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The Role of Immunity and Inflammation in Pulmonary Fibrosis
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The Role of Immunity and Inflammation in Pulmonary Fibrosis

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Immunology".

Deadline for manuscript submissions: closed (30 June 2023) | Viewed by 4611

Special Issue Editor

Dr. Tingting Weng

E-Mail Website
Guest Editor
Department of Biochemistry and Molecular Biology, McGovern Medical School, UTHealth at Houston, Houston, TX 77030, USA
Interests: pulmonary fibrosis; scleroderma; alternative polyadenylation; adenosine; immunopathology; host defense

Special Issue Information

Dear Colleagues,

Inflammatory response to injuries or infections, in combination with dysregulated wound repair and fibroblast activation, lead to the excessive deposition of extracellular matrix proteins and massive tissue remodeling seen in end-stage pulmonary fibrosis. However, the role of inflammation, as an important component of pulmonary fibrosis, is controversial. Inflammatory mechanisms may not be the primary triggers for idiopathic pulmonary fibrosis, but prominently contribute to systemic sclerosis, and pulmonary fibrosis results from severe acute respiratory distress syndrome. We believe that a better understanding of immunity and inflammation in lung fibrosis will provide important preclinical evidence for the treatment of this disease.

This Special Issue will collect research and review articles focusing on novel studies that aimed to investigate the role of immunopathology in pulmonary fibrosis. All researchers are welcome to submit studies related to immunopathology, inflammation, aging immune system, auto-immune responses, crosstalk between immune cells and other cells during the pathogenesis of pulmonary fibrosis, etc.

Dr. Tingting Weng
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

  • immunopathology and diseases
  • inflammation
  • aging immune system
  • crosstalk between immune cells and other cells
  • immunotherapy
  • auto-immune responses
  • early fibrotic markers

Published Papers (2 papers)

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16 pages, 4749 KiB  
Article
Adenosine A3 Receptor (A3AR) Agonist for the Treatment of Bleomycin-Induced Lung Fibrosis in Mice
by Silvia Sgambellone, Silvia Marri, Stefano Catarinicchia, Alessandro Pini, Dilip K. Tosh, Kenneth A. Jacobson, Emanuela Masini, Daniela Salvemini and Laura Lucarini
Int. J. Mol. Sci. 2022, 23(21), 13300; https://doi.org/10.3390/ijms232113300 - 1 Nov 2022
Cited by 5 | Viewed by 2019
Abstract
Adenosine receptors (ARs) are involved in the suppression and development of inflammatory and fibrotic conditions. Specifically, AR activation promotes differentiation of lung fibroblasts into myofibroblasts, typical of a fibrotic event. Pulmonary fibrosis is a severe disease characterized by inflammation and fibrosis of unknown [...] Read more.
Adenosine receptors (ARs) are involved in the suppression and development of inflammatory and fibrotic conditions. Specifically, AR activation promotes differentiation of lung fibroblasts into myofibroblasts, typical of a fibrotic event. Pulmonary fibrosis is a severe disease characterized by inflammation and fibrosis of unknown etiology and lacking an effective treatment. The present investigation explored the action of MRS5980, a new, highly potent and selective A3AR agonist, in an established murine model of lung fibrosis. The effects of either vehicle or MRS5980 were studied in mice following intratracheal bleomycin administration. We evaluated the role of the A3AR agonist on lung stiffness, studying the airway resistance to inflation, oxidative stress (8-OHdG and MDA), inflammation, pro- and anti-inflammatory marker levels (IL-1β, IL-6, TNF-α, IL-10 and IL-17A) and fibrosis establishment, evaluating transforming growth factor (TGF)-β expression and α-smooth muscle actin (α-SMA) deposition in lungs. Bleomycin administration increased lung stiffness, TGF-β levels, α-SMA deposition, and inflammatory and oxidative stress markers. The treatment with MRS5980 attenuated all the analyzed functional, biochemical and histopathological markers in a dose-dependent manner. Our findings support the therapeutic potential of A3AR agonists in lung fibrosis by demonstrating reduced disease progression, as indicated by decreased inflammation, TGF-β expression and fibrotic remodeling. Full article
(This article belongs to the Special Issue The Role of Immunity and Inflammation in Pulmonary Fibrosis)
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16 pages, 326 KiB  
Review
Interstitial Lung Disease in Systemic Lupus Erythematosus and Systemic Sclerosis: How Can We Manage the Challenge?
by Patricia Richter, Anca Cardoneanu, Nicoleta Dima, Ioana Bratoiu, Ciprian Rezus, Alexandra Maria Burlui, Damiana Costin, Luana Andreea Macovei and Elena Rezus
Int. J. Mol. Sci. 2023, 24(11), 9388; https://doi.org/10.3390/ijms24119388 - 28 May 2023
Cited by 1 | Viewed by 2162
Abstract
Interstitial lung disease (ILD) is a severe and frequent manifestation of connective tissue diseases (CTD). Due to its debilitating potential, it requires serious evaluation and treatment. The prevalence of ILD in systemic lupus erythematosus (SLE) is still controversial. Therefore, in order to establish [...] Read more.
Interstitial lung disease (ILD) is a severe and frequent manifestation of connective tissue diseases (CTD). Due to its debilitating potential, it requires serious evaluation and treatment. The prevalence of ILD in systemic lupus erythematosus (SLE) is still controversial. Therefore, in order to establish the diagnosis of ILD, an overlap syndrome must be excluded. Increasing the identification of SLE-associated ILD cases should become a target. To treat this complication, various therapies are now being proposed. To date, no placebo-controlled studies were conducted. Regarding another CTD, systemic sclerosis (SSc), SSc-associated ILD is considered one of the leading causes of mortality. The incidence of ILD varies among disease subtypes, being influenced by diagnostic method, but also by disease duration. Due to the high prevalence of this complication, all SSc patients should be investigated for ILD at the time of SSc diagnosis and during the course of the disease. Fortunately, progress was made in terms of treatment. Nintedanib, a tyrosine kinases inhibitor, showed promising results. It appeared to decrease the rate of progression of ILD compared to placebo. This review aimed to provide up-to-date findings related to SLE-associated ILD and SSc-associated ILD, in order to raise awareness of their diagnosis and management. Full article
(This article belongs to the Special Issue The Role of Immunity and Inflammation in Pulmonary Fibrosis)
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