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Inflammatory Airway Diseases: Diagnosis, Pathology, Molecular Mechanisms and Treatment Options
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Inflammatory Airway Diseases: Diagnosis, Pathology, Molecular Mechanisms and Treatment Options

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: 20 April 2025 | Viewed by 1613

Special Issue Editor

Dr. Stefanie Krick

E-Mail Website
Guest Editor
Pulmonary, Allergy and Critical Care Medicine, Division of Pulmonary, Allergy and Critical Care Medicine, 1900 University Blvd. Tinsley Harrison Tower, Suite 422, Birmingham, AL 35294, USA
Interests: pulmonary medicine; pulmonary physiology and cell biology; aging research
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Acute and chronic airway inflammation are hallmarks of several pulmonary diseases including, but not limited to, chronic obstructive pulmonary disease (COPD), asthma, cystic fibrosis (CF) and non-CF bronchiectasis.

While airway inflammation can be the natural response to harmful stimuli such as pathogens, airway injury and irritants and initiate a healing process, it can also carry a pathological role and promote sustained inflammation and chronic inflammation, which has been recognized as inflammation in aging-related lung diseases.

Despite ongoing research in this topic, diagnosis can be tricky, especially when dealing with overlapping disease entities, the pathomechanisms of multiple of these diseases, especially the role of inflammation, are not well understood and most of those diseases do not have curative treatment strategies with persistent and heavy symptom burden for all patients. Therefore, it is particularly important to explore the pathological mechanisms and molecular treatments of inflammatory airway diseases.

This Special Issue invites authors to submit original research articles, review articles and case reports that summarize current molecular research advances in diagnostic, prevention, and therapy of inflammatory airway diseases. The goal of this Special Issue is to present new ideas and data to help characterize those diseases better and identify potential novel treatment strategies.

Dr. Stefanie Krick
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • inflammatory airway diseases
  • asthma
  • COPD
  • anti-inflammatory

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Published Papers (2 papers)

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Research

10 pages, 1493 KiB  
Article
Cytokines Measured in Nasal Lavage Compared to Induced Sputum in Patients with Mild Cystic Fibrosis
by Teresa Fuchs, Artemis Vasiliadis, Manuela Zlamy, Anja Siedl, Katharina Niedermayr, Dorothea Appelt, Verena Gasser, Johannes Eder and Helmut Ellemunter
Int. J. Mol. Sci. 2024, 25(20), 11081; https://doi.org/10.3390/ijms252011081 - 15 Oct 2024
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Abstract
The measurement of cytokines in induced sputum and nasal lavage (NL) samples has been performed for years in people with cystic fibrosis (CF). The aim of this study was to directly compare sputum and NL samples and interpret results based on disease severity [...] Read more.
The measurement of cytokines in induced sputum and nasal lavage (NL) samples has been performed for years in people with cystic fibrosis (CF). The aim of this study was to directly compare sputum and NL samples and interpret results based on disease severity in patients who were categorized as having mild or severe lung disease. The categorization was based primarily on structural abnormalities detected on lung computed tomography and secondarily on lung function. The serum inflammatory markers neutrophil elastase (NE), IL-1β, 2, 6, 8, 10 and 17a were measured in each sputum and NL sample. Thirty-two sample pairs from 29 patients were included in this study (13 mild, 19 severe). In the patients classified as severe, many systemic inflammatory markers as well as sputum cytokines were significantly higher compared to those in the mild patients. However, all the markers measured in the NL were higher in the mild patients (p =< 0.05 for NE, IL-6 and IL-8). In addition, many cytokines in the NL correlated negatively with those in the sputum samples. Major differences in the cytokine levels were shown although the samples were obtained at the same time in the same patient. Advanced structural lung disease was closely related to systemic and lower airway inflammation, whereas preserved lung function was associated with higher levels in the NL. We hypothesize that the main part of the immune response takes place in the nasal mucosa in patients with minor pulmonary changes. Our results suggest that inflammation must be interpreted individually depending on the compartment in which it is measured. Further research is needed to accurately understand inflammatory markers measured in NL. Full article
(This article belongs to the Special Issue Inflammatory Airway Diseases: Diagnosis, Pathology, Molecular Mechanisms and Treatment Options)
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12 pages, 2034 KiB  
Article
Broncho-Vaxom Attenuates Lipopolysaccharide-Induced Inflammation in a Mouse Model of Acute Lung Injury
by Min-Seok Woo, Dang Long Cao, Eun-Jin Kim, Yi Yeong Jeong and Dawon Kang
Int. J. Mol. Sci. 2024, 25(13), 7135; https://doi.org/10.3390/ijms25137135 - 28 Jun 2024
Viewed by 920
Abstract
Acute lung injury (ALI) is a condition associated with acute respiratory failure, resulting in significant morbidity and mortality. It involves cellular changes such as disruption of the alveolar–capillary membrane, excessive neutrophil migration, and release of inflammatory mediators. Broncho-Vaxom® (BV), a lyophilized product [...] Read more.
Acute lung injury (ALI) is a condition associated with acute respiratory failure, resulting in significant morbidity and mortality. It involves cellular changes such as disruption of the alveolar–capillary membrane, excessive neutrophil migration, and release of inflammatory mediators. Broncho-Vaxom® (BV), a lyophilized product containing cell membrane components derived from eight bacteria commonly found in the respiratory tract, is known for its potential to reduce viral and bacterial lung infections. However, the specific effect of BV on ALI has not been clearly defined. This study explored the preventive effects of BV and its underlying mechanisms in a lipopolysaccharide (LPS)-induced ALI mouse model. Oral BV (1 mg/kg) gavage was administered one hour before the intratracheal injection of LPS to evaluate its preventive effect on the ALI model. The pre-administration of BV significantly mitigates inflammatory parameters, including the production of inflammatory mediators, macrophage infiltration, and NF-κB activation in lung tissue, and the increase in inflammatory cells in bronchoalveolar lavage fluid (BALF). Moreover, BV (3 μg/mL) pretreatment reduced the expression of M1 macrophage markers, interleukins (IL-1β, IL-6), tumor necrosis factor α, and cyclooxygenase-2, which are activated by LPS, in both mouse alveolar macrophage MH-S cells and human macrophage THP-1 cells. These findings showed that BV exhibits anti-inflammatory effects by suppressing inflammatory mediators through the NF-κB pathway, suggesting its potential to attenuate bronchial and pulmonary inflammation. Full article
(This article belongs to the Special Issue Inflammatory Airway Diseases: Diagnosis, Pathology, Molecular Mechanisms and Treatment Options)
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