Antioxidant Treatment Ameliorates Respiratory Syncytial Virus–induced Disease and Lung Inflammation

Protective T cell immunity against respiratory syncytial virus is efficiently induced by recombinant BCG

“…2A, significant weight loss was observed for unimmunized animals or mice immunized either with UV-RSV or WT-BCG, as well as BCG-OVA (data not shown). These data are consistent with previous studies indicating that naive mice challenged with RSV can show significant weight loss as early as 24 h after infection (35)(36)(37). In sharp contrast, mice immunized with either BCG-N or BCG-M2 showed no significant weight loss after RSV challenge, similarly to uninfected mice (Fig.…”

Dual Role of NOX2 in Respiratory Syncytial Virus- and Sendai Virus-Induced Activation of NF-κB in Airway Epithelial Cells

“…Indeed, treatment of mice with BHA significantly reduced RSV-induced cytokines and chemokines production and recruitment of inflammatory cells, especially neutrophils, to the lung (44). However, this study used a general antioxidant and did not target the specific source of ROS responsible for NF-B regulation.…”

“…Interestingly, it was recently shown that the absence of NOX2 led to reduced virus titer, increased Th1 cytokines in the airways, and a reduced inflammatory infiltrate into the lung parenchyma in influenza virus-infected mice (43). Similarly, antioxidant treatment was recently found to improve the final outcome of RSV infection in mice by significantly reducing cytokine and chemokine production and recruitment of inflammatory cells, especially neutrophils, to the lung (44), but the source of ROS in this context remains elusive. Given the observed potential of targeting ROS production to limit the RSV-induced inflammatory response (44), we examined the molecular mechanisms involved in the redox regulation of cytokine and chemokine gene expression in AEC.…”

Respiratory Viral Infections and Subversion of Cellular Antioxidant Defenses

“…In addition to MDA and HNE, 8-isoprostane are also considered markers of cellular oxidative stress, as they are formed in vivofrom the free radical-catalyzed peroxidation of essential fatty acids (primarily arachidonic acid) without the direct action of cyclooxygenase enzymes. The unbalance between ROS formation and antioxidant defenses leads to oxidative stress during the course of RSV infection, as it has been demonstrated by the increased formation of lipid peroxidation products both in vitro and in vivo models of infection [8,61], as well as in patients with primary RSV infection, in which the levels of 8-isoprostane, as well as MDA and HNE present in respiratory secretion correlate with the severity of infection [11].…”

“…BHA treatment significantly attenuated RSV-induced lung oxidative stress, as indicated by decreased markers of oxidative damage in BAL of RSVinfected mice. In addition, lungs of BHA treated mice showed reduced cytokine and chemokine secretion [61]. The beneficial effect of BHA and tBHQ in RSV-induced lung inflammation and oxidative stress could be in part ascribed to the ability of these phenolic compounds to modulate Nrf2-dependent gene expression, in addition to directly scavenging ROS formed in response to the viral infection.…”