• 제목/요약/키워드: host responses

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Effects of nasopharyngeal microbiota in respiratory infections and allergies

  • Kang, Hyun Mi;Kang, Jin Han
    • Clinical and Experimental Pediatrics
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    • 제64권11호
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    • pp.543-551
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    • 2021
  • The human microbiome, which consists of a collective cluster of commensal, symbiotic, and pathogenic microorganisms living in the human body, plays a key role in host health and immunity. The human nasal cavity harbors commensal bacteria that suppress the colonization of opportunistic pathogens. However, dysbiosis of the nasal microbial community is associated with many diseases, such as acute respiratory infections including otitis media, sinusitis and bronchitis and allergic respiratory diseases including asthma. The nasopharyngeal acquisition of pneumococcus, which exists as a pathobiont in the nasal cavity, is the initial step in virtually all pneumococcal diseases. Although the factors influencing nasal colonization and elimination are not fully understood, the adhesion of opportunistic pathogens to nasopharyngeal mucosa receptors and the eliciting of immune responses in the host are implicated in addition to bacterial microbiota properties and colonization resistance dynamics. Probiotics or synbiotic interventions may show promising and effective roles in the adjunctive treatment of dysbiosis; however, more studies are needed to characterize how these interventions can be applied in clinical practice in the future.

2-Undecanone derived from Pseudomonas aeruginosa modulates the neutrophil activity

  • Jeong, Yu Sun;Huh, Sunghyun;Kim, Ji Cheol;Park, Ji Ye;Lee, ChaeEun;Kim, Min-Sik;Koo, JaeHyung;Bae, Yoe-Sik
    • BMB Reports
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    • 제55권8호
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    • pp.395-400
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    • 2022
  • Pseudomonas aeruginosa (P. aeruginosa) is a well-known Gramnegative opportunistic pathogen. Neutrophils play key roles in mediating host defense against P. aeruginosa infection. In this study, we identified a metabolite derived from P. aeruginosa that regulates neutrophil activities. Using gas chromatography-mass spectrometry, a markedly increased level of 2-undecanone was identified in the peritoneal fluid of P. aeruginosa-infected mice. 2-Undecanone elicited the activation of neutrophils in a Gαi-phospholipase C pathway. However, 2-undecanone strongly inhibited responses to lipopolysaccharide and bactericidal activity of neutrophils against P. aeruginosa by inducing apoptosis. Our results demonstrate that 2-undecanone from P. aeruginosa limits the innate defense activity of neutrophils, suggesting that the production of inhibitory metabolites is a strategy of P. aeruginosa for escaping the host immune system.

Photoimmunology -Past, Present and Future-

  • Daynes, Raymond A.;Chung, Hun-Taeg;Roberts, Lee K.
    • 대한미생물학회지
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    • 제21권3호
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    • pp.311-329
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    • 1986
  • The experimental exposure of animals to sources of ultraviolet radiation (UVR) which emit their energy primarily in the UVB region (280-320nm) is known to result in a number of well-described changes in the recipient's immune competence. Two such changes include a depressed capacity to effectively respond immunologically to transplants of syngeneic UVR tumors and a markedly reduced responsiveness to known inducers of delayedtype (DTH) and contact hypersensitivity (CH) reactions. The results of experiments that were designed to elucidate the mechanisms responsible for UVR-induced immunomodulation have implicated: 1) an altered pattern of lymphocyte recirculation, 2) suppressor T cells(Ts), 3) deviations in systemic antigen presenting cell (APC) potential. 4) changes in the production of interleukin-1-like molecules, and 5) the functional inactivation of epidermal Langerhans cells in this process. The exposure of skin to UVR, therefore, causes a number of both local and systemic alterations to the normal host immune system. In spite of this seeming complexity and diversity of responses, our recent studies have established that each of the UVR-mediated changes is probably of equal importance to creating the UVR-induced immunocompromised state. Normal animals were exposed to low dose UVR radiation on their dorsal surfaces under conditions where a $3.0\;cm^2$ area of skin was physically protected from the light energy. Contact sensitization of these animals with DNFB, to either the irradiated or protected back skin, resulted in markedly reduced CH responses. This was observed in spite of a normal responsiveness following the skin sensitization to ventral surfaces of the UVR-exposed animals. Systemic treatment of the low dose UVR recipients with the drug indomethacin (1-3 micrograms/day) during the UVR exposures resulted in a complete reversal of the depressions observed following DNFB sensitization to "protected" dorsal skin while the altered responsiveness found in the group exposed to the skin reactive chemical through directly UVR-exposed sites was maintained. These studies implicate the importance of EC as effective APC in the skin and also suggest that some of the systemic influences caused by UVR exposure involve the production of prostaglandins. This concept was further supported by finding that indomethacin treatment was also capable of totally reversing the systemic depressions in CH responsiveness caused by high dose UVR exposure (30K joules/$m^2$) of mice. Attempts to analyze the cellular mechanisms responsible established that the spleens of all animals which demonstrated altered CH responses, regardless of whether sensitization was through a normal or an irradiated skin site, contained suppressor cells. Interestingly, we also found normal levels of T effector cells in the peripheral lymph nodes of the UVR-exposed mice that were contact sensitized through normal skin. No effector cells were found when skin sensitization took place through irradiated skin sites. In spite of such an apparent paradox, insight into the probable mechanisms responsible for these observations was provided by establishing that UVR exposure of skin results in a striking and dose-dependent blockade of the efferent lymphatic vessels in all peripheral lymph nodes. Therefore, the afferent phases of immune responses can apparently take place normally in UVR exposed animals when antigen is applied to normal skin. The final effector responses, however, appear to be inhibited in the UVR-exposed animals by an apparent block of effector cell mobility. This contrasts with findings in the normal animals. Following contact sensitization, normal animals were also found to simultaneously contain both antigen specific suppressor T cells and lymph node effector cells. However, these normal animals were fully capable of mobilizing their effector cells into the systemic circulation, thereby allowing a localization of these cells to peripheral sites of antigen challenge. Our results suggest that UVR is probably not a significant inducer of suppressor T-cell activity to topically applied antigens. Rather, UVR exposure appears to modify the normal relationship which exists between effector and regulatory immune responses in vivo. It does so by either causing a direct reduction in the skin's APC function, a situation which results in an absence of effector cell generation to antigens applied to UVR-exposed skin sites, inhibiting the capacity of effector cells to gain access to skin sites of antigen challenge or by sequestering the lymphocytes with effector cell potential into the draining peripheral lymph nodes. Each of these situations result in a similar effect on the UVR-exposed host, that being a reduced capacity to elicit a CH response. We hypothesize that altered DTH responses, altered alloresponses, and altered graft-versus-host responses, all of which have been observed in UVR exposed animals, may result from similar mechanisms.

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The Effects of Headquarters' Levels of Control and Subsidiaries' Local Experiences on Competency in Foreign Subsidiaries: A Quadratic Model Investigation of Korean Multinational Corporations

  • Lee, Jae-Eun;Kang, Joo-Yeon;Park, Jung-Min
    • Journal of Korea Trade
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    • 제24권1호
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    • pp.82-98
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    • 2020
  • Purpose - This study aims to overcome the limitations of existing studies, which linearly determine the precedence factors of competency in overseas subsidiaries. The research objectives are as follows. First, what kind of nonlinear effects does the level of control held by Korean headquarters over foreign subsidiaries have in terms of competency in the subsidiaries? Second, what kind of nonlinear effects do the local experiences of overseas subsidiaries have on their competency? Design/methodology - With data on Korean multinational corporations (MNCs), this paper analyzes the effects of control levels of headquarters (HQs) and host-country experiences of foreign subsidiaries regarding competency in overseas subsidiaries. In particular, this study focuses on nonlinear models, differentiating it from previous studies. In order to examine research hypotheses, this study conducted a survey of overseas subsidiaries of Korean corporations. Surveys were conducted through various methods including e-mail, online questionnaires, fax, and telephone calls. Copies of the questionnaire were distributed to a total of 2,246 overseas subsidiaries, and 409 completed responses were collected. Excluding 15 copies that were insufficiently answered, responses from a total of 394 copies were used for analysis. Findings - This study presents the following results. First, there is a U-shaped relationship between levels of HQ control and competency in foreign subsidiaries. This means that higher levels of HQ control negatively impact the competency levels of subsidiaries because strict control undermines autonomy in subsidiaries. However, if the level of HQ control exceeds a certain point, then the transfer of knowledge between HQs and subsidiaries is facilitated. Knowledge transferred from HQs can be used as prior knowledge by foreign subsidiaries to the benefit of all parties. Accordingly, knowledge transfer negates the negative effects of excessive HQ control and positively affects competency in subsidiaries. Second, there is an inverted U-shaped relationship between the local (host-country) experiences of subsidiaries and competency in foreign subsidiaries. This means that foreign subsidiaries can overcome the liabilities of foreignness and contribute to capability building by accumulating unique knowledge about their host countries. However, if local experiences accumulate excessively beyond a certain point, then the host country-specific experiences of foreign subsidiaries will offset the benefits discussed above. Excessive local experiences not only increase organizational inertia, but also create a problem of goal incongruence due to information asymmetry between HQs and subsidiaries. Therefore, excessive local experiences have negative effects on competency in foreign subsidiaries. Originality/value - This study suggests the following implications. First, unlike existing studies based mainly on linear models, this study presents important theoretical implications in its focus on nonlinear models and its analysis of the effects of HQ control and local experiences on competency in foreign subsidiaries from perspectives of organizational learning theory and agency theory. Second, in terms of practical implications, the results of this study suggest that optimally raising levels of HQ control and managing the local experiences of subsidiaries without increasing organizational inertia is important for enhancing competency in foreign subsidiaries.

Host Innate Immunity against Hepatitis E Virus and Viral Evasion Mechanisms

  • Kang, Sangmin;Myoung, Jinjong
    • Journal of Microbiology and Biotechnology
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    • 제27권10호
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    • pp.1727-1735
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    • 2017
  • Hepatitis E virus (HEV) infections cause epidemic or sporadic acute hepatitis, which are mostly self-limiting. However, viral infection in immunocompromised patients and pregnant women may result in serious consequences, such as chronic hepatitis and liver damage, mortality of the latter of which reaches up to 20-30%. Type I interferon (IFN)-induced antiviral immunity is known to be the first-line defense against virus infection. Upon HEV infection in the cell, the virus genome is recognized by pathogen recognition receptors, leading to rapid activation of intracellular signaling cascades. Expression of type I IFN triggers induction of a barrage of IFN-stimulated genes, helping the cells cope with viral infection. Interestingly, some of the HEV-encoded genes seem to be involved in disrupting signaling cascades for antiviral immune responses, and thus crippling cytokine/chemokine production. Antagonistic mechanisms of type I IFN responses by HEV have only recently begun to emerge, and in this review, we summarize known HEV evasion strategies and compare them with those of other hepatitis viruses.

형상기억합금 스트립 작동기를 이용한 구조물의 형상 변형 해석 (Deformation Analysis of the Structures with SMA Strip Actuator)

  • 노진호;한재홍;이인
    • 한국항공우주학회지
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    • 제33권11호
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    • pp.1-6
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    • 2005
  • 본 연구에서는 형상기억합금 작동기의 열-기계적 특성과 구조물의 응용을 살펴보았다. Lagoudas 모델을 기본으로 3-D 형상기억합금의 구성방정식을 FORTRAN으로 해석 알고리즘을 만들어 user material(UMAT) subroutine을 개발하였다. 개발된 형상기억합금 해석 UMAT subroutine을 상용 프로그램 ABAQUS와 연계 해석하여 형상기억합금 작동기와 주 구조물간의 상호 특성을 수치적으로 살펴보았다.

lux Operon과 Heat Shock Promoter 유전자 재조합을 통한 독성물질 탐지용 대장균의 개발 (Construction of Bioluminescent Escherichia coli from lux Operon and Heat Shock Promoter for the Detection of Toxic Substances)

  • 유승오;이은관;김현숙;정계훈;전억한
    • 한국미생물·생명공학회지
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    • 제27권4호
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    • pp.278-285
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    • 1999
  • In order to use heat shock promoter for the detection of toxic substances, dnaK promoter was amplified from E. coli genomic DNA by using a polymerase chain reaction(PCR) followed by sequencing and sub-cloning into the multi-cloning site of the plasmid, pUCD615. The pUCD615 is a broad-host-range vector containing promoterless lux operon originated from V.fischeri. The recombinant plasmid was transfered to E. coli DH5$\alpha$ through electroporation. The recombinant E. coli showed several patterns of bioluminescent responses to ethanol stress. The bioluminescent E. coli also showed responses to other toxic substances including FeK3(CN)6, CdCl2, p-nitrophenol and HgCl2. The increases of RLU(Relative Light Unit) were observed at 100ppm of FeK3(CN)6, 10ppm and 100ppm and 100ppm of CdCl2, 1ppm of 10ppm of p-nitrophenol and at 1ppm of HgCl2.

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FUNDAMENTAL PERFORMANCE OF IMAGE CODING SCHEMES BASED ON MULTIPULSE MODEL

  • Kashiwagi, Takashi;Kobayashi, Daisuke;Koda, Hiromu
    • 한국방송∙미디어공학회:학술대회논문집
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    • 한국방송공학회 2009년도 IWAIT
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    • pp.825-829
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    • 2009
  • In this paper, we examine the fundamental performance of image coding schemes based on multipulse model. First, we introduce several kinds of pulse search methods (i.e., correlation method, pulse overlap search method and pulse amplitude optimization method) for the model. These pulse search methods are derived from auto-correlation function of impulse responses and cross-correlation function between host signals and impulse responses. Next, we explain the basic procedure of multipulse image coding scheme, which uses the above pulse search methods in order to encode the high frequency component of an original image. Finally, by means of computer simulation for some test images, we examine the PSNR(Peak Signal-to-Noise Ratio) and computational complexity of these methods.

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Molecular Mechanisms Involved in Bacterial Speck Disease Resistance of Tomato

  • Kim, Young-Jin;Gregory B. Martin
    • The Plant Pathology Journal
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    • 제20권1호
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    • pp.7-12
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    • 2004
  • An important recent advance in the field of plant-microbe interactions has been the cloning of genes that confer resistance to specific viruses, bacteria, fungi or insects. Disease resistance (R) genes encode proteins with predicted structural motifs consistent with them having roles in signal recognition and transduction. Plant disease resistance is the result of an innate host defense mechanism, which relies on the ability of plant to recognize pathogen invasion and efficiently mount defense responses. In tomato, resistance to the pathogen Pseudomonas syringae pv. tomato is mediated by the specific recognition between the tomato serine/threonine kinase Pto and bacterial protein AvrPto or AvrPtoB. This recognition event initiates signaling events that lead to defense responses including an oxidative burst, the hypersensitive response (HR), and expression of pathogenesis- related genes.

Regulation of Intestinal Homeostasis by Innate Immune Cells

  • Kayama, Hisako;Nishimura, Junichi;Takeda, Kiyoshi
    • IMMUNE NETWORK
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    • 제13권6호
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    • pp.227-234
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    • 2013
  • The intestinal immune system has an ability to distinguish between the microbiota and pathogenic bacteria, and then activate pro-inflammatory pathways against pathogens for host defense while remaining unresponsive to the microbiota and dietary antigens. In the intestine, abnormal activation of innate immunity causes development of several inflammatory disorders such as inflammatory bowel diseases (IBD). Thus, activity of innate immunity is finely regulated in the intestine. To date, multiple innate immune cells have been shown to maintain gut homeostasis by preventing inadequate adaptive immune responses in the murine intestine. Additionally, several innate immune subsets, which promote Th1 and Th17 responses and are implicated in the pathogenesis of IBD, have recently been identified in the human intestinal mucosa. The demonstration of both murine and human intestinal innate immune subsets contributing to regulation of adaptive immunity emphasizes the conserved innate immune functions across species and might promote development of the intestinal innate immunity-based clinical therapy.