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Molecular Mechanisms of Respiratory Diseases

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (30 November 2022) | Viewed by 4513

Special Issue Editor


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Guest Editor
1. Hospital Universitario Virgen del Rocio, Sevilla, Spain
2. Departamento de Medicina, Universidad de Sevilla, Sevilla, Spain
Interests: respiratory diseases

Special Issue Information

Dear Colleagues,

The study of the biological pathways underlying the pathogenesis of respiratory diseases is one of the most relevant fields for biomedical research in respiratory medicine. All conditions directly or indirectly related to the respiratory system have a biological basis, the identification and understanding of which is necessary for the identification of future therapeutic targets. Airway diseases (COPD, asthma, bronchiectasis), pulmonary neoplasms, pulmonary circulation diseases, interstitial pneumopathies, respiratory infections, and processes affecting the upper airway (obstructive sleep apnea, rhinitis) are clear examples of processes with a profound impact on both the patient and the health care system and which require special attention to improve the understanding of their biological determinants. In this context, different laboratory approaches, from simple protein determination and characterization to complex systems biology analyses and high-throughput technologies, constitute a particularly relevant opportunity in these medical contexts. In this Special Issue we would like to call upon the research groups dedicated to respiratory diseases so that, by joining forces, we can improve the knowledge of respiratory diseases. We know that only collaborative research efforts will be the basis for improving the diagnosis and treatment of these processes.

Dr. José Luis López-Campos
Guest Editor

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Published Papers (2 papers)

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12 pages, 1793 KiB  
Article
Severe Obstructive Sleep Apnea Disrupts Vigilance-State-Dependent Metabolism
by Felix Schmidt, Nora Nowak, Patrick Baumgartner, Thomas Gaisl, Stefan Malesevic, Bettina Streckenbach, Noriane A. Sievi, Esther I. Schwarz, Renato Zenobi, Steven A. Brown and Malcolm Kohler
Int. J. Mol. Sci. 2022, 23(22), 14052; https://doi.org/10.3390/ijms232214052 - 14 Nov 2022
Cited by 5 | Viewed by 1877
Abstract
The direct pathophysiological effects of obstructive sleep apnea (OSA) have been well described. However, the systemic and metabolic consequences of OSA are less well understood. The aim of this secondary analysis was to translate recent findings in healthy subjects on vigilance-state-dependent metabolism into [...] Read more.
The direct pathophysiological effects of obstructive sleep apnea (OSA) have been well described. However, the systemic and metabolic consequences of OSA are less well understood. The aim of this secondary analysis was to translate recent findings in healthy subjects on vigilance-state-dependent metabolism into the context of OSA patients and answer the question of how symptomatic OSA influences metabolism and whether these changes might explain metabolic and cardiovascular consequences of OSA. Patients with suspected OSA were assigned according to their oxygen desaturation index (ODI) and Epworth Sleepiness Scale (ESS) score into symptomatic OSA and controls. Vigilance-state-dependent breath metabolites assessed by high-resolution mass spectrometry were used to test for a difference in both groups. In total, 44 patients were eligible, of whom 18 (40.9%) were assigned to the symptomatic OSA group. Symptomatic OSA patients with a median [25%, 75% quartiles] ODI of 40.5 [35.0, 58.8] events/h and an ESS of 14.0 [11.2, 15.8] showed moderate to strong evidence for differences in 18 vigilance-state-dependent breath compounds compared to controls. These identified metabolites are part of major metabolic pathways in carbohydrate, amino acid, and lipid metabolism. Thus, beyond hypoxia per se, we hypothesize that disturbed sleep in OSA patients persists as disturbed sleep-dependent metabolite levels during daytime. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Respiratory Diseases)
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12 pages, 949 KiB  
Article
Effects of Inhaled Corticosteroids on the Innate Immunological Response to Pseudomonas aeruginosa Infection in Patients with COPD
by Noemi Cerón-Pisa, Hanaa Shafiek, Aina Martín-Medina, Javier Verdú, Elena Jordana-Lluch, Maria Escobar-Salom, Isabel M. Barceló, Carla López-Causapé, Antonio Oliver, Carlos Juan, Amanda Iglesias and Borja G. Cosío
Int. J. Mol. Sci. 2022, 23(15), 8127; https://doi.org/10.3390/ijms23158127 - 23 Jul 2022
Cited by 4 | Viewed by 2094
Abstract
Inhaled corticosteroids (ICS) use is associated with an increased risk of Pseudomonas aeruginosa (PA) infection in patients with COPD. We aimed to evaluate the effects of ICS on alveolar macrophages in response to PA in COPD patients with and without baseline ICS treatment [...] Read more.
Inhaled corticosteroids (ICS) use is associated with an increased risk of Pseudomonas aeruginosa (PA) infection in patients with COPD. We aimed to evaluate the effects of ICS on alveolar macrophages in response to PA in COPD patients with and without baseline ICS treatment (COPD and COPD + ICS, respectively) as well as smoker and nonsmoker controls. To do so, cells were infected with PA and cotreated with budesonide (BUD) or fluticasone propionate (FLU). The analysis of NF-κB and c-jun activity revealed a significant increase in both factors in response to PA cotreated with BUD/FLU in smokers but not in COPD or COPD + ICS patients when compared with PA infection alone. The expression of Toll-like receptor 2 (TLR2) and the transcription factor c-jun were induced upon PA infection in nonsmokers only. Moreover, in the smoker and COPD groups, there was a significant increase in TLR2 and a decrease in c-jun expression when treated with BUD/FLU after PA infection, which were not observed in COPD + ICS patients. Therefore, the chronic use of ICS seemingly makes the macrophages tolerant to BUD/FLU stimulation compared with those from patients not treated with ICS, promoting an impaired recognition of PA and activity of alveolar macrophages in terms of altered expression of TLR2 and cytokine production, which could explain the increased risk of PA infection in COPD patients under ICS treatment. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Respiratory Diseases)
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