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Intranasal immunization is one of the most effective methods for eliciting lung mucosal immunity. Multiple intranasal immunization with bacterial polypeptide, termed as a modified PnxIIIA (MP3) protein, is known to elicit production of a specific antibody in mice. In this study, a nasal immuno-inducible sequence (NAIS) was designed to remove the antigenicity of the MP3 protein that can induce mucosal immunity by intranasal immunization, and was examined to induce antigen-specific antibodies against the fused bacterial thioredoxin (Trx) as a model antigen. A NAIS was modified and generated to remove a large number of predicted MHC (Major Histocompatibility Complex)-I and MHC-II binding sites in parent protein PnxIIIA and MP3 in order to reduce the number of antigen epitope sites. For comparative analysis, full-length NAIS291, NAIS230, and NAIS61 fused with Trx and 6× His tag and Trx-fused 6× His tag were used as antigen variants for the intranasal immunization of BALB/c mice every two weeks for three immunizations. Anti-Trx antibody titers in serum and bronchoalveolar lavage fluid (BALF) IgA obtained from NAIS291-fused Trx-immunized mice were significantly higher than those from Trx-immunized mice. The antibody titers against NAIS alone were significantly lower than those against Trx alone in the serum IgG, serum IgA, and BALF IgA. These results indicate that the NAIS contributes to antibody elicitation of the fused antigen as an immunostimulant in intranasal vaccination vaccines. The results indicate that the NAIS and target inactivated antigen fusions can be applied to intranasal vaccine systems. [ABSTRACT FROM AUTHOR]

Background: Tocotrienols exhibit antioxidant and anti-inflammatory activities. RhoA, a small GTPase protein, plays a crucial role in regulating contractility in airway smooth muscle (ASM). Previous studies have demonstrated that γ-tocotrienols reduce ASM proliferation and migration by inhibiting the activation of RhoA. In this present study, we investigate the effect of another vitamin E isoform, β-tocotrienols, on human ASM cell proliferation and migration stimulated by platelet-derived growth factor-BB (PDGF-BB). Methods: Human ASM cells were pre-treated with β-tocotrienol prior to being stimulated with PDGF-BB to induce ASM cell proliferation and migration. The proliferation and migration of PDGF-BB-induced human ASM cells were assessed using colorimetric and transwell migration assays. The intracellular ROS assay kit was employed to quantify reactive oxygen species (ROS) in human ASM cells. Additionally, we explored the effect of β-tocotrienols on the signaling pathways involved in PDGF-BB-induced ASM proliferation and migration. Results: β-tocotrienol inhibited PDGF-BB-induced ASM cell proliferation and migration by reducing RhoA activation and ROS production. However, in this present study, β-tocotrienol did not affect the signaling pathways associated with cyclin D1, phosphorylated Akt1, and ERK1/2. Conclusions: In conclusion, the inhibition of RhoA activation and ROS production by β-tocotrienol, resulting in the reduction in human ASM proliferation and migration, suggests its potential as a treatment for asthma airway remodeling. [ABSTRACT FROM AUTHOR]

It is a problem that influenza virus infection increases susceptibility to secondary bacterial infection in lungs leading to lethal pneumonia. We previously reported that exopolysaccharides (EPS) derived from Lactobacillus delbrueckii ssp. bulgaricus OLL1073R-1 (OLL1073R-1) could prevent against influenza virus infection followed by secondary bacterial infection in vitro. Therefore, the present study assessed whether EPS derived OLL1073R-1 protects the alveolar epithelial barrier disfunction caused by influenza virus infection. After A549 cells treated with EPS or without EPS were infected influenza virus A/Puerto Rico/8/34 (IFV) for 12 h, the levels of tight junction genes expression and inflammatory genes expression were measured by reverse transcription polymerase chain reaction. As results, EPS treatment could protect against low-titer IFV infection, but not high-titer IFV infection, followed by suppression of the increased expression of inflammatory cytokine gene levels and recovery of the decrease in the expression level of ZO-1 gene that was caused by low-titer IFV infection, leading to an improvement trend in the barrier function. Our findings showed that EPS derived from OLL1073R-1 could inhibit low-titer IFV infection leading to maintenance of the epithelial barrier function through the suppression of inflammatory cytokine genes expression. [ABSTRACT FROM AUTHOR]