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Journal of Respiration

Journal of Respiration is an international, peer-reviewed, open access journal on all aspects of respiratory science in humans published quarterly online by MDPI.

All Articles (101)

Asthma, Infections and Immunodeficiency

  • Alberto García de la Fuente,
  • Ebymar Arismendi and
  • Mariona Pascal
  • + 1 author

The relationship between asthma, infections, and immunodeficiencies is complex and affects disease progression. Immune deficiencies can occur independently or because of the inflammatory processes associated with asthma. Early viral infections like respiratory sinticial virus and rhinovirus trigger asthma attacks, while bacteria such as Haemophilus influenzae, Streptococcus pneumoniae, Mycoplasma pneumoniae, and Chlamydia pneumoniae worsen airway inflammation. People with asthma often have defects in innate (mucociliary clearance, interferons, defensins, NK cell, and eosinophils) and adaptive immunity such as immunoglobulin (Ig) deficiencies, making them more vulnerable to lung infections. Combined and selective deficiencies of IgA, IgG, IgM, and IgE are linked to higher asthma rates and reduced effectiveness of treatments, but immunoglobulin therapy can help control symptoms. Biologic therapies also decrease asthma exacerbations during periods of high viral activity by boosting immune responses and airway defenses. However, the link between asthma and higher infection risk is not well studied or understood, so guidelines do not recommend routinely checking for immunodeficiencies in cases of poor treatment response. Further investigation is required to elucidate these relationships and enhance management approaches.

8 December 2025

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Allergic bronchopulmonary aspergillosis (ABPA) is mediated by hypersensitivity reactions to Aspergillus fumigatus, which is ubiquitous in the environment. People with Cystic Fibrosis (PwCF) are at an increased risk for developing ABPA, which can lead to frequent pulmonary exacerbations and progressive decline in lung function. In the age of highly effective modulator therapies (HEMT), PwCF have improved clinical outcomes and overall life expectancy, but they continue to suffer from comorbidities such as ABPA, which may be difficult to diagnose and treat. Establishing the diagnosis of ABPA in PwCF requires high clinical suspicion due to similarities in symptoms with the underlying disease. First-line treatment involves corticosteroids and anti-fungals, which have multiple side effects and drug interactions, especially with HEMT. Given this challenge, biologics have gained attention as potential agents directly targeting the Th-2 inflammatory pathway of ABPA with good tolerability and without significant drug interactions with HEMT. In this review, we discuss the diagnostic process and management of ABPA in PwCF, including a brief overview of the current literature on biologic agents.

14 November 2025

Immune dysregulation in Cystic Fibrosis. A. The periciliary layer of the Cystic Fibrosis airway is dehydrated leading to poor mucociliary clearance as a result of dysfunctional CFTR protein that is normally expressed in airway epithelial cells [47,48]. B. Mucus plugging and biofilm buildup becomes a nidus for inhaled pathogens or allergens such as Aspergillus spp. C. Macrophages with impaired CFTR kill pathogens less efficiently and increase secretion of pro-inflammatory cytokines such as IL-6, IL-4, IL-13, and TNF-α [44,49]. D. CFTR deficient airway epithelial cells lead to increased IL-33 when exposed to allergens, resulting in higher expression of Th2 cell with increased release of IL-5, increased eosinophils, and IL-4 and IL-13, stimulating IgE expression by B cells [50,51]. E. Neutrophils, the predominant type of cell in CF airways, have reduced phagocytosis and can release toxic granule contents (e.g., serine and metalloproteases, oxidants) that can cause tissue damage over time. Neutrophils are known to release neutrophil extracellular traps (NETs), which are DNA fibers that immobilize and kill bacterial and fungal pathogens such as Pseudomonas aeruginosa and Aspergillus fumigatus, respectively. Abundant NET formations may attribute to common colonization of such pathogens in people with CF and reduced lung function; recombinant DNase (e.g., inhaled dornase alfa) improves mucociliary clearance by clearing the NET-DNA meshwork [49,51,52].

Background: The incidence of iatrogenic pneumothorax (IPTX) following transbronchial lung cryobiopsy (TBLCB) ranges from 1.4% to 20.2%. While chest X-ray (CXR) is the standard imaging modality to exclude IPTX, thoracic ultrasound (TUS) has demonstrated superior accuracy in detecting pneumothorax across various contexts. This study evaluates TUS as a reliable alternative to routine CXR for ruling out IPTX after TBLCB. Methods: A retrospective observational study included 51 patients undergoing ambulatory TBLCB. Pre- and post-TBLCB TUS were performed. CXR was reserved for cases where TUS findings were inconclusive (absence of sliding lung [SL] and seashore sign [SS] in any lung zones) or if patients exhibited symptoms or signs of IPTX. Results: TUS findings were concordant in 44 (86.1%) patients, of whom 42 (95.5%) did not require CXR. Two patients (4.5%) with symptomatic IPTX were identified and managed. Among the seven patients (13.7%) requiring CXR due to inconclusive TUS or symptoms, five (71.4%) were negative for IPTX, and two (28.6%) had asymptomatic IPTX. Conclusion: Our TUS protocol effectively ruled out clinically significant IPTX, eliminating routine CXR in 95.5% of patients. TUS is a safe alternative to CXR post-TBLCB, with CXR reserved for inconclusive TUS findings or symptomatic cases.

5 November 2025

Algorithm for the Evaluation and Management of TBLCB—related IPTX. Key: TBLCB—Transbronchial lung cryobiopsy; TUS—Thoracic ultrasound; IPTX—Iatrogenic pneumothorax; CXR—Chest X-ray; *—Patient spontaneously breathing; △—Presence of lung sliding and seashore Sign in all 4 Lung Zones; ○—Lung sliding and/or seashore sign not verifiable in all four lung zones; +—Per American College of Chest Physician’s pneumothorax size criteria.

LAMAs in Real-Life Asthma Management—The 2023 EU-LAMA Survey Results

  • Michał Panek,
  • Robab Breyer-Kohansal and
  • Paschalis Steiropoulos
  • + 5 authors

Background: Triple therapy (long-acting muscarinic antagonists (LAMAs), long-acting beta agonists (LABAs) and inhaled corticosteroids (ICSs)) is a recommended treatment for moderate-to-severe asthma at GINA Steps 4 and 5. However, little is known about the acceptance and use of triple therapy in everyday practice. The EU-LAMA Survey assessed specialists’ knowledge and views on triple therapy in daily practice. Methods: A 19-question survey was administered to 630 pulmonologists, allergologists, general practitioners, and internal medicine specialists in Poland (58%), Greece (27%), Sweden (6.3%), Slovenia (5.4%), and Austria (3.7%) using a dedicated online platform and computer-assisted web interviews. Results: The majority of the physicians were pulmonologists (59%), followed by allergologists (15.7%). For uncontrolled asthma at GINA Step 4, 81% of the respondents preferred increasing the ICS dose to the maximum level, whereas 76% opted to add LAMAs to medium-dose ICSs. At GINA Step 5, 79% of the respondents chose LAMAs first, followed by biological therapy (51%). Oral corticosteroids were favored over increasing the ICS dose and adding LAMAs. Triple therapy was mostly administered in one inhaler (70% and 82% at GINA Steps 4 and 5, respectively). Barriers to the use of LAMAs included a lack of reimbursement (31%), unclear guidelines (24%), lack of experience (18%), insufficient evidence (13%), fear of step-up regimens (10%), and the ease of increasing ICS doses (9%). Conclusion: Many physicians continue to rely on oral corticosteroids at GINA Steps 4 and 5 and infrequently refer patients to triple therapy or biological treatments at GINA Step 5.

31 October 2025

Therapeutic preferences of physicians in patients who are not achieving adequate asthma control at 2023 GINA 4-5. Legend: *—p < 0.05. Note: the level of significance was based on differences within the group and between the GINA 4 and GINA 5. Please see Supplementary Files—Figure S9 to find more details.

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J. Respir. - ISSN 2673-527X