Abstract
Invasive aspergillosis (IA) is a life-threatening fungal disease commonly diagnosed among individuals with immunological deficits, namely hematological patients undergoing chemotherapy or allogeneic hematopoietic stem cell transplantation. Vaccines are not available, and despite the improved diagnosis and antifungal therapy, the treatment of IA is associated with a poor outcome. Importantly, the risk of infection and its clinical outcome vary significantly even among patients with similar predisposing clinical factors and microbiological exposure. Recent insights into antifungal immunity have further highlighted the complexity of host-fungus interactions and the multiple pathogen-sensing systems activated to control infection. How to decode this information into clinical practice remains however, a challenging issue in medical mycology. Here, we address recent advances in our understanding of the host-fungus interaction and discuss the application of this knowledge in potential strategies with the aim of moving toward personalized diagnostics and treatment (theranostics) in immunocompromised patients. Ultimately, the integration of individual traits into a clinically applicable process to predict the risk and progression of disease, and the efficacy of antifungal prophylaxis and therapy, holds the promise of a pioneering innovation benefiting patients at risk of IA.
Highlights
Aspergillosis includes an extensive spectrum of diseases caused by fungi of the genus Aspergillus with clinical manifestations that range from colonization to allergic bronchopulmonary aspergillosis and disseminated forms of infection (Segal, 2009)
Another important feature of dectin-1-mediated signaling in response to A. fumigatus is the activation of the nucleotidebinding oligomerization domain-like receptor family, pyrin domain containing 3 (NLRP3) inflammasome leading to the production of bioactive interleukin (IL)-1β (Said-Sadier et al, 2010)
The inborn deficiency of the phagocyte nicotinamide adenine dinucleotide phosphate (NADPH) oxidase leading to a defective production of reactive oxygen species (ROS) and underlying chronic granulomatous disease (CGD) is the best known example of primary immunodeficiency associated with a distinctive predisposition to Invasive aspergillosis (IA) (Vinh, 2011)
Summary
Aspergillosis includes an extensive spectrum of diseases caused by fungi of the genus Aspergillus with clinical manifestations that range from colonization to allergic bronchopulmonary aspergillosis and disseminated forms of infection (Segal, 2009). The prevalence of invasive aspergillosis (IA) has steadily increased in the last decades, mostly due to the advent of solid organ and hematopoietic stem cell transplantation (HSCT), and the increased use of chemotherapy and immunosuppression (Kontoyiannis et al, 2010; Pagano et al, 2010). The diagnosis of IA has improved, namely because of the introduction of biomarkers such as the detection of galactomannan in the clinical practice (Morrissey et al, 2013), successful treatment is still a challenging endeavor. Established infection is difficult to eradicate, resulting in associated mortality rates ranging from 40 to 90% (Walsh et al, 2008)
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