scholarly journals Plasma S-Adenosylmethionine is Associated with Lung Injury in COVID-19

2021 ◽  
Author(s):  
Evgeny Kryukov ◽  
Alexander Ivanov ◽  
Vladimir Karpov ◽  
Valery Alexandrin ◽  
Alexander Dygai ◽  
...  
Keyword(s):  
Computed Tomography ◽  
Lung Injury ◽  
Interleukin 6 ◽  
Lung Damage ◽  
Methylation Index ◽  
Relative Ratio ◽  
Potential Marker ◽  
Damage Risk ◽  
Cytokine Imbalance

AbstractObjectiveS-Adenosylmethionine (SAM) and S-adenosylhomocysteine (SAH) are indicators of global transmethylation and may play an important role as markers of severity of COVID-19.MethodsThe levels of plasma SAM and SAH were determined in patients admitted with COVID-19 (n = 56, mean age = 61). Lung injury was identified by computed tomography (CT) in accordance with the CT0-4 classification.ResultsSAM was found to be a potential marker of lung damage risk in COVID-19 patients (SAM > 80 nM; CT3,4 vs. CT 0-2: relative ratio (RR) was 3.0; p = 0.0029). SAM/SAH > 6.0 was also found to be a marker of lung injury (CT2-4 vs. CT0,1: RR = 3.47, p = 0.0004). Interleukin-6 (IL-6) levels were associated with SAM (ρ = 0.44, p = 0.01) and SAH (ρ = 0.534, p = 0.001) levels.ConclusionsHigh SAM levels and high methylation index are associated with the risk of lung injury in COVID-19 patients. The association of SAM and SAH with IL-6 indicates an important role of transmethylation in the development of cytokine imbalance in COVID-19 cases.

scholarly journals Plasma S-Adenosylmethionine Is Associated with Lung Injury in COVID-19

2021 ◽  
Vol 2021 ◽  
pp. 1-10
Author(s):  
Evgeny Vladimirovich Kryukov ◽  
Alexander Vladimirovich Ivanov ◽  
Vladimir Olegovich Karpov ◽  
Valery Vasil’evich Aleksandrin ◽  
Alexander Mikhaylovich Dygai ◽  
...  
Keyword(s):  
Lung Injury ◽  
Negative Association ◽  
Lung Damage ◽  
Glutathione Level ◽  
Methylation Index ◽  
Potential Marker ◽  
Damage Risk ◽  
And Oxidative Stress ◽  
Cytokine Imbalance

Objective. S-Adenosylmethionine (SAM) and S-adenosylhomocysteine (SAH) are indicators of global transmethylation and may play an important role as markers of severity of COVID-19. Methods. The levels of plasma SAM and SAH were determined in patients admitted with COVID-19 ( n = 56 , mean   age = 61 ). Lung injury was identified by computed tomography (CT) in accordance with the CT0-4 classification. Results. SAM was found to be a potential marker of lung damage risk in COVID-19 patients ( SAM > 80   nM ; CT3,4 vs. CT 0-2: relative ratio (RR) was 3.0; p = 0.0029 ). SAM / SAH > 6.0 was also found to be a marker of lung injury (CT2-4 vs. CT0,1: RR = 3.47 , p = 0.0004 ). There was a negative association between SAM and glutathione level ( ρ = − 0.343 , p = 0.011 ). Interleukin-6 (IL-6) levels were associated with SAM ( ρ = 0.44 , p = 0.01 ) and SAH ( ρ = 0.534 , p = 0.001 ) levels. Conclusions. A high SAM level and high methylation index are associated with the risk of lung injury in patients with COVID-19. The association of SAM with IL-6 and glutathione indicates an important role of transmethylation in the development of cytokine imbalance and oxidative stress in patients with COVID-19.

scholarly journals The Role of Multidetector Computed Tomography and the Forced Oscillation Technique in Assessing Lung Damage in Adults With Cystic Fibrosis

2017 ◽  
Vol 63 (4) ◽  
pp. 430-440 ◽  
Author(s):  
Letícia S Lacerda ◽  
Agnaldo J Lopes ◽  
Alysson R S Carvalho ◽  
Alan R M Guimarães ◽  
Mônica C Firmida ◽  
...  
Keyword(s):  
Computed Tomography ◽  
Cystic Fibrosis ◽  
Multidetector Computed Tomography ◽  
Forced Oscillation ◽  
Lung Damage ◽  
Forced Oscillation Technique

scholarly journals NADPH Oxidase 4 Signaling in a Ventilator-induced Lung Injury Mouse Model

2021 ◽  
Author(s):  
Sang Hoon Lee ◽  
Mi Hwa Shin ◽  
Ah Young Leem ◽  
Su Hwan Lee ◽  
Kyung Soo Chung ◽  
...  
Keyword(s):  
Lung Injury ◽  
Lavage Fluid ◽  
Lung Damage ◽  
Control Group ◽  
Group 4 ◽  
Ventilator Induced Lung Injury ◽  
Cell Counts ◽  
Group 5 ◽  
Group 2

Abstract For patients with acute respiratory distress syndrome, a ventilator is essential to supply oxygen to tissues, but it may also cause lung damage. We investigated the role of NOX4 in a ventilator-induced lung injury (VILI) model.Wild-type (WT) male C57BL/6J mice and NOX4 knockout (KO) male mice were divided into five groups: (1) control group; (2) high tidal ventilation (HTV) group: WT mice + HTV; (3) NOX4 KO group; (4) NOX4 KO with HTV group; (5) NOX4 inhibitor group: WT mice + HTV + NOX4 inhibitor. In addition, the relationship between EphA2 (which is related to lung injury) and NOX4 was investigated using EphA2 KO mice, and NOX4 levels in the bronchoalveolar lavage fluid (BALF) of 38 patients with pneumonia were examined.In the NOX4 inhibitor group, cell counts and protein concentrations from BALF were significantly lower than those in the HTV group (both, p<0.001). In the NOX4 KO group and the NOX4 inhibitor group, EphA2 levels were significantly lower than those in the HTV group (p<0.001). NOX4 levels were significantly higher in patients with pneumonia and patients who received ventilator treatment in the ICU.In the VILI model, it may be possible to block VILI using NOX4 antibodies.

The Role of Recipient Platelets In the Prevention of Antibody-Mediated Transfusion Related Acute Lung Injury (TRALI)

Blood ◽  
2010 ◽  
Vol 116 (21) ◽  
pp. 3351-3351
Author(s):  
Yuhan Chen ◽  
Michael Kim ◽  
Arata Tabuchi ◽  
Wolfgang M. Kuebler ◽  
Rukhsana Aslam ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Conflicts Of Interest ◽  
Scid Mice ◽  
Lung Damage ◽  
Cell Mediated Immunity ◽  
Shock Lung ◽  
Inflammatory Milieu ◽  
Platelet Depletion

Abstract Abstract 3351 Transfusion related acute lung injury (TRALI) is a serious complication of transfusion. The pathogenesis of TRALI is not fully understood but previous findings have suggested that platelet depletion can protect mice in a two-hit model of TRALI (Looney et al J Clin Invest 119:3450, 2009). To further understand the role of platelets in preventing antibody-mediated TRALI, two mouse models of immune thrombocytopenia (ITP) were utilized. In the passive ITP model, SCID mice were injected with a monoclonal anti-platelet antibody (MWReg30) intraperitoneally (ip, 18 h before TRALI induction) or intravenously (iv, 2 h before TRALI induction). In the active ITP model, SCID mice were transferred with splenocytes from anti-CD61 immune GPIIIa-knockout mice and thrombocytopenia occurred within 2 weeks post transfer (Chow et al Blood 115;1247, 2010). TRALI induction was performed by injecting the various thrombocytopenic SCID mice with a murine monoclonal MHC class I antibody (mAb, 34-1 -2s) iv and several parameters were observed for up to 2 h post antibody injection. In control, non-thrombocytopenic SCID mice, 34-1 -2s injection caused severe systemic shock as noted by reduced rectal temperatures which was associated with significant lung damage and mortality (45%) within 1 hour of 34-1 -2s infusion as previously shown (Fung et al. Blood DOI 10.1182/blood-2010-05-284570). In contrast, while SCID mice depleted of platelets by the passive ip route had systemic shock, lung damage and a 60% mortality rate, those mice made thrombocytopenic by the iv route were completely protected from mortality. On the other hand, in the active ITP model, where the induced thrombocytopenia is associated with a proinflammatory anti-platelet immune response, no mortality was observed in those mice made thrombocytopenic by antibody-mediated immune mechanisms whereas 80% of mice rendered thrombocytopenic by CD8+ T cell-mediated immunity were dead within 1 hr post 34-1 -2s infusion. These results suggest that thrombocytopenia in itself does not protect against antibody-mediated TRALI severity but the nature of the thrombocytopenia induction (e.g. acute passive iv infusion or active ITP immune transfer) is important. In fact, depending on the inflammatory milieu associated with the thrombocytopenia, platelets may actually increase the severity of TRALI. Disclosures: No relevant conflicts of interest to declare.

scholarly journals The Role of Computed Tomography in Pneumonia in Patients with Associated Coronavirus Infection

2021 ◽  
Vol 13 ◽  
Author(s):  
Jonibekov Jasur Jonibekovich
Keyword(s):  
Computed Tomography ◽  
Research Methods ◽  
Lung Damage ◽  
Laboratory Research ◽  
Imaging Data ◽  
Viral Etiology ◽  
Radiation Imaging ◽  
Coronavirus Infection ◽  
Radiation Research

The appearance of COVID-19 has set tasks for healthcare professionals related to rapid diagnosis and provision of medical care to patients. The diagnosis of COVID-19 infection is based on the complex application of clinical, radiological and laboratory research methods[1].Radiation research methods used to diagnose patients with suspected COVID-19 and viral pneumonia of another nature include: radiography, computed tomography and ultrasound examination of the lungs. Radiation imaging data allow us to suspect lung damage of viral etiology (including COVID-19), influence the management of a particular patient, the treatment of complications or the formulation of an alternative diagnosis with a high probability of lung damage of viral etiology.

scholarly journals NADPH Oxidase 4 Signaling in a Ventilator-Induced Lung Injury Mouse Model

2020 ◽  
Author(s):  
Sang Hoon Lee ◽  
Mi Hwa Shin ◽  
Ah Young Leem ◽  
Su Hwan Lee ◽  
Kyung Soo Chung ◽  
...  
Keyword(s):  
Lung Injury ◽  
Lavage Fluid ◽  
Lung Damage ◽  
Control Group ◽  
Nadph Oxidase 4 ◽  
Ventilator Induced Lung Injury ◽  
Oxygen Fraction ◽  
Cell Counts ◽  
The Relationship

Abstract BackgroundFor patients with acute respiratory distress syndrome (ARDS), a ventilator is essential to supply oxygen to tissues, but it may also cause lung damage. In this study, we investigated the role of NOX4 in lung injury using NOX4 knockout (KO) mice and NOX4 inhibitors in a ventilator-induced lung injury (VILI) model.MethodsWild-type male C57BL/6J mice and NOX4 KO male mice were divided into five groups: (1) control group: wild-type (WT) mice + non-ventilator; (2) high tidal ventilation (HTV) group: WT mice + HTV; (3) NOX4 KO group: NOX4 KO + non-ventilator; (4) NOX4 KO with HTV group: NOX4 KO mice + HTV; (5) NOX4 inhibitor group: WT mice + HTV + post-treatment (anti-GKT 137831 inhibitor). In the VILI model, the supine position was maintained at 24 mL/kg volume, 0 cm H2O PEEP, 100/min respiratory rate, and 0.21 inspired oxygen fraction. In the NOX4 inhibitor group, 50 μL anti-GKT 137831 inhibitor was injected intraperitoneally, 2 h after ventilator use. After 5 h of HTV, mice in the ventilator group were euthanized, and their lung tissues were obtained for further analysis. In addition, the relationship between EphA2 (which is related to lung injury) and NOX4 was investigated using EphA2 KO mice, and NOX4 levels in the bronchoalveolar lavage fluid (BALF) of 38 patients with pneumonia were examined.ResultsCell counts from BALFs were significantly lower (p<0.01) in the NOX4 KO with HTV group compared to that in the HTV group. In the NOX4 inhibitor group, cell counts and protein concentrations were significantly lower than those in the HTV group (both, p<0.001). In the NOX4 KO mouse group and the NOX4 inhibitor group, EphA2 levels were significantly lower than those in the HTV group (both, p<0.001). In patients with respiratory disease, NOX4 levels were significantly higher in patients with pneumonia and patients who received ventilator treatment in the intensive care unit.ConclusionsIn the VILI model, NOX4 expression is significantly associated with Eph-ephrin signaling. It may be possible to block VILI using NOX4 antibodies.

scholarly journals Interleukin-6 production in hemorrhagic shock is accompanied by neutrophil recruitment and lung injury

1998 ◽  
Vol 275 (3) ◽  
pp. L611-L621 ◽  
Author(s):  
Christian Hierholzer ◽  
Jörg C. Kalff ◽  
Laurel Omert ◽  
Katsuhiko Tsukada ◽  
J. Eric Loeffert ◽  
...  
Keyword(s):  
Lung Injury ◽  
Hemorrhagic Shock ◽  
Interleukin 6 ◽  
Intratracheal Instillation ◽  
Lung Damage ◽  
Mrna Levels ◽  
Alveolar Cells ◽  
Mobility Shift ◽  
Mobility Shift Assay ◽  
Dna Binding Assay

Hemorrhagic shock (HS) initiates an inflammatory cascade that includes the production of cytokines and recruitment of neutrophils (PMN) and may progress to organ failure, inducing acute respiratory distress syndrome (ARDS). To examine the hypothesis that interleukin-6 (IL-6) contributes to PMN infiltration and lung damage in HS, we examined the lungs of rats subjected to unresuscitated and resuscitated HS for the production of IL-6 and activation of Stat3. Using semiquantitative RT-PCR, we found a striking increase in IL-6 mRNA levels only in resuscitated HS, with peak levels observed 1 h after initiation of resuscitation. Increased IL-6 protein expression was localized to bronchial and alveolar cells. Electrophoretic mobility shift assay of protein extracts from shock lungs exhibited an increase in Stat3 activation with kinetics similar to IL-6 mRNA. In situ DNA binding assay determined Stat3 activation predominantly within alveoli. Intratracheal instillation of IL-6 alone into normal rats resulted in PMN infiltration into lung interstitium and alveoli, marked elevation of bronchoalveolar lavage cellularity, and increased wet-to-dry ratio. These findings indicate that IL-6 production and Stat3 activation occur early in HS and may contribute to PMN-mediated lung injury, including ARDS after HS.

Role Of Interleukin 6 During Acute Lung Injury: Study In A Lipopolysaccharide-induced Murine Model Under Mechanical Ventilation

2010 ◽  
Author(s):  
Guillaume Voiriot ◽  
Aurélie Hervé ◽  
Keyvan Razazi ◽  
Rachid Souktani ◽  
Guillaume Gary-Bobo ◽  
...  
Keyword(s):  
Mechanical Ventilation ◽  
Acute Lung Injury ◽  
Lung Injury ◽  
Murine Model ◽  
Interleukin 6

scholarly journals Role of vascular disorders in lung injury in patients with rheumatoid arthritis

2016 ◽  
Vol 15 (3) ◽  
pp. 15-23 ◽  
Author(s):  
I. I. Nesterovich ◽  
K. V. Nochevnaya ◽  
Y. D. Rabik ◽  
A. A. Speranskaya ◽  
V. P. Zolotnitskaya ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Computed Tomography ◽  
Lung Injury ◽  
Pulmonary Function Tests ◽  
Photon Emission ◽  
Diagnostic Methods ◽  
Control Group ◽  
Emission Computed Tomography ◽  
Vascular Disorders

Introduction. The incidence of respiratory system involvement in patients with rheumatoid arthritis (RA) has currently increased; thereby new diagnostic methods have been developed actively. Meanwhile role of vascular disorders in pathogenesis of lung injury is almost unknown and single-photon emission computed tomography (SPECT) isn't used as method of lung assessment in RA. The detector of endothelial glycocalyx damage syndecan-1 is little known but potentially perspective serum marker of lung injury in RA. Objective. The purpose of the study was to investigate the role of vascular disorders in lung injury in patients with RA. Materials and methods. 61 patients with RA without comorbid lung diseases were enrolled in the study. Control group consisted of 26 healthy persons. Patients underwent survey and physical examination, high-resolution computed tomography (HRCT) and SPECT of the lungs and pulmonary function tests (PFTs). Also serum levels of rheumatoid factor (RF), anti-cyclic citrullinated peptide antibodies (ACCP) and syndecan-1 were measured. Results. All patients developed microcirculation impairment on SPECT. Vascular disorders were according to changes of lung structure detected by HRCT (r = 0.434; p = 0.044). Areas of hypoperfusion matched with ground glass opacities, lung fibrosis, branching linear structures and airway obstruction on HRCT-SPECT fusion scans. Syndecan-1 level was higher in patients with RA compared with healthy controls (р = 0.019). Conclusion. Vascular disorders are important in pathogenesis of lung injury in RA, and SPECT has high sensitivity in lung assessment. Perfusion impairment in lungs correlates with syndecan-1 level, thus syndecan-1 could be used as marker of lung injury in RA thereafter.

scholarly journals Impaired Glucocorticoid Receptor Signaling Aggravates Lung Injury after Hemorrhagic Shock

Cells ◽  
2021 ◽  
Vol 11 (1) ◽  
pp. 112
Author(s):  
Jonathan M. Preuss ◽  
Ute Burret ◽  
Michael Gröger ◽  
Sandra Kress ◽  
Angelika Scheuerle ◽  
...  
Keyword(s):  
Intensive Care Unit ◽  
Lung Injury ◽  
Hemorrhagic Shock ◽  
Lung Tissue ◽  
Lung Inflammation ◽  
Lung Damage ◽  
Lung Mechanics ◽  
Cytokine Signaling ◽  
Pro Inflammatory Cytokines

We previously showed that attenuated lung injury after hemorrhagic shock (HS) coincided with enhanced levels of the glucocorticoid (GC) receptor (GR) in lung tissue of swine. Here, we investigated the effects of impaired GR signaling on the lung during resuscitated HS using a dysfunctional GR mouse model (GRdim/dim). In a mouse intensive care unit, HS led to impaired lung mechanics and aggravated lung inflammation in GRdim/dim mice compared to wildtype mice (GR+/+). After HS, high levels of the pro-inflammatory and pro-apoptotic transcription factor STAT1/pSTAT1 were found in lung samples from GRdim/dim mice. Lungs of GRdim/dim mice revealed apoptosis, most likely as consequence of reduced expression of the lung-protective Angpt1 compared to GR+/+ after HS. RNA-sequencing revealed increased expression of pro-apoptotic and cytokine-signaling associated genes in lung tissue of GRdim/dim mice. Furthermore, high levels of pro-inflammatory cytokines and iNOS were found in lungs of GRdim/dim mice. Our results indicate impaired repression of STAT1/pSTAT1 due to dysfunctional GR signaling in GRdim/dim mice, which leads to increased inflammation and apoptosis in the lungs. These data highlight the crucial role of functional GR signaling to attenuate HS-induced lung damage.

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