• Journal of Microbiology and Biotechnology
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• 제30권11호
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• pp.1626-1639
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• 2020

In Caenorhabditis elegans, SHN-1 is the homologue of SHANK, a scaffolding protein. In this study, we determined the molecular basis for SHN-1/SHANK in the regulation of innate immune response to fungal infection. Mutation of shn-1 increased the susceptibility to Candida albicans infection and suppressed the innate immune response. After C. albicans infection for 6, 12, or 24 h, both transcriptional expression of shn-1 and SHN-1::GFP expression were increased, implying that the activated SHN-1 may mediate a protection mechanism for C. elegans against the adverse effects from fungal infection. SHN-1 acted in both the neurons and the intestine to regulate the innate immune response to fungal infection. In the neurons, GLR-1, an AMPA ionotropic glutamate receptor, was identified as the downstream target in the regulation of innate immune response to fungal infection. GLR-1 further positively affected the function of SER-7-mediated serotonin signaling and antagonized the function of DAT-1-mediated dopamine signaling in the regulation of innate immune response to fungal infection. Our study suggests the novel function of SHN-1/SHANK in the regulation of innate immune response to fungal infection. Moreover, our results also denote the crucial role of neurotransmitter signals in mediating the function of SHN-1/SHANK in regulating innate immune response to fungal infection.

• Molecules and Cells
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• 제39권5호
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• pp.426-438
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• 2016

Plant disease resistance occurs as a hypersensitive response (HR) at the site of attempted pathogen invasion. This specific event is initiated in response to recognition of pathogen-associated molecular pattern (PAMP) and subsequent PAMP-triggered immunity (PTI) and effector-triggered immunity (ETI). Both PTI and ETI mechanisms are tightly connected with reactive oxygen species (ROS) production and disease resistance that involves distinct biphasic ROS production as one of its pivotal plant immune responses. This unique oxidative burst is strongly dependent on the resistant cultivars because a monophasic ROS burst is a hallmark of the susceptible cultivars. However, the cause of the differential ROS burst remains unknown. In the study here, we revealed the plausible underlying mechanism of the differential ROS burst through functional understanding of the Magnaporthe oryzae (M. oryzae) AVR effector, AVR-Pii. We performed yeast two-hybrid (Y2H) screening using AVR-Pii as bait and isolated rice NADP-malic enzyme2 (Os-NADP-ME2) as the rice target protein. To our surprise, deletion of the rice Os-NADP-ME2 gene in a resistant rice cultivar disrupted innate immunity against the rice blast fungus. Malic enzyme activity and inhibition studies demonstrated that AVR-Pii proteins specifically inhibit in vitro NADP-ME activity. Overall, we demonstrate that rice blast fungus, M. oryzae attenuates the host ROS burst via AVR-Pii-mediated inhibition of Os-NADP-ME2, which is indispensable in ROS metabolism for the innate immunity of rice. This characterization of the regulation of the host oxidative burst will help to elucidate how the products of AVR genes function associated with virulence of the pathogen.

• 대한한방소아과학회지
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• 제8권1호
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• pp.39-58
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• 1994

Even though appropriate immune response is necessary for the survival of the individual, excessive or insufficient immune response might cause autoimmune or allergic disease respectively. So the immune response must be controlled to the degree that is beneficial for the well being of the individual. This study was undertaken to know the effects of Junsibaekchulsan(JB) on the immune system od the mouse. For the evalulation of the cell-mediated immunity(CMI), delayed-type hypersensitivity against dinitrofluorobenzene(DNFB) were measured, and humoral immunity, hemagglutinin and hemolysin titers against SRBCs(sheep red blood cells) were measured, and rosette formation of spleen cells with SRBCs were measured. For the evaluation of innate immunity, phagocytic activity of macrophages, natural killer cell activity, and reactive nitrogen and oxygen intermediates were measured. The results are as follows: 1. The administration of JB depressed the antibody formation (hemagglutinin and hemolysin) against SRBCs. 2. The administration of JB did not affect the delayed-type hypersensitivity against DNFB. 3. The administration of JB did not affect the cytotoxic activity of natural killer cells. 4. The administration of JB increased the phagocytic activity of macrophages. 5. The administration of JB increased the rosette formating cells of the spleen cells. 6. The exposure of JB induced the secretion of reactive nitrogen intermediates but administration of JB deperssed the production of reactive oxygen intermediates. Administration of JB selectively depressed the humoral immune response without affecting CMI and innate immunity. These results of JB on the immune system might be useful for the treatment of such.

• 대한한의학회지
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• 제18권2호
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• pp.43-57
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• 1997

It was claimed that the herbal medicine with the function of strengthening the body resistance exerts to enhance the immunity. And the medicine with the effect of eliminating the pathogenic factor is stated to inhibit the immune response. To evaluate the the effects of the herbal medicine on the immune response, the mice were administrated with the herbal medicine for 2 weeks. And the responses were analyzed. As the result, water extract of Radix Astragali, Fructus Psoraleae, Cortex Acanthopanacis, Semen Coicis, Herba Ecliptae, Spica Prunellae, and Radix Sophorae increased the ROI production, while Radix Tripterygia inhibited it. Phagocytic activity was increased after administration of Radix Astragal, Fructus Psoraleae, Cortex Acanthopanacis, Herba Ecliptae, Spica Prunellae and Radix Sophorae. NK cell activity was also significantly inhibited by Radix Tripterygia. Administration of Radix Astragali, Fructus Psoraleae, Cortex Acanthopanacis, Herba Ecliptae, Spica Prunellae and Semen Coicis enhanced the antibodies(hemagglutinin and hemolysin) formation and the appearance of rosette forming cells of the spleen, while Radix Sophorae and Radix Tripterygia decreased it. Radix Sophorae and Radix Tripterygia also decreased the allogenic immune response and mixed-lymphocyte reaction. And all the experimental herbs decreased contact hypersensitivity against dinitroflurobenzene. These results show Radix Astragali, Fructus Psoraleae, Spica Prunellae, Cortex Acanthopanacis, Semen Coicis and Herba Ecliptae enhanced innate immunity, humoral and cellular immune responses. However Radix Sophorae and Radix Tripterygia exert imunosuppressive action. Also these results indicate that the medicine with the action of the strengthening the body resistance enhances the immunity. And the the some of drugs belonging to the eliminating the pathogenic factor also increase the immune responses.

• 한국해양바이오학회지
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• 제2권3호
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• pp.127-132
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• 2007

The innate immune response which is seen as the initial defense mechanism induced upon foreign invasion has been well documented in higher vertebrates. This has also been observed in fish infected with NNV. However, the fish immune system based on fully established genome project has not been fully elucidated. Therefore, in this review, we hope to correlate NNV infection in fish that has devastated the aquaculture industry, to its host immune system. Further, we discuss the potential preventive measures in overcoming the widespread of this neurodisease.

• 대한의생명과학회지
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• 제18권3호
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• pp.181-192
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• 2012

Toll-like receptors (TLRs) induce innate immune responses that are essential for host defense against invading microbial pathogens. In general, TLRs have two major downstream signaling pathways; myeloid differential factor 88 (MyD88) and Toll/IL-1R domain-containing adaptor inducing IFN-${\beta}$ (TRIF) leading to the activation of NF-${\kappa}B$ and IRF3. Numerous studies demonstrated that certain phytochemicals possessing anti-inflammatory effects inhibit NF-${\kappa}B$ activation induced by pro-inflammatory stimuli including lipopolysaccharide and tumor necrosis factor-${\alpha}$ ($TNF{\alpha}$). However, the direct molecular targets for such anti-inflammatory phytochemicals are not fully identified. In this paper, we will discuss about the molecular targets of phytochemicals in TLRs signaling pathways. These results present a novel anti-inflammatory mechanism of phytochemicals in TLRs signaling.

• Journal of Animal Science and Technology
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• 제47권1호
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• pp.29-38
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• 2005

Effect of dietary brown seaweed(Undaria pinnatifida) levels on the anti-oxidant enzyme system was evaluated in blood of broiler chicks activated innate immune response. Day-old broiler chicks were fed diets containing 0.0(basal), 1.0, 2.0 and 4.0 % of brown seaweed for 4 weeks. The innate immune response was activated by injecting Salmonella typhymurium lipopolysaccharide(LPS) i.p. at 8, 10 and 12 day of age. The activation of innate immune response enhanced(p< 0.01) and the brown seaweed 1.0 and 2.0 % diets reduced(P< 0.05) the superoxide dismutase(SOD) activity in erythrocyte cytosol significantly. The activation of innate immune response elevated significantly the levels of peroxide and the activity of peroxidase in plasma, while the levels of dietary brown seaweed resulted in a significant linear increase in peroxidase activity in plasma of normal bird. Experience of the innate immune response in 4 week-old chicks reduced linearly the plasma level of peroxide with the level of brown seaweed and enhanced the plasma peroxidase activity. Also, the plasma of normal birds fed the brown seaweed showed higher level of peroxide and lower activity of peroxidase. The results indicated that dietary brown seaweed affected SOD and peroxidase activities in blood of broiler chicks during activation of innate immune response.

• 한국응용곤충학회:학술대회논문집
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• 한국응용곤충학회 2002년도 추계 합동 특강 및 학술발표대회
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• pp.26-27
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• 2002

• 한국식품영양학회지
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• 제21권3호
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• pp.275-282
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• 2008

Hot-water($100^{\circ}C$) and cold-water($4^{\circ}C$) extracts of Taraxacum officinale root were assessed for the effects of innate and adaptive immune responses in mice. Hot water extracts(TO-100) and cold water extracts(TO-4) did not affect the viability of macrophages at concentrations below to 18 mg/ml and 8 mg/ml, respectively. The thioglycollate-induced macrophages cultured with TO-100 and TO-4 produced a significantly higher quantity of various cytokines, such as IL-6 and IL-12, than those treated with medium. This shows that the extracts potently stimulated the innate immune response. When mice were subcutaneously immunized(sc) with OVA+FIA(Freund's incomplete adjuvant)-emulsified TO-100, TO-100 did not affect the production of IgE, but enhanced the production of IgG1, IgG2a and IgG2b. The culture supernatant obtained from the splenocytes of mice treated with OVA+FIA-emulsified TO-100 also evidenced elevated levels of both OVA-specific Th1-type(IFN-$\gamma$) and Th2-type cytokines(IL-4, IL-6 and IL-10). These results suggested that TO-100 can modulate the immune responses to allergens in mice.

• IMMUNE NETWORK
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• 제10권6호
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• pp.181-187
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• 2010

Excessive alcohol consumption is one of the critical causative factors leading to alcoholic liver disease (ALD). ALD is characterized by a wide spectrum of liver damage, ranging from simple uncomplicated liver steatosis (fatty liver) to steatohepatitis and liver fibrosis/cirrhosis. It has been believed that the obvious underlying cause for ALD is due to hepatocyte death induced by alcohol itself. However, recent sparkling studies have shown that diverse immune responses contribute to ALD because liver is enriched with numerous immune cells. Especially, a line of evidence has suggested that innate immune cells such as Kupffer cells and natural killer (NK)/NKT cells are significantly involved in the pathogenesis of ALD via production of pro-inflammatory cytokines and other mediators. Indeed, more interestingly, hepatic stellate cells (HSCs), known as a major cell inducing liver steatosis and fibrosis, can be killed by liver NK cells, which could be suppressed by chronic alcohol consumption. In this review, with the view of liver as predominant innate immune organ, we describe the pathogenesis of ALD in which what roles of innate immune cells are and how they are interacting with HSCs.