Abstract
Asthma is a chronic debilitating airway disease affecting millions of people worldwide. Although largely thought to be a disease of the first world, it is now clear that it is on the rise in many middle- and lower-income countries. The disease is complex, and its etiology is poorly understood, which explains failure of most treatment strategies. We know that in children, asthma is closely linked to poor lung function in the first 3-years of life, when the lung is still undergoing post-natal alveolarization phase. Epidemiological studies also suggest that environmental factors around that age do play a critical part in the establishment of early wheezing which persists until adulthood. Some of the factors that contribute to early development of asthma in children in Western world are clear, however, in low- to middle-income countries this is likely to differ significantly. The contribution of fungal species in the development of allergic diseases is known in adults and in experimental models. However, it is unclear whether early exposure during perinatal or post-natal lung development influences a protective or promotes allergic asthma. Host immune cells and responses will play a crucial part in early development of allergic asthma. How immune cells and their receptors may recognize fungi and promote allergic asthma or protect by tolerance among other immune mechanisms is not fully understood in this early lung development stage. The aim of this review is to discuss what fungal species are present during early exposure as well as their contribution to the development of allergic responses. We also discuss how the host has evolved to promote tolerance to limit hyper-responsiveness to innocuous fungi, and how host evasion by fungi during early development consequentially results in allergic diseases.
Highlights
Asthma has largely been thought to be a genetic pre-disposition, over the last two decades it is becoming more clear that environment may play a significant role in the development of the disease [1]
Toll-like receptor 3(TLR-3), TLR-9, DECTIN-1 variants were shown to be associated with severe asthma with fungal sensitization (SAFS) induced by Aspergillus fumigatus in a Caucasian older cohort [64, 65]
A full discussion is beyond this review, as we have recently reviewed this topic in great length [68], it is worth highlighting pattern recognition receptors (PRRs) that are implicated in fungal induced asthma
Summary
Asthma has largely been thought to be a genetic pre-disposition, over the last two decades it is becoming more clear that environment may play a significant role in the development of the disease [1]. The relationship between early life exposure to microbes or air pollutants and asthma is complex and is likely to be dependent on many factors, such as the nature of exposure, how and when it takes place, host genetic susceptibility and probably many other factors currently not defined [21] All these do point to the environment being important in asthma pathogenesis. Some fungi are often detected in sputum or lavage fluid in chronic respiratory diseases such as asthma These fungal species exploit a compromised host defense system, often germinating, and colonizing the airways, causing mycosis which precedes sensitization and exacerbation of asthma symptoms [26, 27]. We mainly focus on how some fungi may cause or contribute
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