• Laboraroty Animal Research
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• 제34권4호
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• pp.295-301
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• 2018

Nucleotide-binding domain 1 (Nod1) is a cytosolic receptor that is responsible for the recognition of a bacterial peptidoglycan motif containing meso-diaminophimelic acid. In this study, we sought to identify the role of Nod1 in host defense in vivo against pulmonary infection by multidrug resistant Acinetobacter baumannii. Wildtype (WT) and Nod1-deficient mice were intranasally infected with $3{\times}10^7CFU$ of A. baumannii and sacrificed at 1 and 3 days post-infection (dpi). Bacterial CFUs, cytokines production, histopathology, and mouse ${\beta}$-defensins (mBD) in the lungs of infected mice were evaluated. The production of cytokines in response to A. baumannii was also measured in WT and Nod1-deficient macrophages. The bacterial clearance in the lungs was not affected by Nod1 deficiency. Levels of IL-6, $TNF-{\alpha}$, and $IL-1{\beta}$ in the lung homogenates were comparable at days 1 and 3 between WT and Nod1-deficient mice, except the $TNF-{\alpha}$ level at day 3, which was higher in Nod1-deficient mice. There was no significant difference in lung pathology and expression of mBDs (mBD1, 2, 3, and 4) between WT and Nod1-deficient mice infected with A. baumannii. The production of IL-6, $TNF-{\alpha}$, and NO by macrophages in response to A. baumannii was also comparable in WT and Nod1-deficient mice. Our results indicated that Nod1 does not play an important role in host immune responses against A. baumannii infection.

• IMMUNE NETWORK
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• 제20권3호
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• pp.25.1-25.13
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• 2020

Acinetobacter baumannii is known for its multidrug antibiotic resistance. New approaches to treating drug-resistant bacterial infections are urgently required. Cathelicidin-related antimicrobial peptide (CRAMP) is a murine antimicrobial peptide that exerts diverse immune functions, including both direct bacterial cell killing and immunomodulatory effects. In this study, we sought to identify the role of CRAMP in the host immune response to multidrug-resistant Acinetobacter baumannii. Wild-type (WT) and CRAMP knockout mice were infected intranasally with the bacteria. CRAMP^-/- mice exhibited increased bacterial colony-forming units (CFUs) in bronchoalveolar lavage (BAL) fluid after A. baumannii infection compared to WT mice. The loss of CRAMP expression resulted in a significant decrease in the recruitment of immune cells, primarily neutrophils. The levels of IL-6 and CXCL1 were lower, whereas the levels of IL-10 were significantly higher in the BAL fluid of CRAMP^-/- mice compared to WT mice 1 day after infection. In an in vitro assay using thioglycollate-induced peritoneal neutrophils, the ability of bacterial phagocytosis and killing was impaired in CRAMP^-/- neutrophils compared to the WT cells. CRAMP was also essential for the production of cytokines and chemokines in response to A. baumannii in neutrophils. In addition, the A. baumannii-induced inhibitor of κB-α degradation and phosphorylation of p38 MAPK were impaired in CRAMP^-/- neutrophils, whereas ERK and JNK phosphorylation was upregulated. Our results indicate that CRAMP plays an important role in the host defense against pulmonary infection with A. baumannii by promoting the antibacterial activity of neutrophils and regulating the innate immune responses.

• Journal of Ginseng Research
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• 제48권4호
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• pp.384-394
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• 2024

Background: Herpes simplex virus type 1 (HSV-1), known to latently infect the host's trigeminal ganglion, can lead to severe herpes encephalitis or asymptomatic infection, potentially contributing to neurodegenerative diseases like Alzheimer's. The virus generates reactive oxygen species (ROS) that significantly impact viral replication and induce chronic inflammation through NF-κB activation. Nuclear factor E2-related factor 2 (Nrf2), an oxidative stress regulator, can prevent and treat HSV-1 infection by activating the passive defense response in the early stages of infection. Methods and results: Our study investigated the antiviral effects of ginsenoside Rg5, an Nrf2 activator, on HSV-1 replication and several host cell signaling pathways. We found that HSV-1 infection inhibited Nrf2 activity in host cells, induced ROS/NF-κB signaling, and triggered inflammatory cytokines. However, treatment with ginsenoside Rg5 inhibited ROS/NF-κB signaling and reduced inflammatory cytokines through NRF2 induction. Interestingly, the Nrf2 inhibitor ML385 suppressed the expression of NAD(P)H quinone oxidoreductase 1(NQO1) and enhanced the expression of KEAP1 in HSV-1 infected cells. This led to the reversal of VP16 expression inhibition, a protein factor associated with HSV-1 infection, thereby promoting HSV-1 replication. Conclusion: These findings suggest for the first time that ginsenoside Rg5 may serve as an antiviral against HSV-1 infection and could be a novel therapeutic agent for HSV-1-induced neuroinflammation.

• 한국정보통신학회논문지
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• 제16권12호
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• pp.2649-2656
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• 2012

오늘날 기업에서는 업무의 신속성과 내부의 중요 정보 자산의 보호를 위하여 많은 투자를 하고 있다. 하지만 내부 기업 망 전체를 모두 같은 수준의 방어 시스템으로 구축하기에는 많은 예산과 인력을 투입해야 하는 문제가 있다. 본 논문은 분산 관리되는 기업 망에서 공격자가 다른 신뢰 호스트를 이용하여 목표로 하는 시스템을 공격할 때 신뢰 호스트 상호간 정보 교환을 통하여 IP 스푸핑 공격에 대하여 효율적이면서 신속한 대응이 가능하도록 방어 모델을 설계 하였다.

• The Plant Pathology Journal
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• 제25권2호
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• pp.113-120
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• 2009

Microscopic study of chili pepper (Capsicum annuum L.) infected with Phytophthora capsici, causing Phytophthora blight of chili pepper, was conducted to compare histological and cytological characteristics in the root and stem of susceptible (C. annuum cv. Bugang) and resistant (C. annuum cv. CM334) pepper cultivars. The susceptible pepper roots and stems were extensively penetrated and invaded by the pathogen initially into epidermal cells and later cortical and vascular cells. Host cell walls adjacent to and invaded by the infecting hyphae were partially dissolved and structurally loosened with fine fibrillar materials probably by cell wall-degrading enzymes of the pathogen. In the resistant pepper, the pathogen remained on root epidermal surface at one day after inoculation, embedded and captured in root exudation materials composed of proteins and polysaccharides. Also the pathogen appeared to be blocked in its progression at the early infection stages by thickened middle lamellae. At 3 days after inoculation, the oomycete hyphae were still confined to epidermal cells of the root and at most outer peripheral cortical cells of the stem, resulting from their invasion blocked by wound periderms formed underneath the infection sites and/or cell wall appositions bounding the hyphal protrusions. All of these aspects suggest that limitation of disease development in the resistant pepper may be due to the inhibition of the pathogen penetration, infection, invasion, and colonization by the defense structures such as root exudation materials, thickened middle lamellae, wound peridems and cell wall appositions.

• 동의생리병리학회지
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• 제26권4호
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• pp.409-417
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• 2012

External pathogens such as wind, cold can easily invade the external parts of the body when host's external defense ability is not secure. Herein, we consider the underlying mechanisms against the external contraction at the body surface. During the early period after primary invasion, external defense mechanisms are gradually activated. The classic clinical manifestations are aversion to cold, fever, headache, generalized pain, and nasal congestion. This condition is called by invasion of external pathogen into the body surface. As the disease progress, lung qi is stagnated and thereby up-outward and downward movement action of lung become disturbed. Therefore, when doctor administrate formula to treat the exterior syndrome, doctor must keep in mind not only materia medica, but also underlying mechanisms through which many clinical symptoms appear.

• International Journal of Computer Science & Network Security
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• 제21권12호
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• pp.207-212
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• 2021

A buffer overflow attack is carried out to subvert privileged program functions to gain control of the program and thus control the host. Buffer overflow attacks should be prevented by risk managers by eradicating and detecting them before the software is utilized. While calculating the size, correct variables should be chosen by risk managers in situations where fixed-length buffers are being used to avoid placing excess data that leads to the creation of an overflow. Metamorphism can also be used as it is capable of protecting data by attaining a reasonable resistance level [1]. In addition, risk management teams should ensure they access the latest updates for their application server products that support the internet infrastructure and the recent bug reports [2]. Scanners that can detect buffer overflows' flaws in their custom web applications and server products should be used by risk management teams to scan their websites. This paper presents an experiment of buffer overflow vulnerability and attack. The aims to study of a buffer overflow mechanism, types, and countermeasures. In addition, to comprehend the current detection plus prevention approaches that can be executed to prevent future attacks or mitigate the impacts of similar attacks.

• 한국미생물·생명공학회지
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• 제38권1호
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• pp.1-6
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• 2010

Human milk is frequently the only food source for a newborn during the initial stage of life after birth. Milk provides not only the nutrients necessary for the infant's growth, but also ingredients that may enable the infant to thrive. Human milk oligosaccharides (HMO) are considered to be these beneficial ingredients for the health of infant. It has been reported that around 5 to 10 g unbound oligosaccharides and around 20 to over 130 different HMO are present in 1L of human milk. The suggested health mechanisms of HMO's roles in host defense are 1) blocking bacterial adhesions, 2) binding to a toxin receptor on the extracellular domain, and 3) postbiotic effect resulting from the increase of probiotics such as Bifidobacteria and Lactobacilli. Among the prebiotic oligosaccharides, mixtures of long chain fuetooligosaccharides (10%) and galactooligosaccharides (90%) in infant formula are demonstrated to increase the number of Bifidobacteria and Lactobacilli to the levels seen in human milk fed infants.

• 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.