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      Immunomodulation as a Therapy for Aspergillus Infection: Current Status and Future Perspectives

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          Abstract

          Invasive aspergillosis (IA) is the most serious life-threatening infectious complication of intensive remission induction chemotherapy and allogeneic stem cell transplantation in patients with a variety of hematological malignancies. Aspergillus fumigatus is the most commonly isolated species from cases of IA. Despite the various improvements that have been made with preventative strategies and the development of antifungal drugs, there is an urgent need for new therapeutic approaches that focus on strategies to boost the host’s immune response, since immunological recovery is recognized as being the major determinant of the outcome of IA. Here, we aim to summarize current knowledge about a broad variety of immunotherapeutic approaches against IA, including therapies based on the transfer of distinct immune cell populations, and the administration of cytokines and antibodies.

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          Therapeutic applications of macrophage colony-stimulating factor-1 (CSF-1) and antagonists of CSF-1 receptor (CSF-1R) signaling.

          David A Hume, Kelli P A MacDonald (2012)
          Macrophage-colony stimulating factor (CSF-1) signaling through its receptor (CSF-1R) promotes the differentiation of myeloid progenitors into heterogeneous populations of monocytes, macrophages, dendritic cells, and bone-resorbing osteoclasts. In the periphery, CSF-1 regulates the migration, proliferation, function, and survival of macrophages, which function at multiple levels within the innate and adaptive immune systems. Macrophage populations elicited by CSF-1 are associated with, and exacerbate, a broad spectrum of pathologies, including cancer, inflammation, and bone disease. Conversely, macrophages can also contribute to immunosuppression, disease resolution, and tissue repair. Recombinant CSF-1, antibodies against the ligand and the receptor, and specific inhibitors of CSF-1R kinase activity have been each been tested in a range of animal models and in some cases, in patients. This review examines the potential clinical uses of modulators of the CSF-1/CSF-1R system. We conclude that CSF-1 promotes a resident-type macrophage phenotype. As a treatment, CSF-1 has therapeutic potential in tissue repair. Conversely, inhibition of CSF-1R is unlikely to be effective in inflammatory disease but may have utility in cancer.
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            2006 update of recommendations for the use of white blood cell growth factors: an evidence-based clinical practice guideline.

            Thomas Smith, James Khatcheressian, Gary H Lyman … (2006)
            To update the 2000 American Society of Clinical Oncology guideline on the use of hematopoietic colony-stimulating factors (CSF). The Update Committee completed a review and analysis of pertinent data published from 1999 through September 2005. Guided by the 1996 ASCO clinical outcomes criteria, the Update Committee formulated recommendations based on improvements in survival, quality of life, toxicity reduction and cost-effectiveness. The 2005 Update Committee agreed unanimously that reduction in febrile neutropenia (FN) is an important clinical outcome that justifies the use of CSFs, regardless of impact on other factors, when the risk of FN is approximately 20% and no other equally effective regimen that does not require CSFs is available. Primary prophylaxis is recommended for the prevention of FN in patients who are at high risk based on age, medical history, disease characteristics, and myelotoxicity of the chemotherapy regimen. CSF use allows a modest to moderate increase in dose-density and/or dose-intensity of chemotherapy regimens. Dose-dense regimens should only be used within an appropriately designed clinical trial or if supported by convincing efficacy data. Prophylactic CSF for patients with diffuse aggressive lymphoma aged 65 years and older treated with curative chemotherapy (CHOP or more aggressive regimens) should be given to reduce the incidence of FN and infections. Current recommendations for the management of patients exposed to lethal doses of total body radiotherapy, but not doses high enough to lead to certain death due to injury to other organs, includes the prompt administration of CSF or pegylated G-CSF.
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              Surface hydrophobin prevents immune recognition of airborne fungal spores.

              Vishukumar Aimanianda, Jagadeesh Bayry, Silvia Bozza … (2009)
              The air we breathe is filled with thousands of fungal spores (conidia) per cubic metre, which in certain composting environments can easily exceed 10(9) per cubic metre. They originate from more than a hundred fungal species belonging mainly to the genera Cladosporium, Penicillium, Alternaria and Aspergillus. Although these conidia contain many antigens and allergens, it is not known why airborne fungal microflora do not activate the host innate immune cells continuously and do not induce detrimental inflammatory responses following their inhalation. Here we show that the surface layer on the dormant conidia masks their recognition by the immune system and hence prevents immune response. To explore this, we used several fungal members of the airborne microflora, including the human opportunistic fungal pathogen Aspergillus fumigatus, in in vitro assays with dendritic cells and alveolar macrophages and in in vivo murine experiments. In A. fumigatus, this surface 'rodlet layer' is composed of hydrophobic RodA protein covalently bound to the conidial cell wall through glycosylphosphatidylinositol-remnants. RodA extracted from conidia of A. fumigatus was immunologically inert and did not induce dendritic cell or alveolar macrophage maturation and activation, and failed to activate helper T-cell immune responses in vivo. The removal of this surface 'rodlet/hydrophobin layer' either chemically (using hydrofluoric acid), genetically (DeltarodA mutant) or biologically (germination) resulted in conidial morphotypes inducing immune activation. All these observations show that the hydrophobic rodlet layer on the conidial cell surface immunologically silences airborne moulds.
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                Author and article information

                Journal
                Journal ID (nlm-ta): J Fungi (Basel)
                Journal ID (iso-abbrev): J Fungi (Basel)
                Journal ID (publisher-id): jof
                Title: Journal of Fungi
                Publisher: MDPI
                ISSN (Electronic): 2309-608X
                Publication date (Electronic): 14 December 2018
                Publication date Collection: December 2018
                Volume: 4
                Issue: 4
                Electronic Location Identifier: 137
                Affiliations
                Department of Internal Medicine II, University Hospital Wuerzburg, WÜ4i, Building C11, 97080 Wuerzburg, Germany; Lauruschka_c@ 123456ukw.de (C.D.L.); Einsele_h@ 123456ukw.de (H.E.)
                Author notes
                [* ]Correspondence: Loeffler_j@ 123456ukw.de ; Tel.: +49-931-2013-6412; Fax: +49-931-2013-6409
                Article
                Publisher ID: jof-04-00137
                DOI: 10.3390/jof4040137
                PMC ID: 6308942
                PubMed ID: 30558125
                SO-VID: 62e85cc7-b2ca-4d12-b8bb-74fb4e1319ab
                Copyright © © 2018 by the authors.
                License:

                Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( http://creativecommons.org/licenses/by/4.0/).

                History
                Date received : 15 November 2018
                Date accepted : 10 December 2018
                Categories
                Subject: Review

                Keywords: immunotherapy,invasive aspergillosis,aspergillus fumigatus,fungal infections,innate immunity,adaptive immunity,cell therapy,cytokine therapy
                Data availability:
                Keywords: immunotherapy, invasive aspergillosis, aspergillus fumigatus, fungal infections, innate immunity, adaptive immunity, cell therapy, cytokine therapy

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