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( Chaewon Kwak ),( Quyen Thi Nguyen ),( Jaemoo Kim ),( Tae-hwan Kim ),( Haryoung Poo ) 한국미생물생명공학회(구 한국산업미생물학회) 2021 Journal of microbiology and biotechnology Vol.31 No.2
Vaccination is the most effective way to prevent influenza virus infections. However, conventional vaccines based on hemagglutinin (HA) have to be annually updated because the HA of influenza viruses constantly mutates. In this study, we produced a 3M2e-3HA2-NP chimeric protein as a vaccine antigen candidate using an Escherichia coli expression system. The vaccination of chimeric protein (15 μg) conferred complete protection against A/Puerto Rico/8/1934 (H1N1; PR8) in mice. It strongly induced influenza virus-specific antibody responses, cytotoxic T lymphocyte activity, and antibody-dependent cellular cytotoxicity. To spare the dose and enhance the cross-reactivity of the chimeric, we used a complex of poly-γ-glutamic acid and alum (PGA/alum) as an adjuvant. PGA/alumadjuvanted, low-dose chimeric protein (1 or 5 μg) exhibited higher cross-protective effects against influenza A viruses (PR8, CA04, and H3N2) compared with those of chimeric alone or alumadjuvanted proteins in vaccinated mice. Moreover, the depletion of CD4+ T, CD8+ T, and NK cells reduced the survival rate and efficacy of the PGA/alum-adjuvanted chimeric protein. Collectively, the vaccination of PGA/alum-adjuvanted chimeric protein induced strong protection efficacy against homologous and heterologous influenza viruses in mice, which suggests that it may be a promising universal influenza vaccine candidate.
( Nguyen Hong Phuong ),( Chaewon Kwak ),( Chang-kyu Heo ),( Eun Wie Cho ),( Jihyun Yang ),( Haryoung Poo ) 한국미생물생명공학회(구 한국산업미생물학회) 2018 Journal of microbiology and biotechnology Vol.28 No.5
Influenza, which is a highly contagious disease caused by the influenza A virus, continues to be a major health concern worldwide. Although the accurate and early diagnosis of influenza virus infection is important for controlling the spread of this disease and rapidly initiating antiviral therapy, the current influenza diagnostic kits are limited by their low sensitivity. In this study, we developed several new influenza nucleoprotein (NP)-specific monoclonal antibodies (mAbs) and compared their sensitivity and specificity of those with commercially available anti-NP mAbs. Three mAbs, designated M24.11, M34.3, and M34.33, exhibited higher reactivities to recombinant NPs and A/Puerto Rico/8/1934 (H1N1) viral lysates compared with the commercial mAbs, as assessed using enzyme-linked immunosorbent assays. M34.3 and M34.33 showed higher reactivities with A/California/04/09 (pandemic H1N1) and A/ Philippines/2/82 (H3N2) viral lysates than the commercial mAbs. In contrast, M24.11 had marked reactivity with H3N2 but not with pandemic H1N1. Immunofluorescent confocal microscopy showed that the three mAbs effectively detected the presence of influenza virus in lung tissues of mice infected with A/Puerto Rico/8/1934. These results indicate that the newly developed M34.3 and M34.33 mAbs could be useful for the development of influenza diagnostics.
Ju, In Gyoung,Choi, Jin Gyu,Kim, Namkwon,Kwak, Chaewon,Lee, Jong Kil,Oh, Myung Sook Elsevier 2018 Neuroscience Letters Vol.686 No.-
<P><B>Abstract</B></P> <P>Neuroinflammation is an inflammatory process within the central nervous system that is mediated by microglial activation, which releases pro-inflammatory mediators leading to neurodegeneration. In this study, we investigated the effects of Peucedani Japonici Radix (PJR), a medicinal herb traditionally used in East Asia to treat neuroinflammation both <I>in vitro</I> and <I>in vivo</I>. First, we examined the effects of PJR on pro-inflammatory mediators in lipopolysaccharide (LPS)-stimulated BV-2 microglial cells. The results showed that PJR suppressed the LPS-induced increase of several inflammatory factors, such as nitric oxide, inducible nitric oxide synthase, cyclooxygenase-2, prostaglandin E2, interleukin-1β, and tumor necrosis factor-α. We also revealed that PJR inhibited the nuclear factor kappa B (NF-κB) pathway, which is the upstream modulator of inflammatory processes. Furthermore, to confirm the regulatory effects of PJR on microglia <I>in vivo</I>, we measured the number of ionized calcium-binding adapter molecule 1-positive cells in mouse brains and found that PJR treatment reduced microglial activation. Taken together, these results suggest that PJR inhibits microglia-mediated neuroinflammation through the modulation of NF-κB signaling and has the therapeutic potential to prevent inflammation-related neurodegenerative diseases.</P> <P><B>Highlights</B></P> <P> <UL> <LI> PJR inhibited LPS-induced increase of pro-inflammatory mediators. </LI> <LI> PJR regulated microglial responses <I>via</I> inhibiting NF-kB translocation into nuclear. </LI> <LI> PJR suppressed LPS-induced microglial activation in mouse brain. </LI> </UL> </P> <P><B>Graphical abstract</B></P> <P>[DISPLAY OMISSION]</P>