Publications by authors named "Tommaso Pianigiani"
Online survey on existing sarcoidosis registries and biobanks: an ERN lung initiative.
Sarcoidosis Vasc Diffuse Lung Dis
December 2024
The present survey, promoted by the European Reference Network on rare respiratory diseases (ERN-Lung, Core Networks Sarcoidosis and ILD), aims to assess the existing sarcoidosis registries and biobanks across Europe and to compare the various types of biospecimen collected, the different procedures performed, and the sample storage conditions applied. This survey was initiated by the European Reference Network on rare respiratory diseases (ERN-Lung) Core Network "Sarcoidosis" in April 2023. The survey was launched by ERN-Lung Core Network "Sarcoidosis" in August 2023 and remained active until end of February 2024.
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- Familial Pulmonary Fibrosis (FPF) is a lung disease caused by genetic mutations, and managing it is still a challenge as of 2023.
- A survey conducted in Italy found that more FPF patients are seen at hospitals that treat many interstitial lung disease (ILD) patients each year.
- There were differences in genetic testing services between hospitals, but no major differences in patient care or treatments were found in various medical settings.
Background: Specific biomarkers, such as eosinophilia in peripheral blood or fractional exhaled nitric oxide (FeNO), can guide us in the choice of biologic therapy, allowing a more personalized approach. Although there are multiple evidences in the literature about the role of FeNO as a predictor of response to different biologic treatments, there are no data on the relationship between FeNO changes and clinical response to the four biologic drugs currently in use.
Objective: To evaluate and to compare the expression of multiple-flows FeNO parameters in a cohort of patients with severe asthma (SA) before and during the treatment with biologics to evaluate the performance of these biomarkers in predicting the achievement of clinical remission.
Article Synopsis
- Biological treatments like benralizumab and mepolizumab have improved the management of severe eosinophilic asthma, but their effects on specific immune cells (NK and Treg cells) were previously unknown.
- In a study of fourteen severe asthma patients compared to healthy and mild asthma controls, it was found that severe asthma patients had higher levels of a specific immune cell type (CD4 TEM) at the start.
- Both treatments effectively reduced CD4 TEM cells and increased Treg cells over time, indicating that anti-IL-5 therapies not only improve clinical symptoms but also help rebalance certain immune cell populations in severe asthma patients.
Introduction: The mechanism of action of benralizumab is determined by its afucosylated constant fragment that binds CD16a receptors on the membrane of natural killer cells. Here we analysed changes in Natural Killer and T-cells in Severe asthmatic patients, before and after benralizumab.
Methods: Natural Killer and T-cell subsets were detected through multiparametric flow cytometry.
Background: Fractional exhaled nitric oxide (FeNO) is a biomarker of airway inflammation associated with airway hyper-responsiveness and type-2 inflammation. Its role in the management of severe asthmatic patients undergoing biologic treatment, as well as FeNO dynamics during biologic treatment, is largely unexplored.
Purpose: The aim was to evaluate published data contributing to the following areas: (1) FeNO as a predictive biomarker of response to biologic treatment; (2) the influence of biologic treatment in FeNO values; (3) FeNO as a biomarker for the prediction of exacerbations in patients treated with biologics.
Background: Severe allergic asthma (SAA) is based on type 2 (T2-high) immune responses to allergens promoting type 2 T helper (Th2) cell cytokine responses and production of IgE antibodies. Omalizumab was the first biological drug licensed for clinical use in the management of IgE-mediated SAA. Despite emerging evidence supporting the prominent role of follicular T cells (Tfh), Breg and Treg subsets, in the development and progression of SAA, no data are available on the impact of omalizumab therapy.
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