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      Olfactory mucosa mesenchymal stem cells alleviate pulmonary fibrosis via the immunomodulation and reduction of inflammation

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          Abstract

          Background

          Pulmonary fibrosis (PF) is a progressive fibrosing interstitial pneumonia that leads to respiratory failure and other complications, which is ultimately fatal. Mesenchymal stem cells (MSCs) transplant is a promising strategy to solve this problem, while the procurement of MSCs from the patient for autotransplant remains a challenge.

          Methods

          Here, we presented olfactory mucosa mesenchymal stem cells (OM-MSCs) from mouse turbinate and determined the preventing efficacy of allotransplant for PF. We demonstrated the antiinflammation and immunomodulatory effects of OM-MSCs. Flow cytometric analysis was used to verify the effect of OM-MSCs on monocyte-derived macrophage populations in the lung.

          Results

          Administration of OM-MSCs reduces inflammation, attenuates the matrix metallopeptidase 13 (MMP13) expression level and restores the bleomycin (BLM)-induced pulmonary fibrosis by assessing the architecture of lung, collagen type I; (COL1A1), actin alpha 2, smooth muscle, aorta (ACTA2/α-SMA) and hydroxyproline. This therapeutic effect of OM-MSCs was related to the increase in the ratio of nonclassical monocytes to proinflammatory monocytes in the lung.

          Conclusions

          This study suggests that transplant of OM-MSCs represents an effective and safe treatment for PF.

          Supplementary Information

          The online version contains supplementary material available at 10.1186/s12890-023-02834-5.

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          Most cited references31

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          Idiopathic pulmonary fibrosis.

          Idiopathic pulmonary fibrosis is a prototype of chronic, progressive, and fibrotic lung disease. Healthy tissue is replaced by altered extracellular matrix and alveolar architecture is destroyed, which leads to decreased lung compliance, disrupted gas exchange, and ultimately respiratory failure and death. In less than a decade, understanding of the pathogenesis and management of this disease has been transformed, and two disease-modifying therapies have been approved, worldwide. In this Seminar, we summarise the presentation, pathophysiology, diagnosis, and treatment options available for patients with idiopathic pulmonary fibrosis. This disease has improved understanding of the mechanisms of lung fibrosis, and offers hope that similar approaches will transform the management of patients with other progressive fibrotic lung diseases.
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            Pulmonary fibrosis and COVID-19: the potential role for antifibrotic therapy

            Summary In December, 2019, reports emerged from Wuhan, China, of a severe acute respiratory disease caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). By the end of April, 2020, over 3 million people had been confirmed infected, with over 1 million in the USA alone, and over 215 000 deaths. The symptoms associated with COVID-19 are diverse, ranging from mild upper respiratory tract symptoms to severe acute respiratory distress syndrome. The major risk factors for severe COVID-19 are shared with idiopathic pulmonary fibrosis (IPF), namely increasing age, male sex, and comorbidities such as hypertension and diabetes. However, the role of antifibrotic therapy in patients with IPF who contract SARS-CoV-2 infection, and the scientific rationale for their continuation or cessation, is poorly defined. Furthermore, several licensed and potential antifibrotic compounds have been assessed in models of acute lung injury and viral pneumonia. Data from previous coronavirus infections such as severe acute respiratory syndrome and Middle East respiratory syndrome, as well as emerging data from the COVID-19 pandemic, suggest there could be substantial fibrotic consequences following SARS-CoV-2 infection. Antifibrotic therapies that are available or in development could have value in preventing severe COVID-19 in patients with IPF, have the potential to treat severe COVID-19 in patients without IPF, and might have a role in preventing fibrosis after SARS-CoV-2 infection.
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              Simple method of estimating severity of pulmonary fibrosis on a numerical scale.

              A continuous numerical scale for determining the degree of fibrosis in lung specimens was devised for correlation with other pulmonary variables such as lung function tests or mineral burden. Grading was scored on a scale from 0 to 8, using the average of microscope field scores. The system allows fibrosis to be measured in small samples of tissue (1 cm) which can provide a detailed description of the changes in a lung, currently not possible with most existing methods.
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                Author and article information

                Contributors
                huixie@csu.edu.cn
                liuzhengzhao@gdmu.edu.cn
                Journal
                BMC Pulm Med
                BMC Pulm Med
                BMC Pulmonary Medicine
                BioMed Central (London )
                1471-2466
                5 January 2024
                5 January 2024
                2024
                : 24
                : 14
                Affiliations
                [1 ]Guangdong Provincial Key Laboratory of Autophagy and Major Chronic Non-Communicable Diseases, Key Laboratory of Prevention and Management of Chronic Kidney Disease of Zhanjiang City, Institute of Nephrology, Affiliated Hospital of Guangdong Medical University, ( https://ror.org/04k5rxe29) 524001 Zhanjiang, Guangdong China
                [2 ]GRID grid.216417.7, ISNI 0000 0001 0379 7164, Department of Sports Medicine, Xiangya Hospital, , Central South University, ; 410008 Changsha, Hunan China
                [3 ]GRID grid.216417.7, ISNI 0000 0001 0379 7164, Movement System Injury and Repair Research Center, Xiangya Hospital, , Central South University, ; 410008 Changsha, Hunan China
                [4 ]Department of Neurosurgery, Second affiliated Hospital of Hunan Normal University (921 Hospital of PLA), ( https://ror.org/053w1zy07) 410081 Changsha, Hunan China
                Article
                2834
                10.1186/s12890-023-02834-5
                10768423
                38178092
                db4626bf-f080-4fc4-b4c1-81125cbb0a05
                © The Author(s) 2024

                Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

                History
                : 16 November 2023
                : 28 December 2023
                Funding
                Funded by: Fundamental Research Funds for Central Universities of the Central South University
                Award ID: 2020zzts859
                Funded by: National Natural Science Foundation of China
                Award ID: 82172502
                Categories
                Research
                Custom metadata
                © BioMed Central Ltd., part of Springer Nature 2024

                Respiratory medicine
                olfactory mucosa mesenchymal stem cells,pulmonary fibrosis,monocyte,inflammation,collagen

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