scholarly journals IL-4/IL-13 Remodeling Pathway of Covid-19 Lung Injury

2020 ◽  
Author(s):  
Caroline Busatta Vaz de Paula ◽  
Marina Luise Viola Azevedo ◽  
Seigo Nagashima ◽  
Ana Paula Camargo Martins ◽  
Mineia Alessandra Scaranello Malaquias ◽  
...  
Keyword(s):  
Lung Injury ◽  
Transforming Growth Factor Beta ◽  
Influenza A ◽  
Transforming Growth Factor ◽  
Diffuse Alveolar Damage ◽  
Tissue Expression ◽  
Lung Damage ◽  
Control Group ◽  
M2 Macrophages ◽  
Th17 Response

Abstract Background: The COVID-19 fatality rate is high when compared to the H1N1pdm09 (pandemic Influenza A virus H1N1 subtype) rate, and although both cause an aggravated inflammatory response, the differences in the mechanisms of both pandemic pneumonias need clarification.Objective: To analyze tissue expression of interleukins 4, 13, (IL-4, IL-13), transforming growth factor-beta (TGF-β), and the number of M2 macrophages (Sphingosine-1) in patients who died by COVID-19, comparing with cases of severe pneumopathy caused by H1N1pdm09, and a control group without lung injury.Methods: Six lung biopsy samples of patients who died of SARS-CoV-2 (COVID-19 group) were used and compared with ten lung samples of adults who died from a severe infection of H1N1pdm09 (H1N1 group) and eleven samples of patients who died from different causes without lung injury (CONTROL group). The expression of IL-4, IL-13, TGF-β, and M2 macrophages score (Sphingosine-1) were identified through immunohistochemistry (IHC).Results and conclusion: Significantly higher IL-4 tissue expression and Sphingosine-1 in M2 macrophages was observed in the COVID-19 group when compared to both the H1N1 and the CONTROL groups. Different mechanism of diffuse alveolar damage (DAD) in SARS-CoV-2 compared to H1N1pdm09 infections were observed. IL-4 expression and lung remodeling are phenomena observed in both SARS-COV-2 and H1N1pdm09. However, SARS-CoV-2 seems to promote lung damage through different mechanisms, such as the scarce participation Th1/Th17 response and the higher participation of the Th2. The understanding and management of the aggravated and ineffective immune response elicited by SARS-CoV-2 merits further clarification to improve treatments propose.

scholarly journals IL-4/IL-13 Remodeling Pathway of Covid-19 Lung Injury

2020 ◽  
Author(s):  
Caroline Busatta Vaz de Paula ◽  
Marina Luise Viola Azevedo ◽  
Seigo Nagashima ◽  
Ana Paula Camargo Martins ◽  
Mineia Alessandra Scaranello Malaquias ◽  
...  
Keyword(s):  
Lung Injury ◽  
Transforming Growth Factor Beta ◽  
Influenza A ◽  
Transforming Growth Factor ◽  
Diffuse Alveolar Damage ◽  
Tissue Expression ◽  
Lung Damage ◽  
Control Group ◽  
M2 Macrophages ◽  
Th17 Response

Abstract Background: The COVID-19 fatality rate is high when compared to the H1N1pdm09 (pandemic Influenza A virus H1N1 subtype) rate, and although both cause an aggravated inflammatory response, the differences in the mechanisms of both pandemic pneumonias need clarification.Objective: To analyze tissue expression of interleukins 4, 13, (IL-4, IL-13), transforming growth factor-beta (TGF-β), and the number of M2 macrophages (Sphingosine-1) in patients who died by COVID-19, comparing with cases of severe pneumopathy caused by H1N1pdm09, and a control group without lung injury.Methods: Six lung biopsy samples of patients who died of SARS-CoV-2 (COVID-19 group) were used and compared with ten lung samples of adults who died from a severe infection of H1N1pdm09 (H1N1 group) and eleven samples of patients who died from different causes without lung injury (CONTROL group). The expression of IL-4, IL-13, TGF-β, and M2 macrophages score (Sphingosine-1) were identified through immunohistochemistry (IHC).Results and conclusion: Significantly higher IL-4 tissue expression and Sphingosine-1 in M2 macrophages was observed in the COVID-19 group when compared to both the H1N1 and the CONTROL groups. Different mechanism of diffuse alveolar damage (DAD) in SARS-CoV-2 compared to H1N1pdm09 infections were observed. IL-4 expression and lung remodeling are phenomena observed in both SARS-COV-2 and H1N1pdm09. However, SARS-CoV-2 seems to promote lung damage through different mechanisms, such as the scarce participation Th1/Th17 response and the higher participation of the Th2. The understanding and management of the aggravated and ineffective immune response elicited by SARS-CoV-2 merits further clarification to improve treatments propose.

scholarly journals IL-4/IL-13 Remodeling Pathway of Covid-19 Lung Injury

2020 ◽  
Author(s):  
Caroline Busatta Vaz de Paula ◽  
Marina Luise Viola Azevedo ◽  
Seigo Nagashima ◽  
Ana Paula Camargo Martins ◽  
Mineia Alessandra Scaranello Malaquias ◽  
...  
Keyword(s):  
Lung Injury ◽  
Transforming Growth Factor Beta ◽  
Influenza A ◽  
Transforming Growth Factor ◽  
Diffuse Alveolar Damage ◽  
Tissue Expression ◽  
Lung Damage ◽  
Control Group ◽  
M2 Macrophages ◽  
Th17 Response

Abstract Background: The COVID-19 fatality rate is high when compared to the H1N1pdm09 (pandemic Influenza A virus H1N1 subtype) rate, and although both cause an aggravated inflammatory response, the differences in the mechanisms of both pandemic pneumonias need clarification.Objective: To analyze tissue expression of interleukins 4, 13, (IL-4, IL-13), transforming growth factor-beta (TGF-β), and the number of M2 macrophages (Sphingosine-1) in patients who died by COVID-19, comparing with cases of severe pneumopathy caused by H1N1pdm09, and a control group without lung injury.Methods: Six lung biopsy samples of patients who died of SARS-CoV-2 (COVID-19 group) were used and compared with ten lung samples of adults who died from a severe infection of H1N1pdm09 (H1N1 group) and eleven samples of patients who died from different causes without lung injury (CONTROL group). The expression of IL-4, IL-13, TGF-β, and M2 macrophages score (Sphingosine-1) were identified through immunohistochemistry (IHC).Results and conclusion: Significantly higher IL-4 tissue expression and Sphingosine-1 in M2 macrophages was observed in the COVID-19 group when compared to both the H1N1 and the CONTROL groups. Different mechanism of diffuse alveolar damage (DAD) in SARS-CoV-2 compared to H1N1pdm09 infections were observed. IL-4 expression and lung remodeling are phenomena observed in both SARS-COV-2 and H1N1pdm09. However, SARS-CoV-2 seems to promote lung damage through different mechanisms, such as the scarce participation Th1/Th17 response and the higher participation of the Th2. The understanding and management of the aggravated and ineffective immune response elicited by SARS-CoV-2 merits further clarification to improve treatments propose.

scholarly journals IL-4/IL-13 remodeling pathway of COVID-19 lung injury

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Caroline Busatta Vaz de Paula ◽  
Marina Luise Viola de Azevedo ◽  
Seigo Nagashima ◽  
Ana Paula Camargo Martins ◽  
Mineia Alessandra Scaranello Malaquias ◽  
...  
Keyword(s):  
Lung Injury ◽  
Transforming Growth Factor Beta ◽  
Influenza A ◽  
Transforming Growth Factor ◽  
Diffuse Alveolar Damage ◽  
Tissue Expression ◽  
Lung Damage ◽  
Control Group ◽  
M2 Macrophages ◽  
Th17 Response

Abstract The COVID-19 fatality rate is high when compared to the H1N1pdm09 (pandemic Influenza A virus H1N1 subtype) rate, and although both cause an aggravated inflammatory response, the differences in the mechanisms of both pandemic pneumonias need clarification. Thus, our goal was to analyze tissue expression of interleukins 4, 13, (IL-4, IL-13), transforming growth factor-beta (TGF-β), and the number of M2 macrophages (Sphingosine-1) in patients who died by COVID-19, comparing with cases of severe pneumopathy caused by H1N1pdm09, and a control group without lung injury. Six lung biopsy samples of patients who died of SARS-CoV-2 (COVID-19 group) were used and compared with ten lung samples of adults who died from a severe infection of H1N1pdm09 (H1N1 group) and eleven samples of patients who died from different causes without lung injury (CONTROL group). The expression of IL-4, IL-13, TGF-β, and M2 macrophages score (Sphingosine-1) were identified through immunohistochemistry (IHC). Significantly higher IL-4 tissue expression and Sphingosine-1 in M2 macrophages were observed in the COVID-19 group compared to both the H1N1 and the CONTROL groups. A different mechanism of diffuse alveolar damage (DAD) in SARS-CoV-2 compared to H1N1pdm09 infections were observed. IL-4 expression and lung remodeling are phenomena observed in both SARS-CoV-2 and H1N1pdm09. However, SARS-CoV-2 seems to promote lung damage through different mechanisms, such as the scarce participation Th1/Th17 response and the higher participation of the Th2. Understanding and managing the aggravated and ineffective immune response elicited by SARS-CoV-2 merits further clarification to improve treatments propose.

TGF-beta 1 causes increased endothelial ICAM-1 expression and lung injury

1994 ◽  
Vol 77 (3) ◽  
pp. 1281-1287 ◽  
Author(s):  
Y. Suzuki ◽  
T. Tanigaki ◽  
D. Heimer ◽  
W. Wang ◽  
W. G. Ross ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Lung Injury ◽  
Transforming Growth Factor Beta ◽  
Guinea Pigs ◽  
Transforming Growth Factor ◽  
Weight Ratio ◽  
Control Group ◽  
High Dose ◽  
Albumin Concentration ◽  
Tgf Beta

Neutrophil adherence to vascular endothelium is partially mediated by adhesion molecules, including intracellular adhesion molecule 1 (ICAM-1), on endothelial cells. We examined the effect of transforming growth factor-beta 1 (TGF-beta 1) on the expression of ICAM-1 in human umbilical vein endothelial cells (HUVEC). TGF-beta 1 (1 ng/ml) increased ICAM-1 and ICAM-1 mRNA expression in HUVEC, as assessed by flow cytometry and Northern blot analysis, respectively. In addition, we investigated whether exogenous recombinant TGF-beta 1 can cause neutrophil-mediated lung injury in guinea pigs. The plasma half-life of 125I-labeled TGF-beta 1 in guinea pigs was 4.6 +/- 0.1 min, and the 125I activity was 2.8 +/- 0.2% 8 h after injection. The ratio of 125I-labeled albumin concentration in lung tissue and bronchoalveolar lavage (BAL) fluid to that in plasma, lung wet-to-dry weight ratio, numbers of neutrophils in BAL fluid, and numbers of neutrophils per alveolus in fixed lung sections increased in guinea pigs that received a high dose of TGF-beta 1 (25 micrograms i.v. followed by 2 micrograms/h for 8 h) compared with the control group. These results suggest that TGF-beta 1 causes neutrophil-mediated lung injury, possibly through upregulation of ICAM-1 on endothelial cells, and might be important in the pathogenesis of lung injury.

scholarly journals Alveolar Neutrophilic Recruitment in COVID-19 May Not be Mediated by Th17 Response

2020 ◽  
Author(s):  
Marina L V Azevedo ◽  
Caroline Busatta Vaz de Paula ◽  
Seigo Nagashima ◽  
Cleber Machado de Souza ◽  
Anna Flavia Miggiolaro Ribeiro ◽  
...  
Keyword(s):  
Influenza A ◽  
Group Discussion ◽  
Viral Persistence ◽  
Tissue Expression ◽  
Th2 Cells ◽  
Control Group ◽  
H1n1 Subtype ◽  
Virus H1n1 ◽  
Th17 Response

Abstract Introduction: The COVID-19 current pandemic disease differs from the H1N1pdm09 caused by Influenza A virus H1N1 subtype, by how it induces a pro-inflammatory response in infected lungs. Objective: Investigate the role of Th17 response in the pathogenesis of COVID-19 injury by analyzing the tissue expression of interleukins 8 and 17A and the neutrophils in lung samples of patients who die of COVID-19, comparing to H1N1pdm09. Study design and post-mortem results: Six lung samples from patients SARS-CoV-2 infected (COVID-19 group), and ten lung samples from adults who died from H1N1pdm09 (H1N1 group), were tested. A control group was also added to the study. H&E slides were used for neutrophils scoring. The tissue expression of IL-8 and IL-17A was identified by immunohistochemistry. Tissue expression increasing of IL-17A and IL-8 and a higher number of neutrophils were identified in samples from the H1N1 group when compared to the COVID-19 group. Discussion: It is suggested that the SARS-CoV-2 virus evokes an exacerbated response of the host's immune system but differs from that observed in the H1N1pdm09 disease because it may not be trigger by Th17 response. With the low expression of IL-8, IL-17A, neutrophil recruitment to the site of infection becomes impaired, resulting in viral persistence. On the other hand, in the COVID-19 disease, the immune response by Th2 cells seems to be exacerbated, observed by the extent of the lung injury. This uncontrolled response and, mainly, the lack of a therapeutic target, culminates in disease progression and, consequently, in shorter survival time.

scholarly journals Nebulized Heparin Attenuates Pulmonary Coagulopathy and Inflammation through Alveolar Macrophages in a Rat Model of Acute Lung Injury

2017 ◽  
Vol 117 (11) ◽  
pp. 2125-2134 ◽  
Author(s):  
Laura Chimenti ◽  
Marta Camprubí-Rimblas ◽  
Raquel Guillamat-Prats ◽  
Maria Gomez ◽  
Jessica Tijero ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Inflammatory Response ◽  
Lung Tissue ◽  
Alveolar Macrophages ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Coagulation Cascade ◽  
Control Group ◽  
Proinflammatory Mediators

Objective Alveolar macrophages play a key role in the development and resolution of acute respiratory distress syndrome (ARDS), modulating the inflammatory response and the coagulation cascade in lungs. Anti-coagulants may be helpful in the treatment of ARDS. This study investigated the effects of nebulized heparin on the role of alveolar macrophages in limiting lung coagulation and inflammatory response in an animal model of acute lung injury (ALI). Methods Rats were randomized to four experimental groups. In three groups, ALI was induced by intratracheal instillation of lipopolysaccharide (LPS) and heparin was nebulized at constant oxygen flow: the LPS/Hep group received nebulized heparin 4 and 8 hours after injury; the Hep/LPS/Hep group received nebulized heparin 30 minutes before and 4 and 8 hours after LPS-induced injury; the LPS/Sal group received nebulized saline 4 and 8 hours after injury. The control group received only saline. Animals were exsanguinated 24 hours after LPS instillation. Lung tissue, bronchoalveolar lavage fluid (BALF) and alveolar macrophages isolated from BALF were analysed. Results LPS increased protein concentration, oedema and neutrophils in BALF as well as procoagulant and proinflammatory mediators in lung tissue and alveolar macrophages. In lung tissue, nebulized heparin attenuated ALI through decreasing procoagulant (tissue factor, thrombin–anti-thrombin complexes, fibrin degradation products) and proinflammatory (interleukin 6, tumour necrosis factor alpha) pathways. In alveolar macrophages, nebulized heparin reduced expression of procoagulant genes and the effectors of transforming growth factor beta (Smad 2, Smad 3) and nuclear factor kappa B (p-selectin, CCL-2). Pre-treatment resulted in more pronounced attenuation. Conclusion Nebulized heparin reduced pulmonary coagulopathy and inflammation without producing systemic bleeding, partly by modulating alveolar macrophages.

scholarly journals Alveolar Neutrophilic Recruitment in COVID-19 May Not be Mediated by Th17 Response

2020 ◽  
Author(s):  
Marina L V Azevedo ◽  
Caroline Busatta Vaz de Paula ◽  
Seigo Nagashima ◽  
Cleber Machado de Souza ◽  
Anna Flavia Miggiolaro Ribeiro ◽  
...  
Keyword(s):  
Influenza A ◽  
Group Discussion ◽  
Viral Persistence ◽  
Tissue Expression ◽  
Th2 Cells ◽  
Control Group ◽  
H1n1 Subtype ◽  
Virus H1n1 ◽  
Th17 Response

Abstract Introduction: The COVID-19 current pandemic disease differs from the H1N1pdm09 caused by Influenza A virus H1N1 subtype, by how it induces a pro-inflammatory response in infected lungs. Objective: Investigate the role of Th17 response in the pathogenesis of COVID-19 injury by analyzing the tissue expression of interleukins 8 and 17A and the neutrophils in lung samples of patients who die of COVID-19, comparing to H1N1pdm09. Study design and post-mortem results: Six lung samples from patients SARS-CoV-2 infected (COVID-19 group), and ten lung samples from adults who died from H1N1pdm09 (H1N1 group), were tested. A control group was also added to the study. H&E slides were used for neutrophils scoring. The tissue expression of IL-8 and IL-17A was identified by immunohistochemistry. Tissue expression increasing of IL-17A and IL-8 and a higher number of neutrophils were identified in samples from the H1N1 group when compared to the COVID-19 group. Discussion: It is suggested that the SARS-CoV-2 virus evokes an exacerbated response of the host's immune system but differs from that observed in the H1N1pdm09 disease because it may not be trigger by Th17 response. With the low expression of IL-8, IL-17A, neutrophil recruitment to the site of infection becomes impaired, resulting in viral persistence. On the other hand, in the COVID-19 disease, the immune response by Th2 cells seems to be exacerbated, observed by the extent of the lung injury. This uncontrolled response and, mainly, the lack of a therapeutic target, culminates in disease progression and, consequently, in shorter survival time.

scholarly journals Transforming growth factor beta 1 expression and inflammatory cells in tooth extraction socket after X-ray irradiation

2017 ◽  
Vol 49 (2) ◽  
pp. 87
Author(s):  
Ramadhan Hardani Putra ◽  
Eha Renwi Astuti ◽  
Rini Devijanti Ridwan
Keyword(s):  
Growth Factor ◽  
Treatment Group ◽  
Transforming Growth Factor Beta ◽  
Tooth Extraction ◽  
Transforming Growth Factor ◽  
Inflammatory Cells ◽  
Radiographic Examination ◽  
Control Group ◽  
X Ray ◽  
Growth Factor Beta

Background: Radiographic examination is often used in dentistry to evaluate tooth extraction complications. X-ray used in radiographic examination, however, has negative effects, including damage to DNA and inflammatory response during wound healing process. Purpose: This study aimed to analyze the effects of X-ray irradiation on transforming growth factor beta 1 (TGF-ß1) expression and number of inflammatory cells in tooth extraction sockets. Method: Thirty rats were divided into three groups, which consist of control group (with a radiation of 0 mSv), treatment group 1 (with a radiation of 0.08 mSv), and treatment group 2 (with a radiation of 0.16 mSv). These rats in each group were sacrificed on days 3 and 5 after treatment. Inflammatory cells which were observed in this research were PMN, macrophages, and lymphocytes. Histopathological and immunohistochemical examinations were used to calculate the number of inflammatory cells and TGF-ß1 expression. Obtained data were analyzed using SPSS 16.0 software with one way ANOVA and Tukey’s HSD tests. Result: There was no significant decrease in the number of PMN. On the other hand, there were significant decreases in the number of macrophages and lymphocytes in the sacrificed group on day-5 with the radiation of 0.16 mSv. Similarly, the most significant decreased expression of TGF-ß1 was found in the group sacrificed on day 5 with the radiation of 0.16 mSv. Conclusion: X-ray irradiation with 0.08 mSv and 0.16 mSv doses can decrease TGF-ß1 expression and number of inflammatory cells in tooth extraction sockets on day 3 and 5 post extraction.

microRNA-265 Regulates Bone Marrow Mesenchymal Stem Cells Differentiation and Promotes Sepsis Lung Injury Repair via Transforming Growth Factor Beta 1

2022 ◽  
Vol 12 (2) ◽  
pp. 405-410
Author(s):  
Lian Tan ◽  
Xiongxiong Wang ◽  
Danqi Chen ◽  
Li Xu ◽  
Yudong Xu ◽  
...  
Keyword(s):  
Stem Cells ◽  
Bone Marrow ◽  
Mesenchymal Stem Cells ◽  
Lung Injury ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Alveolar Type ◽  
Injury Repair ◽  
Qrt Pcr ◽  
Marrow Mesenchymal Stem Cells

Our study investigates whether miR-265 regulates the differentiation of rat bone marrow mesenchymal stem cells (BMSCs) into alveolar type II epithelial cells (ATII) through TGF-β1 and promotes lung injury repair in rats with sepsis, thereby inhibiting sepsis progression. 25 patients with sepsis admitted to the Respiratory and Critical Care Medicine Department of the hospital and 17 normal controls were included. TGF-β1 level was measured by ELISA. miR-265 level was measured by qRT-PCR and AT II-related genes and proteins expression was analyzed by western blot and qRT-PCR. miR-265 expression was significantly higher in sepsis patients than normal group. Progenitor BMSCs were long and shuttle-shaped after 1 and 3 days of growth. Cultured MSCs had low expression of the negative antigen CD34 (4.32%) and high expression of the positive antigen CD44 (99.87%). TGF-β1 level was significantly increased with longer induction time, while miR-265 expression was significantly decreased in cell culture medium. miR-265 interference significantly decreased TGF-β1 expression. In conclusion, miR-265 inhibits BMSC differentiation to AT II via regulation of TGF-β1, thereby inhibiting sepsis progression.

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