Submit to Special Issue Submit Abstract to Special Issue Review for IJMS Propose a Special Issue

Journal Menu

Journal Browser

Advances in Lung Inflammation, Injury, and Repair

Special Issue Editors
Special Issue Information
Keywords
Benefits of Publishing in a Special Issue
Published Papers

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 December 2024 | Viewed by 9956

Share This Special Issue

Special Issue Editor

Dr. Andreas Schwingshackl

E-Mail Website
Guest Editor

Department of Pediatrics, Universiy of California Los Angeles, Los Angeles, CA 90095, USA
Interests: acute lung injury; acute respiratory distress syndrome; lung; inflammation; respiratory failure; hyperoxia; mechanical ventilation; cytokines; ion channels; potassium; calcium

Special Issue Information

Dear Colleagues,

Lung inflammation, injury, and repair are pathophysiological processes shared by multiple pulmonary disease entities. Most recently, the COVID-19 pandemic highlighted the catastrophic consequences associated with the dysregulation of these processes and our limited understanding of the underlying molecular mechanisms, which is reflected in the limited therapeutic armamentarium currently available for our patients. In many cases, these pathophysiological findings are grouped together as Acute Respiratory Distress Syndrome (ARDS), but a substantial number of patients suffering from similarly dysregulated lung inflammation, injury, and repair mechanisms are not meeting the ARDS criteria and yet are still at high risk for poor outcomes and short- and long-term morbidity and mortality.

To address these challenges, within the IJMS section of “Molecular Pathology, Diagnostics, and Therapeutics” we are proposing a Special Issue titled “Advances in Lung Inflammation, Injury, and Repair” to create a state-of-the art work product summarizing our current understanding and knowledge gaps in this field and propose future approaches, novel targets, and next-generation experimental models. Since lung injury can be triggered by a variety of insults, including, but not limited to, viral and bacterial infections, sepsis, trauma, blood transfusion, gastric content aspiration, cardio-pulmonary resuscitation, toxic inhalations, medications, and auto-immune processes, this interdisciplinary collection of manuscripts aims to provide a comprehensive resource on molecular pathology, diagnostics, and therapeutics in the fields of lung inflammation, injury, and repair for a large audience including research and medical trainees, pulmonary physiologists and pathologists, general practitioners and pulmonary/critical care specialists, nurses, and respiratory therapists.

Dr. Andreas Schwingshackl
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

lung
inflammation
injury
repair
fibrosis
diagnostics
therapeutics
acute respiratory distress syndrome

Benefits of Publishing in a Special Issue

Ease of navigation: Grouping papers by topic helps scholars navigate broad scope journals more efficiently.
Greater discoverability: Special Issues support the reach and impact of scientific research. Articles in Special Issues are more discoverable and cited more frequently.
Expansion of research network: Special Issues facilitate connections among authors, fostering scientific collaborations.
External promotion: Articles in Special Issues are often promoted through the journal's social media, increasing their visibility.
e-Book format: Special Issues with more than 10 articles can be published as dedicated e-books, ensuring wide and rapid dissemination.

Further information on MDPI's Special Issue polices can be found here.

Published Papers (6 papers)

Download All Papers

Order results

Result details

Show export options Show export options

Select all

Export citation of selected articles as:

Research

Jump to: Review

19 pages, 6363 KiB

Open AccessArticle

RAMP1 Signaling Mitigates Acute Lung Injury by Distinctively Regulating Alveolar and Monocyte-Derived Macrophages

by Atsushi Yamashita, Yoshiya Ito, Mayuko Osada, Hiromi Matsuda, Kanako Hosono, Kazutake Tsujikawa, Hirotsugu Okamoto and Hideki Amano

Int. J. Mol. Sci. 2024, 25(18), 10107; https://doi.org/10.3390/ijms251810107 - 20 Sep 2024

Viewed by 863

Abstract

Acute respiratory distress syndrome (ARDS) is a life-threatening lung injury that induces cytokine hypersecretion. Receptor activity-modifying protein (RAMP) 1, a subunit of the calcitonin gene-related peptide (CGRP) receptor, regulates the production of cytokines. This study examined the role of RAMP1 signaling during lipopolysaccharide (LPS)-induced acute lung injury (ALI). LPS administration to wild-type (WT) mice depleted alveolar macrophages (AMs) and recruited monocyte-derived macrophages (MDMs) and neutrophils. RAMP1-deficient (RAMP1^−/−) mice exhibited higher lung injury scores, cytokine levels, and cytokine-producing neutrophil infiltration. RAMP1-deficient AMs produced more cytokines in response to LPS than WT AMs. Adoptive transfer of RAMP1-deficient AMs to RAMP1^−/− mice increased cytokine levels and neutrophil accumulation compared to the transfer of WT AMs. RAMP1^−/− mice had reduced MDM recruitment and lower pro-inflammatory and reparative macrophage profiles. Cultured bone marrow (BM)-derived RAMP1-deficient macrophages stimulated with LPS showed decreased expression of pro-inflammatory and pro-repairing genes. CGRP administration to WT mice reduced cytokine production and neutrophil accumulation. These findings indicate that RAMP1 signaling mitigates LPS-induced ALI by inactivating AMs and promoting inflammatory and repair activities of MDMs. Targeting RAMP1 signaling presents a potential therapeutic approach for the treatment of ARDS. Full article

(This article belongs to the Special Issue Advances in Lung Inflammation, Injury, and Repair)

► Show Figures

Figure 1

16 pages, 3157 KiB

Open AccessArticle

GPR55 Antagonist CID16020046 Attenuates Obesity-Induced Airway Inflammation by Suppressing Chronic Low-Grade Inflammation in the Lungs

by So-Eun Son, Ye-Ji Lee, Yoon-Jung Shin, Dong-Hyun Kim and Dong-Soon Im

Int. J. Mol. Sci. 2024, 25(13), 7358; https://doi.org/10.3390/ijms25137358 - 4 Jul 2024

Viewed by 1076

Abstract

GPR55 is a receptor for lysophosphatidylinositols (LPIs) in digestive metabolites. Overnutrition leads to obesity, insulin resistance, and increased LPI levels in the plasma. The involvement of LPIs and GPR55 in adiposity, hepatic steatosis, and atherosclerosis has been previously elucidated. However, the therapeutic efficacy of GPR55 antagonists against obesity-induced airway inflammation has not been studied. The present study investigated whether CID16020046, a selective antagonist of GPR55, could modulate obesity-induced airway inflammation caused by a high-fat diet (HFD) in C57BL/6 mice. Administration of CID16020046 (1 mg/kg) inhibits HFD-induced adiposity and glucose intolerance. Analysis of immune cells in BALF showed that CID16020046 inhibited HFD-induced increase in immune cell infiltration. Histological analysis revealed the HFD induced hypersecretion of mucus and extensive fibrosis in the lungs. CID16020046 inhibited these HFD-induced pathological features. qRT-PCR revealed the HFD-induced increase in the expression of Ifn-γ, Tnf-α, Il-6, Il-13, Il-17A, Il-1β, Nlrp3, and Mpo mRNAs in the lungs. CID16020046 inhibited the HFD-induced increases in these genes. The expression levels of adipokines were regulated by the HFD and CID16020046. AdipoQ in the lungs and gonadal white adipose tissue was decreased by the HFD and reversed by CID16020046. In contrast, Lep was increased by the HFD and suppressed by CID16020046. The findings suggest the potential application of the GPR55 antagonist CID16020046 in obesity-induced airway inflammation. Full article

(This article belongs to the Special Issue Advances in Lung Inflammation, Injury, and Repair)

► Show Figures

Figure 1

17 pages, 4226 KiB

Open AccessArticle

C-Phycocyanin Prevents Oxidative Stress, Inflammation, and Lung Remodeling in an Ovalbumin-Induced Rat Asthma Model

by Zayra Mundo-Franco, Julieta Luna-Herrera, Jorge Ismael Castañeda-Sánchez, José Iván Serrano-Contreras, Plácido Rojas-Franco, Vanessa Blas-Valdivia, Margarita Franco-Colín and Edgar Cano-Europa

Int. J. Mol. Sci. 2024, 25(13), 7031; https://doi.org/10.3390/ijms25137031 - 27 Jun 2024

Cited by 1 | Viewed by 1379

Abstract

Asthma is a chronic immunological disease related to oxidative stress and chronic inflammation; both processes promote airway remodeling with collagen deposition and matrix thickening, causing pulmonary damage and lost function. This study investigates the immunomodulation of C-phycocyanin (CPC), a natural blue pigment purified from cyanobacteria, as a potential alternative treatment to prevent the remodeling process against asthma. We conducted experiments using ovalbumin (OVA) to induce asthma in Sprague Dawley rats. Animals were divided into five groups: (1) sham + vehicle, (2) sham + CPC, (3) asthma + vehicle, (4) asthma + CPC, and (5) asthma + methylprednisolone (MP). Our findings reveal that asthma promotes hypoxemia, leukocytosis, and pulmonary myeloperoxidase (MPO) activity by increasing lipid peroxidation, reactive oxygen and nitrogen species, inflammation associated with Th2 response, and airway remodeling in the lungs. CPC and MP treatment partially prevented these physiological processes with similar action on the biomarkers evaluated. In conclusion, CPC treatment enhanced the antioxidant defense system, thereby preventing oxidative stress and reducing airway inflammation by regulating pro-inflammatory and anti-inflammatory cytokines, consequently avoiding asthma-induced airway remodeling. Full article

(This article belongs to the Special Issue Advances in Lung Inflammation, Injury, and Repair)

► Show Figures

Figure 1

13 pages, 3056 KiB

Open AccessArticle

Inflammatory Cytokine Elaboration Following Secondhand Smoke (SHS) Exposure Is Mediated in Part by RAGE Signaling

by Katrina L. Curtis, Kyle M. Homer, Ryan A. Wendt, Brendan M. Stapley, Evan T. Clark, Kaden Harward, Ashley Chang, Derek M. Clarke, Juan A. Arroyo and Paul R. Reynolds

Int. J. Mol. Sci. 2023, 24(21), 15645; https://doi.org/10.3390/ijms242115645 - 27 Oct 2023

Cited by 4 | Viewed by 1337

Abstract

The receptor for advanced glycation end products (RAGE) is a key contributor to immune and inflammatory responses in myriad diseases. RAGE is a transmembrane pattern recognition receptor with a special interest in pulmonary anomalies due to its naturally abundant pulmonary expression. Our previous studies demonstrated an inflammatory role for RAGE following acute 30-day exposure to secondhand smoke (SHS), wherein immune cell diapedesis and cytokine/chemokine secretion were accentuated in part via RAGE signaling. However, the chronic inflammatory mechanisms associated with RAGE have yet to be fully elucidated. In this study, we address the impact of long-term SHS exposure on RAGE signaling. RAGE knockout (RKO) and wild-type (WT) mice were exposed to SHS using a nose-only delivery system (Scireq Scientific, Montreal, Canada) for six months. SHS-exposed animals were compared to mice exposed to room air (RA) only. Immunoblotting was used to assess the phospho-AKT and phospho-ERK activation data, and colorimetric high-throughput assays were used to measure NF-kB. Ras activation was measured via ELISAs. Bronchoalveolar lavage fluid (BALF) cellularity was quantified, and a mouse cytokine antibody array was used to screen the secreted cytokines. The phospho-AKT level was decreased, while those of phospho-ERK, NF-kB, and Ras were elevated in both groups of SHS-exposed mice, with the RKO + SHS-exposed mice demonstrating significantly decreased levels of each intermediate compared to those of the WT + SHS-exposed mice. The BALF contained increased levels of diverse pro-inflammatory cytokines in the SHS-exposed WT mice, and diminished secretion was detected in the SHS-exposed RKO mice. These results validate the role for RAGE in the mediation of chronic pulmonary inflammatory responses and suggest ERK signaling as a likely pathway that perpetuates RAGE-dependent inflammation. Additional characterization of RAGE-mediated pulmonary responses to prolonged exposure will provide a valuable insight into the cellular mechanisms of lung diseases such as chronic obstructive pulmonary disease. Full article

(This article belongs to the Special Issue Advances in Lung Inflammation, Injury, and Repair)

► Show Figures

Figure 1

11 pages, 5656 KiB

Open AccessArticle

Blood Immunophenotypes of Idiopathic Pulmonary Fibrosis: Relationship with Disease Severity and Progression

by Nuria Mendoza, Sandra Casas-Recasens, Núria Olvera, Fernanda Hernandez-Gonzalez, Tamara Cruz, Núria Albacar, Xavier Alsina-Restoy, Alejandro Frino-Garcia, Gemma López-Saiz, Lucas Robres, Mauricio Rojas, Alvar Agustí, Jacobo Sellarés and Rosa Faner

Int. J. Mol. Sci. 2023, 24(18), 13832; https://doi.org/10.3390/ijms241813832 - 7 Sep 2023

Cited by 7 | Viewed by 2358

Abstract

(1) The role of the immune response in the pathogenesis of idiopathic pulmonary fibrosis (IPF) remains controversial. We hypothesized that peripheral blood immune phenotypes will be different in IPF patients and may relate to the disease severity and progression. (2) Whole blood flow cytometry staining was performed at diagnosis in 32 IPF patients, and in 32 age- and smoking-matched healthy controls. Thirty-one IPF patients were followed up for one year and categorized as stable or progressors based on lung function, deterioration and/or death. At 18–60 months, immunophenotypes were characterized again. (3) The main results showed that: (1) compared to matched controls, at diagnosis, patients with IPF showed more neutrophils, CD8⁺HLA-DR⁺ and CD8⁺CD28⁻ T cells, and fewer B lymphocytes and naïve T cells; (2) in IPF, circulating neutrophils, eosinophils and naïve T cells were associated with lung function abnormalities; (3) patients whose disease progressed during the 12 months of follow-up showed evidence of cytotoxic dysregulation, with increased CD8⁺CD28⁻ T cells, decreased naïve T cells and an inverted CD4/CD8 ratio at baseline; and (4) blood cell alterations were stable over time in survivors. (4) IPF is associated with abnormalities in circulating immune cells, particularly in the cytotoxic cell domain. Patients with progressive IPF, despite antifibrotic therapy, present an over-activated and exhausted immunophenotype at diagnosis, which is maintained over time. Full article

(This article belongs to the Special Issue Advances in Lung Inflammation, Injury, and Repair)

► Show Figures

Figure 1

Review

Jump to: Research

34 pages, 30833 KiB

Open AccessReview

Multidisciplinary Approach to the Diagnosis of Idiopathic Interstitial Pneumonias: Focus on the Pathologist’s Key Role

by Stefano Lucà, Francesca Pagliuca, Fabio Perrotta, Andrea Ronchi, Domenica Francesca Mariniello, Giovanni Natale, Andrea Bianco, Alfonso Fiorelli, Marina Accardo and Renato Franco

Int. J. Mol. Sci. 2024, 25(7), 3618; https://doi.org/10.3390/ijms25073618 - 23 Mar 2024

Cited by 1 | Viewed by 2039

Abstract

Idiopathic Interstitial Pneumonias (IIPs) are a heterogeneous group of the broader category of Interstitial Lung Diseases (ILDs), pathologically characterized by the distortion of lung parenchyma by interstitial inflammation and/or fibrosis. The American Thoracic Society (ATS)/European Respiratory Society (ERS) international multidisciplinary consensus classification of the IIPs was published in 2002 and then updated in 2013, with the authors emphasizing the need for a multidisciplinary approach to the diagnosis of IIPs. The histological evaluation of IIPs is challenging, and different types of IIPs are classically associated with specific histopathological patterns. However, morphological overlaps can be observed, and the same histopathological features can be seen in totally different clinical settings. Therefore, the pathologist’s aim is to recognize the pathologic–morphologic pattern of disease in this clinical setting, and only after multi-disciplinary evaluation, if there is concordance between clinical and radiological findings, a definitive diagnosis of specific IIP can be established, allowing the optimal clinical–therapeutic management of the patient. Full article

(This article belongs to the Special Issue Advances in Lung Inflammation, Injury, and Repair)

► Show Figures

Journal Menu

Journal Browser

Advances in Lung Inflammation, Injury, and Repair

Share This Special Issue

Special Issue Editor

Special Issue Information

Keywords

Benefits of Publishing in a Special Issue

Published Papers (6 papers)

Research

Review

Further Information

Guidelines

MDPI Initiatives

Follow MDPI