Article Sidebar
Article Details
Submission of a manuscript to this journal is a representation that the manuscript has not been published previously and is not under consideration for publication elsewhere.
All authors named in each manuscript would be required to sign a form (to be supplied by the Editor) so that they may retain their copyright in the article but to assign to us (the Publishers) and its licensees in perpetuity, in all forms, formats and media (whether known or created in the future) to (i) publish, reproduce, distribute, display and store the contribution, (ii) translate the contribution into other languages, create adaptations, reprints, include within collections and create summaries, extracts and/or abstracts of the contribution, (iii) create any other derivative works(s) based on the contribution, (iv) to exploit all subsidiary rights in the contribution, (v) the inclusion of electronic links from the contribution to third party material where-ever it may be located, and (vi) license any thrid party to do any or all of the above.
Main Article Content
Bryostatin 1 alleviates respiratory syncytial virus pneumonia in a mice model via down-regulation of inflammatory cytokines
Abstract
Purpose: To investigate the effect of bryostatin 1 on respiratory syncytial virus (RSV) infection in vitro in lung alveolar cells and in vivo in a mice model.
Methods: RSV infection in the mice was induced by the administration of 2 x 106 PFU viral particles intranasally in the left nostril. Reverse transcription-polymerase chain reaction (RT-PCR) and western blotting were used for the determination of changes in interleukin expression.
Results: Bryostatin 1 treatment of RSV-infected BEAS-2B cells significantly (p < 0.05) inhibited viability. The mortality of mice infected with RSV markedly decreased on treatment with bryostatin 1. The pulmonary damage induced by RSV infection was also prevented in mice treated with bryostatin 1. Treatment of the RSV infected mice with bryostatin 1 caused a dose-based suppression of IL 1β/ 18 and TNF α generation (p < 0.05). Bryostatin 1 pre-treatment at doses 2, 6 and 12 mg/kg led to reduction of NLRP3, ASC and caspase 1 proteins, as well as a significant decrease in the expression of mRNA corresponding to NLRP3, ASC and caspase 1 (p< 0.05).
Conclusion: The results demonstrate that bryostatin 1 treatment of RSV-infected BEAS-2B cells prevents reduction in its viability. Moreover, pre-treatment of RSV-infected mice with bryostatin 1 improves mortality and prevents pulmonary tissue damage by down-regulating NLRP3 activation. Therefore, bryostatin 1 may be an option for the development of an effective treatment for pneumonia
