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. 2014 Apr 15:4:14.
doi: 10.1186/2045-7022-4-14. eCollection 2014.

Fungal allergy in asthma-state of the art and research needs

David W Denning  1 , Catherine Pashley  2 , Domink Hartl  3 , Andrew Wardlaw  2 , Cendrine Godet  4 , Stefano Del Giacco  5 , Laurence Delhaes  6 , Svetlana Sergejeva  7
Affiliations

Fungal allergy in asthma-state of the art and research needs

David W Denning et al. Clin Transl Allergy. .

Abstract

Sensitization to fungi and long term or uncontrolled fungal infection are associated with poor control of asthma, the likelihood of more severe disease and complications such as bronchiectasis and chronic pulmonary aspergillosis. Modelling suggests that >6.5 million people have severe asthma with fungal sensitizations (SAFS), up to 50% of adult asthmatics attending secondary care have fungal sensitization, and an estimated 4.8 million adults have allergic bronchopulmonary aspergillosis (ABPA). There is much uncertainty about which fungi and fungal allergens are relevant to asthma, the natural history of sensitisation to fungi, if there is an exposure response relationship for fungal allergy, and the pathogenesis and frequency of exacerbations and complications. Genetic associations have been described but only weakly linked to phenotypes. The evidence base for most management strategies in ABPA, SAFS and related conditions is weak. Yet straightforward clinical practice guidelines for management are required. The role of environmental monitoring and optimal means of controlling disease to prevent disability and complications are not yet clear. In this paper we set out the key evidence supporting the role of fungal exposure, sensitisation and infection in asthmatics, what is understood about pathogenesis and natural history and identify the numerous areas for research studies.

Keywords: ABPA; ABPM; Aspergillus; Corticosteroid; Eosinophil; Hypertonic saline; IgE; Itraconazole; SAFS; Severe asthma.

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Figures

Figure 1
Figure 1
Patterns of fungal interactions with humans, illustrating different host pathogen interactions, based on the host damage response framework[9].
Figure 2
Figure 2
Two contrasting disease models (A and B), with common elements of risk and exposure, but different outcomes. Model A illustrates a linear relationship between disease and complications, whereas model B provides independent consequences of fungal exposure, which may or may not be associated. In both models, it is proposed that airway colonization/infection with fungus, and possibly fungal impaction from breathing airborne non-pathogenic fungi, and/or bacterial infection, continue to drive the inflammatory process.
See this image and copyright information in PMC

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