• Parasites, Hosts and Diseases
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• 제23권2호
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• pp.247-252
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• 1985

In the present study, the effect of primary infection to reinfection with Ascaris suum larvae was experimented in mouse model. Mice were challenged with 1,000 infective stage eggs of Ascaris suum. The embryonated eggs were directly introduced into stomach of mice. Reinfection was performed at 50 days after the primary infection with same method as primary infection. Mice were sacrificed 3, 5, 7, 10, 15 and 20 days after infection in both groups respectively. Larvae collected from livers and lungs with Baermann's apparatus were enumerated and measured after sacrifice. Sera of mice were also collected at same time. The results of the experiment were as follows: With antigen prepared from coelomic fluid of adult Ascaris suum and sera collected from mice before reinfection, the production of antibody in experimental mice was confirmed by the gel-diffusion technique. In the livers of reinfected mice, the larvae were recovered up to 10 days after challenge, otherwhile in the primary infected mice, the larvae were observed up to 7 days. The maximum number of larvae were observed in the lungs of primary infected mice on 10 days after inoculation. In the lungs of reinfected mice, maximum number of larvae were recovered on 7 days after, only few larvae were recovered on 10 days after reinfection. As regards the growth of the larvae, the third stage larvae, over $500{\mu\textrm{m}}$ in length, appeared in livers at 5 days after reinfection, but it couldn't be found on 7 days and 10 days after challenge. The third stage larvae continuously developed were observed in lungs of mice from 5 days after reinfection. In conclusion, it was found that development of larvae in livers of immune mice were probably repressed by the immune mechanisms being rises in livers and defence mechanism is also acting by interfering with the process of larval penetration into the lung from the liver.

• Restorative Dentistry and Endodontics
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• 제40권4호
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• pp.306-313
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• 2015

Objectives: Molecular mechanism of the pathogenicity of Enterococcus faecalis (E. faecalis), a suspected endodontic pathogen, has not yet been adequately elucidated due to limited information on its virulence factors. Here we report the identification of in vivo expressed antigens of E. faecalis by using a novel immunoscreening technique called change-mediated antigen technology (CMAT) and an experimental animal model of endodontic infection. Materials and Methods: Among 4,500 E. coli recombinant clones screened, 19 positive clones reacted reproducibly with hyperimmune sera obtained from rabbits immunized with E. faecalis cells isolated from an experimental endodontic infection. DNA sequences from 16 of these in vivo-induced (IVI) genes were determined. Results: Identified protein antigens of E. faecalis included enzymes involved in housekeeping functions, copper resistance protein, putative outer membrane proteins, and proteins of unknown function. Conclusions: In vivo expressed antigens of E. faecalis could be identified by using a novel immune-screening technique CMAT and an experimental animal model of endodontic infection. Detailed analysis of these IVI genes will lead to a better understanding of the molecular mechanisms involved in the endodontic infection of E. faecalis.

• Journal of Ginseng Research
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• 제38권3호
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• pp.215-219
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• 2014

Background: Biological control of plant pathogens using benign or beneficial microorganisms as antagonistic agents is currently considered to be an important component of integrated pest management in agricultural crops. In this study, we evaluated the potential of Bacillus subtilis strain HK-CSM-1 as a biological control agent against Colletotrichum panacicola. Methods: The potential of B. subtilis HK-CSM-1 as a biological control agent for ginseng anthracnose was assessed. C. panacicola was inoculated to ginseng plants and the incidence and severity of disease was assessed to examine the efficacy of the bacterium as a biological control against C. panacicola. Results: Inoculation of Panax ginseng plants with B. subtilis significantly suppressed the number of disease lesions of C. panacicola and was as effective as the chemical fungicide iminoctadine tris(albesilate). The antifungal activity of B. subtilis against C. panacicola was observed on a co-culture medium. Interestingly, treatment with B. subtilis did not significantly affect the diameter of the lesions, suggesting that the mechanism of protection was through the reduction in the incidence of infection related to the initial events of the infection cycle, including penetration and infection via spore germination and appressorium formation rather than by the inhibition of invasive growth after infection. Conclusion: Our results suggest that B. subtilis HK-CSM-1 can be used as an effective and ecologically friendly biological control agent for anthracnose in P. ginseng.

• The Plant Pathology Journal
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• 제32권5호
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• pp.377-387
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• 2016

Tomato yellow leaf curl virus (TYLCV), a member of the genus Begomovirus, is one of the most important viruses of cultivated tomatoes worldwide, mainly causing yellowing and curling of leaves with stunting in plants. TYLCV causes severe problems in sub-tropical and tropical countries, as well as in Korea. However, the mechanism of TYLCV infection remains unclear, although the function of each viral component has been identified. TYLCV C4 codes for a small protein involved in various cellular functions, including symptom determination, gene silencing, viral movement, and induction of the plant defense response. In this study, through yeast-two hybrid screenings, we identified TYLCV C4-interacting host proteins from both healthy and symptom-exhibiting tomato tissues, to determine the role of TYLCV C4 proteins in the infection processes. Comparative analyses of 28 proteins from healthy tissues and 36 from infected tissues showing interactions with TYLCV C4 indicated that TYLCV C4 mainly interacts with host proteins involved in translation, ubiquitination, and plant defense, and most interacting proteins differed between the two tissues but belong to similar molecular functional categories. Four proteins-two ribosomal proteins, S-adenosyl-L-homocysteine hydrolase, and 14-3-3 family protein-were detected in both tissues. Furthermore, the identified proteins in symptom-exhibiting tissues showed greater involvement in plant defenses. Some are key regulators, such as receptor-like kinases and pathogenesis-related proteins, of plant defenses. Thus, TYLCV C4 may contribute to the suppression of host defense during TYLCV infection and be involved in ubiquitination for viral infection.

• 대한수의학회지
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• 제33권4호
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• pp.679-691
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• 1993

As a series of studies to investigate the effect of immunosuppression on Ascaris suum infection in undefinitive hosts, a delicate relationship between host and parasite, rabbits were divided into experiment 1(control group) and experiment 2(immnunosuppressive group treated with prednisolone acetate) and inoculated with a single dose of 5,000 embryonated A suum eggs. The recovery rates, sizes and morphology of the larvae and immunological responses in the rabbits were chronologically monitored according to somatic migration. In both experiments, the larvae failed to develop into the adults, but young adults in the experiment 2 grew somewhat faster and survied later than those in the experiment 1. The mast cells of small intestinal mucosa and mesenteric lymph nodes and the goblet cells of small intestinal mucosa in the worm detected cases of experiment 2 decreased remarkably in number comparing with those of experiment 1. Considering the experimental results. the expulsion mechanism of somatic migrant larvae may he related to the temporary increasing tendency of the mast cells, the goblet cells, T-cells of mesenteric lymph nodes and spleens, eosinophils in peripheral blood, degranulation rates of peritoneal mast cells and the migration inhibition rates of leucocytes. In addition, patent infection of A suum in the rabbits was not obviously observed despite of immunosuppression by prednisolone acetate.

• Biomolecules & Therapeutics
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• 제29권3호
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• pp.249-262
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• 2021

The most effective way to control newly emerging infectious disease, such as the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) pandemic, is to strengthen preventative or therapeutic public health strategies before the infection spreads worldwide. However, global health systems remain at the early stages in anticipating effective therapeutics or vaccines to combat the SARS-CoV-2 pandemic. While maintaining social distance is the most crucial metric to avoid spreading the virus, symptomatic therapy given to patients on the clinical manifestations helps save lives. The molecular properties of SARS-CoV-2 infection have been quickly elucidated, paving the way to therapeutics, vaccine development, and other medical interventions. Despite this progress, the detailed biomolecular mechanism of SARS-CoV-2 infection remains elusive. Given virus invasion of cells is a determining factor for virulence, understanding the viral entry process can be a mainstay in controlling newly emerged viruses. Since viral entry is mediated by selective cellular proteases or proteins associated with receptors, identification and functional analysis of these proteins could provide a way to disrupt virus propagation. This review comprehensively discusses cellular machinery necessary for SARS-CoV-2 infection. Understanding multifactorial traits of the virus entry will provide a substantial guide to facilitate antiviral drug development.

• Parasites, Hosts and Diseases
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• 제55권6호
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• pp.613-622
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• 2017

IL-12 and IL-23 are closely related in structure, and have been shown to play crucial roles in regulation of immune responses. However, little is known about the regulation of these cytokines in T cells. Here, we investigated the roles of PI3K and MAPK pathways in IL-12 and IL-23 production in human Jurkat T cells in response to Toxoplasma gondii and LPS. IL-12 and IL-23 production was significantly increased in T cells after stimulation with T. gondii or LPS. T. gondii and LPS increased the phosphorylation of AKT, ERK1/2, p38 MAPK, and JNK1/2 in T cells from 10 min post-stimulation, and peaked at 30-60 min. Inhibition of the PI3K pathway reduced IL-12 and IL-23 production in T. gondii-infected cells, but increased in LPS-stimulated cells. IL-12 and IL-23 production was significantly reduced by ERK1/2 and p38 MAPK inhibitors in T. gondii- and LPS-stimulated cells, but not in cells treated with a JNK1/2 inhibitor. Collectively, IL-12 and IL-23 production was positively regulated by PI3K and JNK1/2 in T. gondii-infected Jurkat cells, but negatively regulated in LPS-stimulated cells. And ERK1/2 and p38 MAPK positively regulated IL-12 and IL-23 production in Jurkat T cells. These data indicate that T. gondii and LPS induced IL-12 and IL-23 production in Jurkat T cells through the regulation of the PI3K and MAPK pathways; however, the mechanism underlying the stimulation of IL-12 and IL-23 production by T. gondii in Jurkat T cells is different from that of LPS.

• Journal of Microbiology and Biotechnology
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• 제31권11호
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• pp.1583-1590
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• 2021

Studies have demonstrated that PE_PGRS45 is constitutively expressed under various environmental conditions (such as nutrient depletion, hypoxia, and low pH) of the in vitro growth conditions examined, indicating that PE_PGRS45 protein is critical to the basic functions of Mycobacterium tuberculosis. However, there are few reports about the biochemical function and pathogenic mechanism of PE_PGRS45 protein. The fact that this M. tuberculosis gene is not easily expressed in E. coli may be mainly due to the high content of G+C and the use of unique codons. Fusion tags are indispensable tools used to improve the soluble expression of recombinant proteins and accelerate the characterization of protein structure and function. In the present study, His6, Trx, and His6-MBP were used as fusion tags, but only MBP-PE_PGRS45 was expressed solubly. The purification using His6-MBP tag-specific binding to the Ni column was easy to separate after the tag cleavage. We used the purified PE_PGRS45 to immunize New Zealand rabbits and obtained anti-PE_PGRS45 serum. We found that the titer of polyclonal antibodies against PE_PGR45 was higher than 1:256000. The result shows that purified PE_PGRS45 can induce New Zealand rabbits to produce high-titer antibodies. In conclusion, the recombinant protein PE_PGRS45 was successfully expressed in E. coli and specific antiserum was prepared, which will be followed by further evaluation of these specific antigens to develop highly sensitive and specific diagnostic tests for tuberculosis.

• 한국통신학회논문지
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• 제41권9호
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• pp.1103-1107
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• 2016

현재까지 내부 네트워크에 접근하는 단말의 무결성을 검증하기 위한 방안으로 네트워크 접근제어 시스템 NAC(Network Access Control), 백신, 망분리, MDM(Mobile Device Management) 등 다양한 방법들을 이용하여 내부 네트워크의 자산을 보호하고자 하였다. 그러나 기존의 접근제어 시스템에서 사용하는 정책은 획일화 되어 사용자에게 적용되고 있고, 또한 APT(Advance Persistent Threat) 대응 솔루션, 방화벽, 백신 등의 보안 솔루션은 단말이 내부 네트워크에 접근한 이후에 이상 트래픽 등이 발생 시 이를 감지하고 처리하는 형태이므로 근본적으로 무결성 검사를 수행한 이후에 내부 네트워크에 접근하는 등의 방안이 필요하다. 따라서 본 논문에서는 악성코드에 감염된 단말이 내부 네트워크에 접속하기 이전에 이를 검증하고 조치하는 방안에 대한 보안네트워크 설계를 제시하고자 한다.

• Journal of Microbiology and Biotechnology
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• 제18권4호
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• pp.799-804
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• 2008

Retrovirus tropism can be restricted by host cell factors such as Fv1, TRIM5${\alpha}$, and LvI that inhibit infection by targeting the incoming viral capsid. The Fv1 gene inhibits murine leukemia virus infection in mice, but the precise mechanism of Fv1-mediated restriction is poorly understood. Our previous studies had demonstrated that Fv1-mediated viral tropism can be determined within the capsid protein at position 114. To study the interaction between Fv1 and CA, we introduced amino acid substitution and deletion at this site in the N-tropic AKV capsid gene. The mutated two-LTR proviral DNAs were introduced into SC-1 cells by transfection. After transfection, cell supernatants collected from transfected cells were tested for host range susceptibility. The result indicated that substitution of amino acids did not alter tropism, but the deletion of 114His produced a virus with unusual tropism. The novel phenotype produced here failed to replicate in Fv1-expressing cells. This mutant virus showing such an extreme restriction pattern would be useful for studying the mechanism of Fv1-mediated restriction.