Sepsis-induced acute respiratory distress syndrome with fatal outcome is associated to increased serum transforming growth factor beta-1 levels

2012 ◽  
Vol 23 (4) ◽  
pp. 358-362 ◽  
Author(s):  
Raúl de Pablo ◽  
Jorge Monserrat ◽  
Eduardo Reyes ◽  
David Díaz ◽  
Manuel Rodríguez-Zapata ◽  
...  
2015 ◽  
Vol 36 (4) ◽  
pp. 1644-1658 ◽  
Author(s):  
Gisele P. Oliveira ◽  
Johnatas D. Silva ◽  
Patricia S. Marques ◽  
Cassiano F. Gonçalves-de-Albuquerque ◽  
Heloísa L. Santos ◽  
...  

Background/Aims: Evidence suggests that tyrosine-kinase inhibitors may attenuate lung inflammation and fibrosis in experimental acute respiratory distress syndrome (ARDS). We hypothesized that dasatinib, a tyrosine-kinase inhibitor, might act differently depending on the ARDS etiology and the dose. Methods: C57/BL6 mice were divided to be pre-treated with dasatinib (1mg/kg or 10mg/kg) or vehicle (1% dimethyl-sulfoxide) by oral gavage. Thirty-minutes after pre-treatment, mice were subdivided into control (C) or ARDS groups. ARDS animals received Escherichia coli lipopolysaccharide intratracheally (ARDSp) or intraperitoneally (ARDSexp). A new dose of dasatinib or vehicle was administered at 6 and 24h. Results: Forty-eight hours after ARDS induction, dasatinib 1mg/kg yielded: improved lung morphofunction and reduced cells expressing toll-like receptor (TLR)-4 in lung, independent of ARDS etiology; reduced neutrophil and levels of interleukin (IL)-6, IL-10 and transforming growth factor (TGF)-β in ARDSp. The higher dose of dasatinib caused no changes in lung mechanics, diffuse alveolar damage, neutrophil, or cells expressing TLR4, but increased IL-6, vascular endothelial growth factor (VEGF), and cells expressing Fas receptor in lung in ARDSp. In ARDSexp, it improved lung morphofunction, increased VEGF, and reduced cells expressing TLR4. Conclusion: Dasatinib may have therapeutic potential in ARDS independent of etiology, but careful dose monitoring is required.


PLoS ONE ◽  
2018 ◽  
Vol 13 (11) ◽  
pp. e0206105 ◽  
Author(s):  
Jean-Marie Forel ◽  
Christophe Guervilly ◽  
Catherine Farnarier ◽  
Stéphane-Yannis Donati ◽  
Sami Hraiech ◽  
...  

2021 ◽  
Vol 8 (3) ◽  
pp. 474
Author(s):  
Sanjukta Mishra ◽  
Amaresh Mishra ◽  
Swarnalata Das

The current onset and expeditious increase of COVID-19, caused by severe acute respiratory distress syndrome coronavirus (SARS-CoV-2), has established a global health predicament. Declared as pandemic and public health emergency by the World Health Organization (WHO), it follows an extremely heterogeneous course from mild flu like symptoms to severe acute respiratory distress syndrome. This outbreak intimidates the public with human to human escalation, which is the primary concern worldwide with a still unforeseeable result. With limited data on plausible therapy and vaccination, it is significant to unravel the virulence mechanism of SARS-CoV-2 to delineate chemoprevention that might curb the fatal outcome. It may be acknowledged here that the primary stage of disease prevention depends on the protective immune response to eliminate the virus. This postulation kindles interest in the intervention of vitamin D micronutrient, which might unfold the feasibility of slowing disease advancement and decreasing the risk of mortality. Taking into account, the wide spectrum of beneficial effects ascribed to vitamin D like antiviral, immunomodulatory, anti-inflammatory, and antioxidant action, it can be administered to affect immune cell proliferation and angiotensin-converting enzyme (ACE) 2 expression, which is the basis of pathogenesis of transmission of SARS-CoV-2. Recently, several observational clinical and epidemiological studies underline the hypothesis regarding mean vitamin D level and COVID-19 mortality. More so some retrospective analysis reported the correlation between vitamin D level and disease severity. Nevertheless, potential clinical researches and randomised control trials are recommended in COVID-19 patients with different levels of disease extremity to appraise the useful outcomes. 


Sign in / Sign up

Export Citation Format

Share Document