• Title/Summary/Keyword: host resistant

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Current perspectives on atypical pneumonia in children

  • Shim, Jung Yeon
    • Clinical and Experimental Pediatrics
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    • v.63 no.12
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    • pp.469-476
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    • 2020
  • The major pathogens that cause atypical pneumonia are Mycoplasma pneumoniae, Chlamydophila pneumoniae, and Legionella pneumophila. Community-acquired pneumonia (CAP) caused by M. pneumoniae or C. pneumoniae is common in children and presents as a relatively mild and self-limiting disease. CAP due to L. pneumophila is very rare in children and progresses rapidly, with fatal outcomes if not treated early. M. pneumoniae, C. pneumoniae, and L. pneumophila have no cell walls; therefore, they do not respond to β-lactam antibiotics. Accordingly, macrolides, tetracyclines, and fluoroquinolones are the treatments of choice for atypical pneumonia. Macrolides are the first-line antibiotics used in children because of their low minimum inhibitory concentrations and high safety. The incidence of pneumonia caused by macrolide-resistant M. pneumoniae that harbors point mutations has been increasing since 2000, particularly in Korea, Japan, and China. The marked increase in macrolide-resistant M. pneumoniae pneumonia (MRMP) is partly attributed to the excessive use of macrolides. MRMP does not always lead to clinical nonresponsiveness to macrolides. Furthermore, severe complicated MRMP responds to corticosteroids without requiring a change in antibiotic. This implies that the hyper-inflammatory status of the host can induce clinically refractory pneumonia regardless of mutation. Empirical macrolide therapy in children with mild to moderate CAP, particularly during periods without M. pneumoniae epidemics, may not provide additional benefits over β-lactam monotherapy and can increase the risk of MRMP.

Characterization of Heterodera sojae Virulence Phenotypes in Korea

  • Kang, Heonil;Ko, Hyoungrai;Park, Byeongyong;Choi, Insoo
    • The Plant Pathology Journal
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    • v.38 no.4
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    • pp.366-371
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    • 2022
  • The white soybean cyst nematode Heterodera sojae, isolated from the roots of soybean in Korea, is widespread in most provinces of the country and has the potential to be as harmful to soybean as H. glycines. Determining the virulence phenotypes of H. sojae is essential to devising management strategies that use resistant cultivars. Consequently, virulence phenotypes of 15 H. sojae populations from Korea were determined on seven soybean lines and one susceptible check variety. Two different HS types were found to be present in Korea; the more common HS type 2.5.7, comprising 73.3% of the H. sojae populations and the less common HS type 0, constituting only 26.7% of the tested populations. Considering the high frequency of H. sojae adaptation to soybean indicator lines, the PI 88788 group may not be a possible source of resistance while PI 548402, PI 90763, PI 437654, and PI 89772 can be used as resistance sources for soybean breeding programs aimed at developing H. sojae-resistant soybean cultivars in Korea.

Effects of $aroP^{-}$ mutation on the tryptophan excretion in escherichia coli ($aroP^{-}$변이가 E.coli에서 트립토판 방출에 미치는 영향)

  • 지연태;안병우;이세영
    • Korean Journal of Microbiology
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    • v.23 no.1
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    • pp.9-12
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    • 1985
  • As a part of the host cell development for a amplified recombinant trp operon, $aroP^-$ mutation was introduced in a E. coli host strain. $aroP^-$ mutation was induced by transposon Tn10 and transduced into the E. coli host cell by bacteriophage P1Kc. The effect of $aroP^-$ mutation on the excretion of tryptophan in E. coli $trpR^{-ts}/ColE_1 -trp^+$ cells was investigated. Mutant lacking the general aromatic transport system was resistant to ${\beta}-2-thienylalanine\;(2{\times}10^{-4}\;M)$, p-fluorophenylalanine $(2{\times}10^{-4}M)$, or 5-methyltryptophan $(2{\times}10^{-4}\;M.)[^3H]-tryptophan$ uptake of the $aroP^-$ mutant strain was reduced considerably as compared with $aroP^+$ counterpart. The rate of $[^3H]-tryptophan$ uptake of the $aroP^-$ mutant strain treated with $NaN_3(3{\times}10^{-2}\;M)$ was much less affected than that of $aroP^+$ counterpart. The $aroP^-$ transductants increased the tryptophan excretion from E. coli $trpR^{-ts}/ColE_1 -trp^+$ four times more than $aroP^+$ counterpart.

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Immune Responses to Viral Infection (바이러스 감염에 대한 면역반응)

  • Hwang, Eung-Soo;Park, Chung-Gyu;Cha, Chang-Yong
    • IMMUNE NETWORK
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    • v.4 no.2
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    • pp.73-80
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    • 2004
  • Viruses are obligate intracellular parasites which cause infection by invading and replicating within cells. The immune system has mechanisms which can attack the virus in extracellular and intracellular phase of life cycle, and which involve both non-specific and specific effectors. The survival of viruses depends on the survival of their hosts, and therefore the immune system and viruses have evolved together. Immune responses to viral infection may be variable depending on the site of infection, the mechanism of cell-to-cell spread of virus, physiology of the host, host genetic variation, and environmental condition. Viral infection of cells directly stimulates the production of interferons and they induce antiviral state in the surrounding cells. Complement system is also involved in the elimination of viruses and establishes the first line of defence with other non-specific immunity. During the course of viral infection, antibody is most effective at an early stage, especially before the virus enters its target cells. The virus- specific cytotoxic T lymphocytes are the principal effector cells in clearing established viral infections. But many viruses have resistant mechanism to host immune responses in every step of viral infection to cells. Some viruses have immune evasion mechanism and establish latency or persistency indefinitely. Furthermore antibodies to some viruses can enhance the disease by the second infection. Immune responses to viral infection are very different from those to bacterial infection.

Fate of Genetically Engineered 2,4-D-Degrading Microorganisms in Natural Soils and Waters

  • Hong, Seok-Myeong;Lee, Yin-Won;Kim, Chi-Kyung;Ka, Jong-Ok
    • Journal of Microbiology
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    • v.34 no.4
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    • pp.320-326
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    • 1996
  • To analyze the effects of host versus plasmid on survival of 2, 4-degrading bacteria in environmental samples, strains Pseudomonas cepacia/pJP4, Alcaligenes JMP228/pJP4, P. cepacia/p712, and Alcaligenes JMP228/p712 were separately inoculated into samples of field soil, paddy soil, lake water, and river water, and then the changes of their populations were measured. The strains used contained a 2, 4-D degradative plasmid, either pJP4 conferring fast-growing property to the host or p712 conferring slow-growing property, and were resistant to antibiotics such that the inoculated strains could be enumerated against the indigenous microbial populations. In sterile environmental samples, these strains were stably maintained at the levels used for inoculation, except in sterile paddy soil where Alcaligenes JMP228 strains died drapidly. In natural soil samples for four strains declined steadily with time, but in naturla water samples their polulations fell rapidly at the early phase and then remained almost constant. When the environmentla samples were treated with 2, 4-D, P. cepacia/pJP4 and P. cepacia/p712 maintained significant numbers, while Alcaligenes JMP228/pJP4 and Alcaligenes JMP228/p712 declined significantly in most of the samples. The results indicated that the survivability of genetically modified microorganisms could vary depending on the environments and that their abundance in the environments under s2, 4-D selection was markedly influenced by the nature of the 2, 4-D degradative plasmid as well as type of the host strain.

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Evaluation of Host Resistance of 18 Warm-Season and 20 Cool-Season Turfgrass Species and Cultivars to Spodoptera depravata(Butler) (잔디밤나방에 대한 난지형 잔디와 한지형 잔디의 내충성 평가)

  • 박봉주
    • Journal of the Korean Institute of Landscape Architecture
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    • v.31 no.4
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    • pp.74-81
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    • 2003
  • The need for insect and mite resistant turfgrass cultivars arose because of problems associated with pesticide use. Representative cultivars and genotypes of 18 warm-season turfgrass [Zoysia japonica Steud., Z. japonica${\times}$Z. metrella hybrids, Z. japonica${\times}$Z. tenuifotia hybrids, Z. matrella (L.) Merr., Cynodon dactylon (L.) Pers., C. dactylon${\times}$C. transvallensis hybrids, Paspalum notatum Flugge., P. vaginatum Swartz., Stenotaphrum secundatum (Walt.) Kuntze, Eremochloa ophiuroides (Munro.) and Buchloe dactyloides (Nutt.) Engelm.] and 20 cool-season turfgrasses [Poa pratensis L., Festuca arundinacea Schreb., F. rubra L., F. rubra var. commutata Gaud., F. ovina var. duriuscula L. Koch. Agrostis tenuis Sibth., A. palustris Huds., and Latium perenne L.] were evaluated for host resistance to feeding by the Spodoptera depravata (Butler) in the laboratory. Two experiments were set up in the laboratory using 8.5cm diameter${\times}$4.0cm deep plastic petri dishes as larvae feeding chambers. In experiment 1, one neonate larvae were place on the grass in each dish and the dishes were arranged with 5 replicates each within an environmental chamber maintained at $25^{\circ}C$ and 15h light: 9h dark Larval survival and larval weights at 7d and 14d, pupal weights, and days to pupation were compared among turfgrasses. In Experiment 2, 4cm sections of all grasses were oriented equidistant from each other in a pattern resembling the spokes of a wheel. Five one neonate larvae were introduced to the center of each dish. Dishes were immediately placed in an environmental chamber held at $25^{\circ}C$, 15h light: 9h dark Larvae were allowed to feed for 24h. Damage was rated from 0(no damage) to 9(completely consumed) were made for eachturfgrass. Resistance as antibiosis (high mortality, slowed growth, and least preference) was identified in Z. japonica${\times}$Z. tenuifolia hybirids ‘Emerald’, Z. japonica${\times}$Z. metrella hybirds ‘Miyako’ and Eremochloa ophiuroides (Munro.). Cool-season turfgrasses tested were susceptible to feeding by Spodoptera depravata (Butler).

Isolation and Characterization of Bacteriophages Against Pseudomonas syringae pv. actinidiae Causing Bacterial Canker Disease in Kiwifruit

  • Yu, Ji-Gang;Lim, Jeong-A;Song, Yu-Rim;Heu, Sunggi;Kim, Gyoung Hee;Koh, Young Jin;Oh, Chang-Sik
    • Journal of Microbiology and Biotechnology
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    • v.26 no.2
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    • pp.385-393
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    • 2016
  • Pseudomonas syringae pv. actinidiae causes bacterial canker disease in kiwifruit. Owing to the prohibition of agricultural antibiotic use in major kiwifruit-cultivating countries, alternative methods need to be developed to manage this disease. Bacteriophages are viruses that specifically infect target bacteria and have recently been reconsidered as potential biological control agents for bacterial pathogens owing to their specificity in terms of host range. In this study, we isolated bacteriophages against P. syringae pv. actinidiae from soils collected from kiwifruit orchards in Korea and selected seven bacteriophages for further characterization based on restriction enzyme digestion patterns of genomic DNA. Among the studied bacteriophages, two belong to the Myoviridae family and three belong to the Podoviridae family, based on morphology observed by transmission electron microscopy. The host range of the selected bacteriophages was confirmed using 18 strains of P. syringae pv. actinidiae, including the Psa2 and Psa3 groups, and some were also effective against other P. syringae pathovars. Lytic activity of the selected bacteriophages was sustained in vitro until 80 h, and their activity remained stable up to 50℃, at pH 11, and under UV-B light. These results indicate that the isolated bacteriophages are specific to P. syringae species and are resistant to various environmental factors, implying their potential use in control of bacterial canker disease in kiwifruits.

Nucleotide-binding oligomerization domain 1 is dispensable for host immune responses against pulmonary infection of Acinetobacter baumannii in mice

  • Kang, Min-Jung;Choi, Jin-A;Choi, Joo-Hee;Jang, Ah-Ra;Park, Ji-Yeon;Ahn, Jae-Hun;Lee, Tae-Sung;Kim, Dong-Yeon;Park, Jong-Hwan
    • Laboraroty Animal Research
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    • v.34 no.4
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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.

Insights into Tan Spot and Stem Rust Resistance and Susceptibility by Studying the Pre-Green Revolution Global Collection of Wheat

  • Abdullah, Sidrat;Sehgal, Sunish Kumar;Jin, Yue;Turnipseed, Brent;Ali, Shaukat
    • The Plant Pathology Journal
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    • v.33 no.2
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    • pp.125-132
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    • 2017
  • Tan spot (TS), caused by the fungus Pyrenophora tritici-repentis (Died) Drechs, is an important foliar disease of wheat and has become a threat to world wheat production since the 1970s. In this study a globally diverse pre-1940s collection of 247 wheat genotypes was evaluated against Ptr ToxA, P. tritici-repentis race 1, and stem rust to determine if; (i) acquisition of Ptr ToxA by the P. tritici-repentis from Stagonospora nodorum led to increased pathogen virulence or (ii) incorporation of TS susceptibility during development stem rust resistant cultivars led to an increase in TS epidemics globally. Most genotypes were susceptible to stem rust; however, a range of reactions to TS and Ptr ToxA were observed. Four combinations of diseasetoxin reactions were observed among the genotypes; TS susceptible-Ptr ToxA sensitive, TS susceptible-Ptr ToxA insensitive, TS resistant-Ptr ToxA insensitive, and TS resistant-Ptr ToxA toxin sensitive. A weak correlation (r = 0.14 for bread wheat and -0.082 for durum) was observed between stem rust susceptibility and TS resistance. Even though there were no reported epidemics in the pre-1940s, TS sensitive genotypes were widely grown in that period, suggesting that Ptr ToxA may not be an important factor responsible for enhanced prevalence of TS.

Transformation Conditions of Bacillus subtilis by Streptomyces rimosus Plasmid DNA (Streptomyces rimosus Plasmid DNA에 의한 Bacillus subtilis의 형질전환 조건)

  • Hong, Yong-Ki;Seu, Jung-Hwn
    • Microbiology and Biotechnology Letters
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    • v.11 no.1
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    • pp.75-79
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    • 1983
  • To exploit a suitable vector and recipient strain for molecular cloning in Bacillus subtilis, oxytetracycline-resistant plasmic DNA has been prepared from Streptomyces rimosus by phenol-buffer extraction of lysozyme-lysed cells and introduced into B. subtilis KPM 60 [St $r^{R}$-mutant of RM 125 (leu A8, arg 15, hsm $M^{-10}$ , hsr $M^{-10}$ )] by transformation. Oxitetracycline-resistant plasmid was well transferred into B. subtilis KPM 60 with average frequency of 10$^{-4}$ per $\mu\textrm{g}$ of DNA. The highest frequency of plasmid transformation was obtained after 3 hours incubation of recipient cells in the growth medium and 30 to 60 minutes incubation in the competence medium, and then 20 minutes contact of DNA and host cells. Optimum pH for competence was 7.5, and optimum temperature for transformation was 2$0^{\circ}C$.>.

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