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Review
. 2013 Oct 19;382(9901):1360-72.
doi: 10.1016/S0140-6736(13)61536-6. Epub 2013 Sep 13.

Asthma

Fernando D Martinez  1 , Donata Vercelli
Affiliations
Review

Asthma

Fernando D Martinez et al. Lancet. .

Abstract

Asthma is a heterogeneous group of conditions that result in recurrent, reversible bronchial obstruction. Although the disease can start at any age, the first symptoms occur during childhood in most cases. Asthma has a strong genetic component, and genome-wide association studies have identified variations in several genes that slightly increase the risk of disease. Asthma is often associated with increased susceptibility to infection with rhinoviruses and with changes in the composition of microbial communities colonising the airways, but whether these changes are a cause or consequence of the disease is unknown. There is currently no proven prevention strategy; however, the finding that exposure to microbial products in early life, particularly in farming environments, seems to be protective against asthma offers hope that surrogates of such exposure could be used to prevent the disease. Genetic and immunological studies point to defective responses of lung resident cells, especially those associated with the mucosal epithelium, as crucial elements in the pathogenesis of asthma. Inhaled corticosteroids continue to be the mainstay for the treatment of mild and moderate asthma, but limited adherence to daily inhaled medication is a major obstacle to the success of such therapy. Severe asthma that is refractory to usual treatment continues to be a challenge, but new biological therapies, such as humanised antibodies against IgE, interleukin 5, and interleukin 13, offer hope to improve the quality of life and long-term prognosis of severe asthmatics with specific molecular phenotypes.

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Conflict of interest statement

Conflicts of interest

FDM has received honoraria from Abbott Laboratories for invited lectures. DV has participated in peer discussion groups supported by Merck.

Figures

Figure 1:
Figure 1:. Changes in lung function during the course of mild and moderate asthma
In mild disease, change in lung function is not substantially different from that in people without asthma. In more severe asthma, deficits have already been detected at birth, but most of the postnatal loss in lung function seems to occur during the preschool years.
Figure 2:
Figure 2:. Asthma genes identified through genome-wide association studies (GWAS)
The National Human Genome Research Institute catalogue of published GWAS was searched using asthma as disease, and childhood asthma as trait.
Figure 3:
Figure 3:. Clinical phenotypes of adult asthma, identified by cluster analysis
Clusters of patients are plotted according to their relative level of symptoms and eosinophilic inflammation. The plot highlights that patients with greater discordance between symptoms and inflammation are more difficult to treat and should usually be followed up in specialised asthma centres.
Figure 4:
Figure 4:. Major immune pathways involved in asthma pathogenesis
Innate and adaptive components of allergic inflammation are shown, including the recently discovered ILC2 cells that release Th2 cytokines in response to epithelial damage. The links between immune responses and structural changes in the lung are also depicted. TLR=toll-like receptor. TSLP= thymic stromal lymphopoietin. TGFβ1=transforming growth-factor β1. TCR=T-cell receptor. Treg=regulatory T cell. Th=T-helper cell. Th2=T-helper-type-2 cell.
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