scholarly journals The Interaction Between Pulmonary Fibrosis and COVID-19 and the Application of Related Anti-Fibrotic Drugs

2022 ◽  
Vol 12 ◽  
Author(s):  
Hao Shen ◽  
Nu Zhang ◽  
Yuqing Liu ◽  
Xuerong Yang ◽  
Yuanyuan He ◽  
...  
Keyword(s):  
Pulmonary Fibrosis ◽  
Drug Treatment ◽  
Immune Cells ◽  
Distress Syndrome ◽  
Potential Interaction ◽  
Inflammatory Factors ◽  
Treatment Programs ◽  
Cytokine Storm ◽  
Potential Mechanism ◽  
Drug Treatment Program

COVID-19 is a highly contagious respiratory disease, which mainly affects the lungs. Critically ill patients are easily complicated by cytokine storms, acute respiratory distress syndrome (ARDS), and respiratory failure, which seriously threaten their lives. Pulmonary fibrosis (PF) is a common interstitial lung disease, and its pathogenesis may involve the participation of a variety of immune cells and inflammatory factors. Current studies have shown that patients with COVID-19 may be complicated by pulmonary fibrosis, and patients with pulmonary fibrosis may also be at higher risk of contracting COVID-19 than healthy people. Pulmonary fibrosis is an important risk factor leading to the aggravation of COVID-19 disease. COVID-19 complicated by cytokine storm and ARDS mechanism pathways are similar to the pathogenesis of pulmonary fibrosis. The potential interaction between pulmonary fibrosis and COVID-19 can cause acute exacerbation of the patient’s condition, but the potential mechanism between the two has not been fully elucidated. Most of the drug treatment programs for COVID-19-related pulmonary fibrosis are currently formulated about the relevant guidelines for idiopathic pulmonary fibrosis (IPF), and there is no clear drug treatment program recommendation. This article aims to summarize the relevant mechanism pathways of COVID-19 and pulmonary fibrosis, explore the interrelationships and possible mechanisms, and discuss the value and risks of existing and potential COVID-19-related pulmonary fibrosis treatment drugs, to provide reference for anti-fibrosis treatment for patients.

scholarly journals Protective Effect of Arbidol Against Pulmonary Fibrosis and Sepsis in Mice

2021 ◽  
Vol 11 ◽  
Author(s):  
Hailong Li ◽  
Rui Liu ◽  
Ruotong Zhang ◽  
Shanshan Zhang ◽  
Yiying Wei ◽  
...  
Keyword(s):  
Pulmonary Fibrosis ◽  
Mouse Model ◽  
Antiviral Drug ◽  
Dynamic Compliance ◽  
Serum Levels ◽  
Inflammatory Factors ◽  
Cytokine Storm ◽  
Viral Immunology ◽  
Sepsis Induction ◽  
Sepsis Score

From the perspective of epidemiology, viral immunology and current clinical research, pulmonary fibrosis may become one of the complications of patients with Coronavirus Disease 2019 (COVID-19). Cytokine storm is a major cause of new coronavirus death. The purpose of this study was to explore the effects of antiviral drug arbidol on cytokine storm and pulmonary fibrosis. Here, we use a mouse model of bleomycin-induced pulmonary fibrosis and a mouse model of fecal dilution-induced sepsis to evaluate the effects of arbidol on pulmonary fibrosis and cytokine storm. The results showed that arbidol significantly reduced the area of pulmonary fibrosis and improved lung function (reduced inspiratory resistance, lung dynamic compliance and forced vital capacity increased). Treatment with arbidol promoted reduced sepsis severity 48 h after sepsis induction, based on weight, murine sepsis score and survival rate. Arbidol observably alleviates inflammatory infiltrates and injury in the lungs and liver. Finally, we also found that arbidol reduced serum levels of pro-inflammatory factors such as TNF-α and IL-6 induced by fecal dilution. In conclusion, our results indicate that arbidol can alleviate the severity of pulmonary fibrosis and sepsis, and provide some reference for the treatment of cytokine storm and sequelae of pulmonary fibrosis in patients with COVID-19.

scholarly journals Increased circulating microparticles and inflammatory factors aggravate coronavirus disease 2019 (COVID-19)

2020 ◽  
Author(s):  
DA-ZHI GUO ◽  
Yan Lv ◽  
Ya’nan Qi ◽  
Shuyi Pan
Keyword(s):  
Distress Syndrome ◽  
Pearson Correlation ◽  
Inflammatory Factors ◽  
Control Group ◽  
Cytokine Storm ◽  
Circulating Microparticles ◽  
Pearson Correlation Analysis ◽  
Early Inhibition ◽  
Important Therapeutic Target ◽  
Healthy Persons

Abstract Background The outbreak of coronavirus disease 2019 (COVID-19) caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has posed tremendous challenges to the world's public health. The conditions of some patients can quickly progress to acute respiratory distress syndrome and even death. Current studies suggest that an outbreak of inflammatory response known as cytokine storm may play a key role in the process. This study was performed to investigate the relativity of the production of circulating microparticles (cMPs) and the expression of inflammatory factors (interleukin [IL]-6, IL-8 and IL-10) expression in the blood on the degree of COVID-19. Methods A total of 89 patients infected with SARS-CoV-2 were divided into four groups, namely, mild, moderate, severe and critically ill groups, according to China's COVID-19 Diagnosis and Treatment Program (6th trial version), and 30 healthy persons were selected as the control group. The groups were compared in terms of cMP production and IL-6, IL-8 and IL-10 levels in their blood, and the correlation between cMP production and the expression of inflammatory factors with the degree of COVID-19 were analysed. Results Differences in cMP production and IL-6, IL-8 and IL-10 expression levels among the five groups were statistically significant (P<0.05). Pearson correlation analysis showed a positive correlation between cMP production or the expression of IL-6, IL-8 and IL-10 and the degree of COVID-19 (cMP, r=0.981; IL-6, r=0.954; IL-8, r=0.863; IL-10, r=0.895; P<0.05). Conclusion Increased levels of cMP, IL-6, IL-8 and IL-10 aggravate COVID-19. cMP production and the expression of IL-6, IL-8 and IL-10 may predict the degree of COVID-19 to a certain extent. The early inhibition of cMP overproduction and IL-6, IL-8 and IL-10 expression may be an important therapeutic target for the prevention of COVID-19 progression.

scholarly journals Commonalities Between ARDS, Pulmonary Fibrosis and COVID-19: The Potential of Autotaxin as a Therapeutic Target

2021 ◽  
Vol 12 ◽  
Author(s):  
Konstantinos Ntatsoulis ◽  
Theodoros Karampitsakos ◽  
Eliza Tsitoura ◽  
Elli-Anna Stylianaki ◽  
Alexios N. Matralis ◽  
...  
Keyword(s):  
Pulmonary Fibrosis ◽  
Lysophosphatidic Acid ◽  
Immune Cells ◽  
Therapeutic Target ◽  
Lung Diseases ◽  
Distress Syndrome ◽  
Severe Disease ◽  
Interstitial Lung Diseases ◽  
Extracellular Production ◽  
Increased Risk

Severe COVID-19 is characterized by acute respiratory distress syndrome (ARDS)-like hyperinflammation and endothelial dysfunction, that can lead to respiratory and multi organ failure and death. Interstitial lung diseases (ILD) and pulmonary fibrosis confer an increased risk for severe disease, while a subset of COVID-19-related ARDS surviving patients will develop a fibroproliferative response that can persist post hospitalization. Autotaxin (ATX) is a secreted lysophospholipase D, largely responsible for the extracellular production of lysophosphatidic acid (LPA), a pleiotropic signaling lysophospholipid with multiple effects in pulmonary and immune cells. In this review, we discuss the similarities of COVID-19, ARDS and ILDs, and suggest ATX as a possible pathologic link and a potential common therapeutic target.

scholarly journals Δ9-Tetrahydrocannabinol Prevents Mortality from Acute Respiratory Distress Syndrome through the Induction of Apoptosis in Immune Cells, Leading to Cytokine Storm Suppression

2020 ◽  
Vol 21 (17) ◽  
pp. 6244
Author(s):  
Amira Mohammed ◽  
Hasan F.K. Alghetaa ◽  
Kathryn Miranda ◽  
Kiesha Wilson ◽  
Narendra P. Singh ◽  
...  
Keyword(s):  
Acute Respiratory Distress Syndrome ◽  
Respiratory Distress Syndrome ◽  
Respiratory Distress ◽  
Single Cell ◽  
Rna Sequencing ◽  
Immune Cells ◽  
Distress Syndrome ◽  
Elevated Serum ◽  
Cytokine Storm ◽  
Single Cell Rna Sequencing

Acute Respiratory Distress Syndrome (ARDS) causes up to 40% mortality in humans and is difficult to treat. ARDS is also one of the major triggers of mortality associated with coronavirus-induced disease (COVID-19). We used a mouse model of ARDS induced by Staphylococcal enterotoxin B (SEB), which triggers 100% mortality, to investigate the mechanisms through which Δ9-tetrahydrocannabinol (THC) attenuates ARDS. SEB was used to trigger ARDS in C3H mice. These mice were treated with THC and analyzed for survival, ARDS, cytokine storm, and metabolome. Additionally, cells isolated from the lungs were used to perform single-cell RNA sequencing and transcriptome analysis. A database analysis of human COVID-19 patients was also performed to compare the signaling pathways with SEB-mediated ARDS. The treatment of SEB-mediated ARDS mice with THC led to a 100% survival, decreased lung inflammation, and the suppression of cytokine storm. This was associated with immune cell apoptosis involving the mitochondrial pathway, as suggested by single-cell RNA sequencing. A transcriptomic analysis of immune cells from the lungs revealed an increase in mitochondrial respiratory chain enzymes following THC treatment. In addition, metabolomic analysis revealed elevated serum concentrations of amino acids, lysine, n-acetyl methionine, carnitine, and propionyl L-carnitine in THC-treated mice. THC caused the downregulation of miR-185, which correlated with an increase in the pro-apoptotic gene targets. Interestingly, the gene expression datasets from the bronchoalveolar lavage fluid (BALF) of human COVID-19 patients showed some similarities between cytokine and apoptotic genes with SEB-induced ARDS. Collectively, this study suggests that the activation of cannabinoid receptors may serve as a therapeutic modality to treat ARDS associated with COVID-19.

Cancer stemness as a target for immunotherapy is shaped by pro-inflammatory stress.

2020 ◽  
Vol 15 ◽  
Author(s):  
Nese Unver
Keyword(s):  
Stem Cells ◽  
Stem Cell ◽  
Cancer Stem Cells ◽  
Immune Cells ◽  
Tumor Recurrence ◽  
Inflammatory Factors ◽  
Cancer Stemness ◽  
Self Renewal ◽  
Inflammatory Stress ◽  
Factors Affecting

: Cancer stem cells represent a rare subpopulation of cancer cells carrying self-renewal and differentiation features in the multi-step tumorigenesis, tumor recurrence and metastasis. Pro-inflammatory stress is highly associated with cancer stemness via induction of cytokines, tumor-promoting immune cells and cancer stemness-related signaling pathways. This review summarizes the major pro-inflammatory factors affecting cancer stem cell characteristics and the critical immunotherapeutic strategies to eliminate cancer stem cells.

scholarly journals Lipopolysaccharides promote pulmonary fibrosis in silicosis through the aggravation of apoptosis and inflammation in alveolar macrophages

2020 ◽  
Vol 15 (1) ◽  
pp. 598-605
Author(s):  
Shiyi Tan ◽  
Shang Yang ◽  
Mingke Chen ◽  
Yurun Wang ◽  
Li Zhu ◽  
...  
Keyword(s):  
Pulmonary Fibrosis ◽  
Alveolar Macrophages ◽  
Inflammatory Factors ◽  
Necrosis Factor Alpha ◽  
Defensive Role ◽  
Factor Alpha ◽  
Apoptosis And Inflammation ◽  
The Relationship ◽  
Lps Treatment ◽  
Necrosis Factor

AbstractAlveolar macrophages (AMs) play an important defensive role by removing dust and bacteria from alveoli. Apoptosis of AMs is associated with lung fibrosis; however, the relationship between this apoptotic event and environmental factors, such as the presence of lipopolysaccharides (LPSs) in the workplace, has not yet been addressed. To investigate whether exposure to LPS can exacerbate fibrosis, we collected AMs from 12 male workers exposed to silica and incubated them in the presence and absence of LPS for 24 h. We show that the levels of cleaved caspase-3 and pro-inflammatory cytokines interleukin (IL)-1β, IL-6, and tumor necrosis factor-alpha were increased in these AMs following LPS treatment. Moreover, we demonstrate that LPS exposure aggravated apoptosis and the release of inflammatory factors in AMs in a mouse model of silicosis, which eventually promoted pulmonary fibrosis. These results suggest that exposure to LPS may accelerate the progression of pulmonary fibrosis in silicosis by increasing apoptosis and inflammation in AMs.

scholarly journals Recent Findings on Cell-Based Therapies for COVID19-Related Pulmonary Fibrosis

2021 ◽  
Vol 30 ◽  
pp. 096368972199621
Author(s):  
Hong-Meng Chuang ◽  
Li-Ing Ho ◽  
Horng-Jyh Harn ◽  
Ching-Ann Liu
Keyword(s):  
Stem Cells ◽  
Clinical Trials ◽  
Pulmonary Fibrosis ◽  
Tissue Repair ◽  
Immune Modulation ◽  
Distress Syndrome ◽  
Clinical Symptoms ◽  
The United States ◽  
Past Experiences ◽  
Respiratory Tract Inflammation

COVID-19 has spread worldwide, including the United States, United Kingdom, and Italy, along with its site of origin in China, since 2020. The virus was first found in the Wuhan seafood market at the end of 2019, with a controversial source. The clinical symptoms of COVID-19 include fever, cough, and respiratory tract inflammation, with some severe patients developing an acute and chronic lung injury, such as acute respiratory distress syndrome (ARDS) and pulmonary fibrosis (PF). It has already claimed approximately 300 thousand human lives and the number is still on the rise; the only way to prevent the infection is to be safe till vaccines and reliable treatments develop. In previous studies, the use of mesenchymal stem cells (MSCs) in clinical trials had been proven to be effective in immune modulation and tissue repair promotion; however, their efficacy in treating COVID-19 remains underestimated. Here, we report the findings from past experiences of SARS and MSCs, and how SARS could also induce PF. Such studies may help to understand the rationale for the recent cell-based therapies for COVID-19.

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