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1. High frequencies of allergic sensitization in non-cystic fibrosis bronchiectasis
2. Hypersensitivity pneumonitis: recent advances
3. Hypersensitivity pneumonitis: radiologic phenotypes, survival time and pulmonary function trajectory
4. Laundry detergents disrupt the epithelial barrier in the airways
5. Shared and distinct genetic risk factors for childhood-onset and adult-onset asthma

High frequencies of allergic sensitization in non-cystic fibrosis bronchiectasis

M. Mac Aogáin  AJRCCM 2019 199 7 apr 01 830 - 841

To determine the frequency and geographic variability that exists in a sensitization pattern to common and specific allergens, and clinical outcomes in non-cystic-fibrosis bronchiectasis of adults, the authors recruited patients in Asia (Singapore and Malaysia) and the United Kingdom (Scotland) (n = 238), a cohort which matched on age, sex, and bronchiectasis severity. Specific IgE response against a range of common allergens was determined, combined with airway immune-inflammatory status. Clinically relevant patient clusters, based on sensitization pattern and airway immune profiles (“immunoallertypes”), were determined. The main result was:                                                                  

1) A high and unexpected frequency of sensitization to multiple allergens in bronchiectasis, exceeding that in a comparator cohort with allergic rhinitis (n = 149). Sensitization was associated with poor clinical outcomes, including decreased pulmonary function and more severe disease.

2)  “Sensitized bronchiectasis” was classified into two immunoallertypes: one fungal driven and pro-inflammatory, the other house dust mite driven and chemokine dominant, with the former demonstrating poorer clinical out.                              

3) In conclusion: Allergic sensitization occurs at high frequency in patients with bronchiectasis recruited from different global centers. Improving endophenotyping of sensitized bronchiectasis, allows therapeutic intervention in appropriate patients and improve stratification in future bronchiectasis research.

Hypersensitivity pneumonitis: recent advances

D.A.Lynch CHEST 2019 April 155 4 655-656
P.A.Greenberger JACI 2019April 143 4 1295-1301

Hypersensitivity pneumonitis (HP) is a TH1 lymphocyte–based fibrosing alveolitis caused by antigens ranging from avian excreta, fungi, thermophilic actinomycetes (cf picture), bacteria, and protozoa to reactive chemicals found in the workplace. The first example described was the mythical Farmer’s Lung “ published in Europe by J. Pepys then Cl. Molina, and immortalized in the famous painting from Millet : “The Winnower”. Mimicking a viral syndrome, acute exposures to inciting antigens cause abrupt onset of nonproductive cough, dyspnea, and chills with arthralgias or malaise usually from 4 to 8 hours later so that the temporal relationship between antigen exposure and symptoms might be unsuspected. The presence of serum precipitating antibodies reveals the role of immune response (type III of Gell and Coombs classification) The histology of HP shows prominent lymphocyte infiltrates that thicken the alveolar septa with poorly formed granulomas or giant cells.  Bronchoalveolar lavage fluid demonstrates greater than 20% lymphocytes in nearly all patients. Abnormalities on CT computed range from nodular centrilobular opacities in acute/subacute disease to increased reticular markings ground-glass opacities and honeycombing fibrosis, which typically are predominant in the upper lobes, in patients with advanced disease. The diagnosis is often difficult with nonspecific interstitial pneumonia or idiopathic pulmonary fibrosis IPF. Clinicians require a high level of suspicion to make an early diagnosis of HP before extensive pulmonary fibrosis or restrictive lung disease has occurred which may drive, in absence of drug treatment, to pulmonary transplantation.

Hypersensitivity pneumonitis: radiologic phenotypes, survival time and pulmonary function trajectory

Salisbury et al. April 2019 Volume 155, Issue 4, Pages 699–711

Hypersensitivity pneumonitis (HP) is an interstitial lung disease with a better prognosis, on average, than idiopathic pulmonary fibrosis (IPF). The authors compare survival time and pulmonary function trajectory in patients with HP and IPF by radiologic phenotype.
HP (n = 117) was diagnosed if surgical/transbronchial lung biopsy, BAL, and exposure history results suggested this diagnosis. IPF (n = 152) was clinically and histo-pathologically diagnosed. All participants had a baseline high-resolution CT (HRCT) scan and FVC % predicted. Survival time is from HRCT scan to death or lung transplant.
Subjects were grouped by clinical diagnosis and three mutually exclusive radiologic phenotypes: honeycomb present, non-honeycomb fibrosis (traction bronchiectasis and reticulation) present, and nonfibrotic. Nonfibrotic HP had the longest event-free median survival (> 14.73 years) and improving FVC % predicted. HP with non-honeycomb fibrosis had longer survival than IPF (> 7.95 vs 5.20 years), and both groups experienced a significant decline in FVC % predicted. Subjects with HP and IPF with honeycombing had poor survival (2.76 and 2. years, respectively) and significant decline in FVC % predicted.             Conclusion: Three prognostically distinct, radiologically defined phenotypes are identified among patients with HP. The importance of pursuing a specific diagnosis (eg, HP vs IPF) among patients with non-honeycomb fibrosis is highlighted. When radiologic honeycombing is present, invasive diagnostic testing directed at determining the diagnosis may be of limited value given a uniformly poor prognosis.


Laundry detergents disrupt the epithelial barrier in the airways

M.Wang et al JACI 2019 143 5 1892-1903

Persons highly exposed to detergents both in the workplace and at home are at high risk of allergen sensitization and asthma. In this issue, the international team driven by C. Akdis reports the influence of laundry detergents on human bronchial epithelial cells (HBECs) with the following findings:                
Laundry detergents, even at a very high dilution, show significant cell-toxicity and have disruptive effects on barrier integrity of HBECs from healthy control subjects, asthmatic patients, and patients with chronic obstructive pulmonary disease.
Laundry detergent residue remaining on clothes after rinsing still kills the HBECs and disrupts their barrier integrity.                                                                         
Genes of lipid metabolism, apoptosis, and epithelial derived allergic inflammation inducing molecules such as IL-33 and thymic stromal lymphopoietin (TSLP) are upregulated, whereas cell adhesion–related genes are downregulated by 1:50.000 times diluted laundry detergent.
These findings suggest a mechanism for high penetration of allergens, irritants, and pathogens through the mucosa that may promote the development of asthma and allergic diseases.

Shared and distinct genetic risk factors for childhood-onset and adult-onset asthma

M. Pividoriet & al. The Lancet Resp April 26 2019 – In press.

The goal of this study from the Chicago team is to identify shared and distinct genetic risk loci for childhood-onset and adult-onset asthma by genome-wide and transcriptome-wide studies, using data from the UK Biobank, including adults with childhood-onset asthma (onset before 12 years), adults with adult-onset asthma (onset between 26 and 65 years), and adults without asthma (controls aged older than 38).
Of 376 358 British white individuals, were included 37 846 with self-reports - 9433 adults with childhood-onset asthma; 21 564 adults with adult-onset asthma; and an additional 6849 young adults asthmatics with onset between 12 and 25 years of age.
Sixty-one independent asthma loci were detected: 23 were childhood-onset specific, one was adult-onset specific, and 37 were shared. 19 loci were associated with age of asthma onset. The most significant asthma-associated locus was at 17q12 in the childhood-onset GWAS. Genes at the childhood onset-specific loci were most highly expressed in skin, blood, and small intestine; genes at the adult onset-specific loci were most highly expressed in lung, blood, small intestine, and spleen. SNP-based heritability estimates were more than three times larger for childhood-onset asthma (0.327) than for adult-onset disease (0.098). The onset of disease in childhood was associated with additional genes with relatively large effect sizes, the largest odds ratio being observed at the FLG locus at 1q21.3.                                                                                   
In conclusion genetic risk factors for adult-onset asthma are largely a subset of the genetic risk for childhood-onset asthma but with overall smaller effects, suggesting a greater role for non-genetic risk factors in adult-onset asthma more lung-centered and environmentally determined. It is suggested that the establishment of disease in children is driven more by dysregulated allergy and epithelial barrier function genes, the immune-mediated mechanisms driving disease progression in both children and adults.

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Please find the previous bibliographic updates of allergology below:
- Archive of 2018
- Archive of 2017
- Archive of 2016
- Archive of 2015
- Archive of 2014
- Archive of 2013
- Archive of 2012
- Archive of 2011
Last updated 28 May 2019
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