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New Advances in Inflammation and Repair in Respiratory Diseases
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New Advances in Inflammation and Repair in 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: 31 December 2024 | Viewed by 9595

Special Issue Editors

Dr. Solleti Siva Kumar

E-Mail Website
Guest Editor
School of Medicine and Dentistry, University of Rochester Medical Center, 601 Elmwood Ave, Box 850, Rochester, NY 14642, USA
Interests: respiratory diseases
Dr. Ravi S. Misra

E-Mail Website
Guest Editor
Division of Neonatology, Department of Pediatrics, University of Rochester Medical Center, Rochester, NY 14642, USA
Interests: vaccine responses; infectious diseases; inflammatory lung diseases
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The respiratory system is under constant threat from various invading factors, and the occurrence of respiratory diseases has increased dramatically in the past decade. An aberrant immune response can result in various respiratory diseases, such as chronic obstructive pulmonary disease, asthma, pulmonary fibrosis, respiratory distress, broncho pulmonary dysplasia, and various respiratory pathogen infections. Although respiratory diseases differ in presentation, they all originate from unresolved inflammation.

Lung injury, inflammation, and repair involve a variety of cell types and structures of the respiratory system that can be injured. The coordinated interaction between structural and nonstructural cells mediated by signaling molecules results in a complex orchestration of mechanistic events to shield against pathogens and repair or regenerate tissue. The COVID-19 pandemic has demonstrated the need for an in-depth and broadened understanding of the cellular-, molecular-, and tissue-level mechanisms driving respiratory diseases and accelerated the need for strides forward in the discovery of novel therapeutics.

In spite of novel technological advances, understanding the key regulators of inflammation and repair in respiratory diseases remains a major obstacle. This Special Issue aims to present an up-to-date overview on the current understanding of respiratory diseases, novel druggable targets, and molecular mechanisms, as well as their translation into novel therapeutics and treatments for lung diseases.

Dr. Solleti Siva Kumar
Dr. Ravi S. Misra
Guest Editors

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Keywords

  • asthma
  • COPD
  • emphysema
  • pulmonary fibrosis
  • airway epithelium
  • lung fibroblast
  • alveolar macrophages
  • innate immunity
  • inflammasomes
  • translational research
  • animal model
  • signaling
  • chemokines
  • cytokines
  • novel therapy

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Published Papers (4 papers)

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Research

15 pages, 2972 KiB  
Article
Inhaled CD24-Enriched Exosomes (EXO-CD24) as a Novel Immune Modulator in Respiratory Disease
by Shiran Shapira, Reut Schwartz, Sotirios Tsiodras, Amir Bar-Shai, Ariel Melloul, Sarah Borsekofsky, Michael Peer, Nimrod Adi, Ronan MacLoughlin and Nadir Arber
Int. J. Mol. Sci. 2024, 25(1), 77; https://doi.org/10.3390/ijms25010077 - 20 Dec 2023
Cited by 4 | Viewed by 1950
Abstract
Acute Respiratory Distress Syndrome (ARDS) is a major health concern with urgent unmet need for treatment options. There are three million new ARDS cases annually, and the disease’s mortality rate is high (35–46%). Cluster of differentiation 24 (CD24), a long-known protein with multifaceted [...] Read more.
Acute Respiratory Distress Syndrome (ARDS) is a major health concern with urgent unmet need for treatment options. There are three million new ARDS cases annually, and the disease’s mortality rate is high (35–46%). Cluster of differentiation 24 (CD24), a long-known protein with multifaceted functions, is a small, heavily glycosylated, membrane-anchored protein which functions as an immune checkpoint control. CD24 allows for immune discrimination between Damage-Associated Molecular Patterns and Pathogen-Associated Molecular Patterns derived from pathogens. Exosomes are intraluminal vesicles which play an important role in intercellular communication. Exosomes offer the advantage of targeted delivery, which improves safety and efficacy. The safety and efficacy of EXO-CD24 is promising, as was shown in >180 ARDS patients in phase 1b/2a, phase 2b, and compassionate use. CD24 binds Damage-associated molecular patterns (DAMPs) and inhibits the activation of the NF-ĸB pathway, a pivotal mediator of inflammatory responses. In contrast to anti-inflammatory therapies that are cytokine-specific or steroids that shut down the entire immune system, EXO-CD24 acts upstream, reverting the immune system back to normal activity. Herein, the safety and efficacy of mEXO-CD24 is shown in murine models of several pulmonary diseases (sepsis, allergic asthma, Chronic Obstructive Pulmonary Disease(COPD), fibrosis). EXO CD24 can suppress the hyperinflammatory response in the lungs in several pulmonary diseases with a significant unmet need for treatment options. Full article
(This article belongs to the Special Issue New Advances in Inflammation and Repair in Respiratory Diseases)
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13 pages, 4508 KiB  
Article
Resistin-like Molecule α and Pulmonary Vascular Remodeling: A Multi-Strain Murine Model of Antigen and Urban Ambient Particulate Matter Co-Exposure
by Nedim Durmus, Wen-Chi Chen, Sung-Hyun Park, Leigh M. Marsh, Sophia Kwon, Anna Nolan and Gabriele Grunig
Int. J. Mol. Sci. 2023, 24(15), 11918; https://doi.org/10.3390/ijms241511918 - 25 Jul 2023
Cited by 2 | Viewed by 1552
Abstract
Pulmonary hypertension (PH) has a high mortality and few treatment options. Adaptive immune mediators of PH in mice challenged with antigen/particulate matter (antigen/PM) has been the focus of our prior work. We identified key roles of type-2- and type-17 responses in C57BL/6 mice. [...] Read more.
Pulmonary hypertension (PH) has a high mortality and few treatment options. Adaptive immune mediators of PH in mice challenged with antigen/particulate matter (antigen/PM) has been the focus of our prior work. We identified key roles of type-2- and type-17 responses in C57BL/6 mice. Here, we focused on type-2-response-related cytokines, specifically resistin-like molecule (RELM)α, a critical mediator of hypoxia-induced PH. Because of strain differences in the immune responses to type 2 stimuli, we compared C57BL/6J and BALB/c mice. A model of intraperitoneal antigen sensitization with subsequent, intranasal challenges with antigen/PM (ovalbumin and urban ambient PM2.5) or saline was used in C57BL/6 and BALB/c wild-type or RELMα−/− mice. Vascular remodeling was assessed with histology; right ventricular (RV) pressure, RV weights and cytokines were quantified. Upon challenge with antigen/PM, both C57BL/6 and BALB/c mice developed pulmonary vascular remodeling; these changes were much more prominent in the C57BL/6 strain. Compared to wild-type mice, RELMα−/− had significantly reduced pulmonary vascular remodeling in BALB/c, but not in C57BL/6 mice. RV weights, RV IL-33 and RV IL-33-receptor were significantly increased in BALB/c wild-type mice, but not in BALB/c-RELMα−/− or in C57BL/6-wild-type or C57BL/6-RELMα−/− mice in response to antigen/PM2.5. RV systolic pressures (RVSP) were higher in BALB/c compared to C57BL/6J mice, and RELMα−/− mice were not different from their respective wild-type controls. The RELMα−/− animals demonstrated significantly decreased expression of RELMβ and RELMγ, which makes these mice comparable to a situation where human RELMβ levels would be significantly modified, as only humans have this single RELM molecule. In BALB/c mice, RELMα was a key contributor to pulmonary vascular remodeling, increase in RV weight and RV cytokine responses induced by exposure to antigen/PM2.5, highlighting the significance of the genetic background for the biological role of RELMα. Full article
(This article belongs to the Special Issue New Advances in Inflammation and Repair in Respiratory Diseases)
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25 pages, 2026 KiB  
Article
Co-Expression Analysis of Airway Epithelial Transcriptome in Asthma Patients with Eosinophilic vs. Non-Eosinophilic Airway Infiltration
by Pawel Kozlik-Siwiec, Sylwia Buregwa-Czuma, Izabela Zawlik, Sylwia Dziedzina, Aleksander Myszka, Joanna Zuk-Kuwik, Andzelika Siwiec-Kozlik, Jacek Zarychta, Krzysztof Okon, Lech Zareba, Jerzy Soja, Bogdan Jakiela, Michał Kepski, Jan G. Bazan and Stanislawa Bazan-Socha
Int. J. Mol. Sci. 2023, 24(4), 3789; https://doi.org/10.3390/ijms24043789 - 14 Feb 2023
Cited by 1 | Viewed by 3006
Abstract
Asthma heterogeneity complicates the search for targeted treatment against airway inflammation and remodeling. We sought to investigate relations between eosinophilic inflammation, a phenotypic feature frequent in severe asthma, bronchial epithelial transcriptome, and functional and structural measures of airway remodeling. We compared epithelial gene [...] Read more.
Asthma heterogeneity complicates the search for targeted treatment against airway inflammation and remodeling. We sought to investigate relations between eosinophilic inflammation, a phenotypic feature frequent in severe asthma, bronchial epithelial transcriptome, and functional and structural measures of airway remodeling. We compared epithelial gene expression, spirometry, airway cross-sectional geometry (computed tomography), reticular basement membrane thickness (histology), and blood and bronchoalveolar lavage (BAL) cytokines of n = 40 moderate to severe eosinophilic (EA) and non-eosinophilic asthma (NEA) patients distinguished by BAL eosinophilia. EA patients showed a similar extent of airway remodeling as NEA but had an increased expression of genes involved in the immune response and inflammation (e.g., KIR3DS1), reactive oxygen species generation (GYS2, ATPIF1), cell activation and proliferation (ANK3), cargo transporting (RAB4B, CPLX2), and tissue remodeling (FBLN1, SOX14, GSN), and a lower expression of genes involved in epithelial integrity (e.g., GJB1) and histone acetylation (SIN3A). Genes co-expressed in EA were involved in antiviral responses (e.g., ATP1B1), cell migration (EPS8L1, STOML3), cell adhesion (RAPH1), epithelial–mesenchymal transition (ASB3), and airway hyperreactivity and remodeling (FBN3, RECK), and several were linked to asthma in genome- (e.g., MRPL14, ASB3) or epigenome-wide association studies (CLC, GPI, SSCRB4, STRN4). Signaling pathways inferred from the co-expression pattern were associated with airway remodeling (e.g., TGF-β/Smad2/3, E2F/Rb, and Wnt/β-catenin). Full article
(This article belongs to the Special Issue New Advances in Inflammation and Repair in Respiratory Diseases)
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10 pages, 1458 KiB  
Article
PD1, CTLA4 and TIGIT Expression on T and NK Cells in Granulomatous Diseases: Sarcoidosis and ANCA-Associated Vasculitis
by Miriana d’Alessandro, Edoardo Conticini, Laura Bergantini, Fabrizio Mezzasalma, Paolo Cameli, Stefano Baglioni, Martina Armati, Marta Abbritti and Elena Bargagli
Int. J. Mol. Sci. 2023, 24(1), 256; https://doi.org/10.3390/ijms24010256 - 23 Dec 2022
Cited by 4 | Viewed by 2053
Abstract
Sarcoidosis is a granulomatous diseases affecting the lungs. Anti-neutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV) is a histologically granulomatous B-mediated disorder characterized by activated T cells. The expression of immune checkpoint (IC) molecules (PD1, CTLA4, TIGIT) on T- and NK-cells negatively regulate the T-cell [...] Read more.
Sarcoidosis is a granulomatous diseases affecting the lungs. Anti-neutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV) is a histologically granulomatous B-mediated disorder characterized by activated T cells. The expression of immune checkpoint (IC) molecules (PD1, CTLA4, TIGIT) on T- and NK-cells negatively regulate the T-cell immune function. The present study aimed to explore the peripheral distribution of IC molecules to better elucidate their peripheral tolerance failure, which might reflect the development of diseases. Patients referred to Respiratory Diseases and Rheumatology Unit of Siena University Hospital were prospectively and consecutively enrolled. Healthy subjects were also enrolled as a control group. Multicolor flow cytometric analysis was performed to detect IC molecules in the peripheral blood of patients. Twenty-three patients were consecutively and prospectively enrolled in the study: 11 patients had an AAV diagnosis and 12 had sarcoidosis. CD4+PD1+ cells were higher in sarcoidosis and GPA than in HC (p = 0.0250 and p = 0.0253, respectively). CD56+CTLA4+ were higher in sarcoidosis than GPA, MPA and HC (p = 0.0085, p = 0.0042 and p = 0.0004, respectively). CTLA4+NK cells clustered for 100% of sarcoidosis patients according to decision tree analysis, while PD1+CD4 and CD8 cells for clustered for 100% of GPA patients. Our analyses showed substantial differences between sarcoidosis and AAV, further confirming the immunological peculiarity of this disease. Despite these advances, the pathogenesis remains incompletely understood, indicating an urgent need for further research to reveal the distinct immunological events in this process, with the hope to open up new therapeutic avenues and, if possible, to develop preventive measures. Full article
(This article belongs to the Special Issue New Advances in Inflammation and Repair in Respiratory Diseases)
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