%) patients with low CD19. Ten (7%) patients had isolated CD19 lymphopenia, 18 (13%) had isolated CD56 lymphopenia, and 15 (10%) had combined CD19 and CD56 lymphopenia only. Forty-eight (33%) patients had low CD3 and 46 (32%) had low CD8 counts. Twenty-five (17%) patients had low CD4, 15 (10%) of whom had absolute CD4 counts <200/μL. Multivariable logistic regression showed associations between: low CD19 and pulmonary sarcoidosis (Odds Ratio (OR), 5.53; 95% Confidence Interval (CI), 1.43–21.33; p = 0.013), and emphysema (OR, 4.58; 95% CI; 1.36–15.38; p = 0.014), low CD56 and no bronchiectasis (OR, 0.27; 95% CI, 0.10–0.77; p = 0.014), low CD3 and both multicavitary CPA disease (OR, 2.95; 95% CI, 1.30–6.72; p = 0.010) and pulmonary sarcoidosis (OR, 4.94; 95% CI, 1.39–17.57; p = 0.014). Several subtle immune defects are found in CPA. Full article
(This article belongs to the Special Issue Host–Fungus Interactions)
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Review

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Review
The Role of IL-17 in Protection against Mucosal Candida Infections
J. Fungi 2017, 3(4), 52; https://doi.org/10.3390/jof3040052 - 27 Sep 2017
Cited by 52 | Viewed by 2927
Abstract
Interleukin-17 (IL-17) is a proinflammatory cytokine produced by adaptive CD4+ T helper cells and innate lymphocytes, such as γδ-T cells and TCRβ+ “natural” Th17 cells. IL-17 activates signaling through the IL-17 receptor, which induces other proinflammatory cytokines, antimicrobial peptides and neutrophil chemokines that [...] Read more.
Interleukin-17 (IL-17) is a proinflammatory cytokine produced by adaptive CD4+ T helper cells and innate lymphocytes, such as γδ-T cells and TCRβ+ “natural” Th17 cells. IL-17 activates signaling through the IL-17 receptor, which induces other proinflammatory cytokines, antimicrobial peptides and neutrophil chemokines that are important for antifungal activity. The importance of IL-17 in protective antifungal immunity is evident in mice and humans, where various genetic defects related to the IL-17-signaling pathway render them highly susceptible to forms of candidiasis such oropharyngeal candidiasis (OPC) or more broadly chronic mucocutaneous candidiasis (CMC), both caused mainly by the opportunistic fungal pathogen Candida albicans. OPC is common in infants and the elderly, HIV/AIDS and patients receiving chemotherapy and/or radiotherapy for head and neck cancers. This review focuses on the role of IL-17 in protection against candidiasis, and includes a brief discussion of non-Candida albicans fungal infections, as well as how therapeutic interventions blocking IL-17-related components can affect antifungal immunity. Full article
(This article belongs to the Special Issue Host–Fungus Interactions)
Review
Fungal Strategies to Evade the Host Immune Recognition
J. Fungi 2017, 3(4), 51; https://doi.org/10.3390/jof3040051 - 23 Sep 2017
Cited by 55 | Viewed by 7257
Abstract
The recognition of fungal cells by the host immune system is key during the establishment of a protective anti-fungal response. Even though the immune system has evolved a vast number of processes to control these organisms, they have developed strategies to fight back, [...] Read more.
The recognition of fungal cells by the host immune system is key during the establishment of a protective anti-fungal response. Even though the immune system has evolved a vast number of processes to control these organisms, they have developed strategies to fight back, avoiding the proper recognition by immune components and thus interfering with the host protective mechanisms. Therefore, the strategies to evade the immune system are as important as the virulence factors and attributes that damage the host tissues and cells. Here, we performed a thorough revision of the main fungal tactics to escape from the host immunosurveillance processes. These include the composition and organization of the cell wall, the fungal capsule, the formation of titan cells, biofilms, and asteroid bodies; the ability to undergo dimorphism; and the escape from nutritional immunity, extracellular traps, phagocytosis, and the action of humoral immune effectors. Full article
(This article belongs to the Special Issue Host–Fungus Interactions)
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Review
Immune Recognition of Fungal Polysaccharides
J. Fungi 2017, 3(3), 47; https://doi.org/10.3390/jof3030047 - 28 Aug 2017
Cited by 45 | Viewed by 5745
Abstract
The incidence of fungal infections has dramatically increased in recent years, in large part due to increased use of immunosuppressive medications, as well as aggressive medical and surgical interventions that compromise natural skin and mucosal barriers. There are relatively few currently licensed antifungal [...] Read more.
The incidence of fungal infections has dramatically increased in recent years, in large part due to increased use of immunosuppressive medications, as well as aggressive medical and surgical interventions that compromise natural skin and mucosal barriers. There are relatively few currently licensed antifungal drugs, and rising resistance to these agents has led to interest in the development of novel preventative and therapeutic strategies targeting these devastating infections. One approach to combat fungal infections is to augment the host immune response towards these organisms. The polysaccharide-rich cell wall is the initial point of contact between fungi and the host immune system, and therefore, represents an important target for immunotherapeutic approaches. This review highlights the advances made in our understanding of the mechanisms by which the immune system recognizes and interacts with exopolysaccharides produced by four of the most common fungal pathogens: Aspergillus fumigatus, Candida albicans, Cryptococcus neoformans, and Histoplasma capsulatum. Work to date suggests that inner cell wall polysaccharides that play an important structural role are the most conserved across diverse members of the fungal kingdom, and elicit the strongest innate immune responses. The immune system senses these carbohydrates through receptors, such as lectins and complement proteins. In contrast, a greater diversity of polysaccharides is found within the outer cell walls of pathogenic fungi. These glycans play an important role in immune evasion, and can even induce anti-inflammatory host responses. Further study of the complex interactions between the host immune system and the fungal polysaccharides will be necessary to develop more effective therapeutic strategies, as well as to explore the use of immunosuppressive polysaccharides as therapeutic agents to modulate inflammation. Full article
(This article belongs to the Special Issue Host–Fungus Interactions)
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Review
Innate Immune Responses to Cryptococcus
J. Fungi 2017, 3(3), 35; https://doi.org/10.3390/jof3030035 - 02 Jul 2017
Cited by 16 | Viewed by 2724
Abstract
Cryptococcus species are encapsulated fungi found in the environment that predominantly cause disease in immunocompromised hosts after inhalation into the lungs. Even with contemporary antifungal regimens, patients with cryptococcosis continue to have high morbidity and mortality rates. The development of more effective therapies [...] Read more.
Cryptococcus species are encapsulated fungi found in the environment that predominantly cause disease in immunocompromised hosts after inhalation into the lungs. Even with contemporary antifungal regimens, patients with cryptococcosis continue to have high morbidity and mortality rates. The development of more effective therapies may depend on our understanding of the cellular and molecular mechanisms by which the host promotes sterilizing immunity against the fungus. This review will highlight our current knowledge of how Cryptococcus, primarily the species C. neoformans, is sensed by the mammalian host and how subsequent signaling pathways direct the anti-cryptococcal response by effector cells of the innate immune system. Full article
(This article belongs to the Special Issue Host–Fungus Interactions)
Review
NK Cells and Their Role in Invasive Mold Infection
J. Fungi 2017, 3(2), 25; https://doi.org/10.3390/jof3020025 - 19 May 2017
Cited by 5 | Viewed by 1830
Abstract
There is growing evidence that Natural Killer (NK) cells exhibit in vitro activity against both Aspergillus and non-Aspergillus molds. Cytotoxic molecules such as NK cell-derived perforin seem to play an important role in the antifungal activity. In addition, NK cells release a [...] Read more.
There is growing evidence that Natural Killer (NK) cells exhibit in vitro activity against both Aspergillus and non-Aspergillus molds. Cytotoxic molecules such as NK cell-derived perforin seem to play an important role in the antifungal activity. In addition, NK cells release a number of cytokines upon stimulation by fungi, which modulate both innate and adaptive host immune responses. Whereas the in vitro data of the antifungal activity of NK cells are supported by animal studies, clinical data are scarce to date. Full article
(This article belongs to the Special Issue Host–Fungus Interactions)
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