• Title/Summary/Keyword: Infection Mechanism

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장애환자에서 치성감염에 의한 아관긴급과 구강피부누공의 관리 (CARE OF TRISMUS AND OROCUTANEOUS FISTULA BY ODONTOGENIC INFECTION IN A DISABLED PATIENT)

  • 오지현;손정석;유재하;김종배
    • 대한장애인치과학회지
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    • 제9권2호
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    • pp.111-117
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    • 2013
  • Some odontogenic infections erode into fascial spaces directly and spread toward lymphatic tissues and blood streams. The principal maxillary primary spaces are the canine, buccal, and infratemporal space, the next secondary spaces are the masseteric, temporal and pharygeal space. As a result of the infection, trismus and orocutaneous fistula may be occurred. Trismus is owing to conditions not associated with temporomandibular joint itself and may be of myogenic, neurogenic, or psychogenic nature. Muscular trismus is due to infection adjacent to the elevator muscles of the jaw. The four principles of treatment of infection are as follows: (1) removal of the cause, (2) establishment of drainage, (3) institution of antibiotic therapy, and (4) provision of supportive care, including rest, nutrition and physiotherapy. Jaw physiotherapy is necessary to increase the amount of mouth opening and regain normal muscle tone. If proper care of odontogenic infection could be attained, the orocutaneous fistula will heal and close spontaneously by wound contraction mechanism of natural homeostatic response. This is a case report of the care of trismus and orocutaneous fistula due to fascial space abscess by advanced odontogenic infection in a physically disabled patient.

Positive association of breastfeeding on respiratory syncytial virus infection in hospitalized infants: a multicenter retrospective study

  • Jang, Min Jeong;Kim, Yong Joo;Hong, Shinhye;Na, Jaeyoon;Hwang, Jong Hee;Shin, Son Moon;Ahn, Yong Min
    • Clinical and Experimental Pediatrics
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    • 제63권4호
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    • pp.135-140
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    • 2020
  • Background: Breastfeeding reportedly reduces the overall frequency of infections. Respiratory syncytial virus (RSV), the most common respiratory pathogen in infants, involves recurrent wheezing and has a pathogenic mechanism related to airway structural damage. Purpose: This study aimed to investigate whether breastfeeding has a beneficial effect against RSV-induced respiratory infection compared to formula feeding among infants in Korea. Methods: We retrospectively reviewed the medical records of infants under 1 year of age who were admitted with RSV infection between January 2016 and February 2018 at the department of pediatrics of 4 hospitals. We investigated the differences in clinical parameters such as cyanosis, chest retraction, combined infection, fever duration, oxygen use, oxygen therapy duration, intensive care unit (ICU) admission, and corticosteroid treatment of exclusive breast milk feeding (BMF), artificial milk formula fed (AMF), and mixed feeding (MF) groups. Results: Among the 411 infants included in our study, 94, 161, and 156 were included in the BMF, MF, and AMF groups, respectively. The rates of oxygen therapy were significantly different among the BMF (4.3%), MF (8.1%), and AMF (13.5 %) groups (P=0.042). The odds ratios (ORs) for oxygen therapy was significantly higher in the AMF group than in the BMF group (adjusted OR, 3.807; 95% confidence interval, 1.22-11.90; P=0.021). The ICU admission rate of the BMF group (1.1%) was lower than that of the MF (3.5%) and AMF (4.5%) groups; however, the dissimilarity was not statistically significant (P=0.338). Conclusion: The severity of RSV infection requiring oxygen therapy was lower in the BMF than the AMF group. This protective role of human milk on RSV infection might decrease the need for oxygen therapy suggesting less airway damage.

Nitro oxide in human cytomegalovirus replication and gene expression

  • Lee, Jee-Yeon;Lee, Chan-Hee
    • Journal of Microbiology
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    • 제35권2호
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    • pp.152-157
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    • 1997
  • Infection of human fibroblast (HF) cells with human cytomegalovirus (HCMV) result in changes in the intracellular level of second messengers. Since nitric oxide (NO) production has been known to be related with other second messengers, it is probable that HCMV infection of HF cells may involve NO. To test this possibility, the amount of NO was measured following ogenous addition of NO generators such as sodium nitroprusside (SNP) or S-nitroso-N-a-cetylpenicillamine (SNAP) immediately after HCMV infection, however, inhibited virus multiplication. Furthermore, immunoblot experiment using monoclonal antibody to HCMV major immediate early (MIE) proteins or CAT assay using pCMVIE/CAT (plasmid containing CAT gene driven by HCMV MIE promoter) revealed that SNP or SNAP blocked the MIE gene expression. SNP was more effective than SNAP in hibiting HCMV multiplication or MIE gene expression. SNP produced more NO than SNAP in inhibiting HCMV multiplication or MIE gene expression. SNP produced more NO than SNAP. Although the mechanism for the inhibition of HCMV multiplication and MIE gene expression by NO is still elusive some correlation with NO-mediated inhibition of HCMV-induced increase in cytosolic free Ca$\^$2+/ concentration ([Ca$\^$2+/]) was observed. The increase of [Ca$\^$2+/] following HCMV infection was inhibited by SNP, and less effectively by SNAP. Raising [Ca$\^$2+/ with bromo-A23187 partially reversed the SNP block of MIE gene expression. Thus, there appear to e some relationships among NO. [Ca$\^$2+/], and HCMV MIE gene expression.

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Mycobacterium tuberculosis-induced expression of granulocyte-macrophage colony stimulating factor is mediated by PI3-K/MEK1/p38 MAPK signaling pathway

  • Cho, Jang-Eun;Park, Sangjung;Lee, Hyeyoung;Cho, Sang-Nae;Kim, Yoon Suk
    • BMB Reports
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    • 제46권4호
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    • pp.213-218
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    • 2013
  • Members of the colony stimulating factor cytokine family play important roles in macrophage activation and recruitment to inflammatory lesions. Among them, granulocyte-macrophage colony stimulating factor (GM-CSF) is known to be associated with immune response to mycobacterial infection. However, the mechanism through which Mycobacterium tuberculosis (MTB) affects the expression of GM-CSF is poorly understood. Using PMA-differentiated THP-1 cells, we found that MTB infection increased GM-CSF mRNA expression in a dose-dependent manner. Induction of GM-CSF mRNA expression peaked 6 h after infection, declining gradually thereafter and returning to its basal levels at 72 h. Secretion of GM-CSF protein was also elevated by MTB infection. The increase in mRNA expression and protein secretion of GM-CSF caused by MTB was inhibited in cells treated with inhibitors of p38 MAPK, mitogen-activated protein kinase kinase (MEK-1), and PI3-K. These results suggest that up-regulation of GM-CSF by MTB is mediated via the PI3-K/MEK1/p38 MAPK-associated signaling pathway.

Distinct Molecular Mechanisms Characterizing Pathogenesis of SARS-CoV-2

  • Lee, Su Jin;Kim, Yu-Jin;Ahn, Dae-Gyun
    • Journal of Microbiology and Biotechnology
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    • 제32권9호
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    • pp.1073-1085
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    • 2022
  • The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) pandemic has continued for over 2 years, following the outbreak of coronavirus-19 (COVID-19) in 2019. It has resulted in enormous casualties and severe economic crises. The rapid development of vaccines and therapeutics against SARS-CoV-2 has helped slow the spread. In the meantime, various mutations in the SARS-CoV-2 have emerged to evade current vaccines and therapeutics. A better understanding of SARS-CoV-2 pathogenesis is a prerequisite for developing efficient, advanced vaccines and therapeutics. Since the outbreak of COVID-19, a tremendous amount of research has been conducted to unveil SARS-CoV-2 pathogenesis, from clinical observations to biochemical analysis at the molecular level upon viral infection. In this review, we discuss the molecular mechanisms of SARS-CoV-2 propagation and pathogenesis, with an update on recent advances.

돼지호흡기복합증후군(Porcine respiratory disease complex, PRDC)에 대한 발생상황의 분석 및 cytokine의 변화 (Prevalence and Expression Pattern of Cytokines in Porcine Respiratory Disease Complex (PRDC))

  • 이경현;송재찬
    • 생명과학회지
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    • 제24권10호
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    • pp.1118-1124
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    • 2014
  • 국내에서 발생하는 돼지호흡기복합증후군(Porcine respiratory disease complex, PRDC)의 발생 상황 및 원인체의 검출 방법의 비교와 PRDC에서 cytokine의 발현변화 여부를 확인하기 위해서 481건의 시료에 대해 PRDC 발생상황을 조사하였다. 총 481건 중 단독감염은 113건(23.5%), 2종 이상의 원인체에 의한 발병이 348(72.3%)건으로 나타났다. PRDC 발생상황을 주령별로 분석한 결과, 총 348건에서 3주령에서 10주령미만의 돼지에서 258건(74.1%)으로 가장 많이 나타났다. PRDC의 주 원인체로 알려진 PRRSV, PCV2, SIV에 대한 감별진단을 위해 면역조직화학염색법(IHC)과 PCR에 의한 검출을 원인체 검출을 비교한 결과, 결과 PCR 방법이 IHC보다 원인균인 PRRSV, PCV-2의 검출에 효과적인 것으로 나타났으며 이러한 결과를 근거로 PRDC를 유발하는 원인체에 대해서는 임상적으로는 PCV-2는 감염되더라도 병리소견을 발현하지 않는 예가 있어 임상증상을 나타내는 PRDC의 주요 원인체는 PRRSV로 확인되었다. PRDC로 진단된 시료 중 2종 및 3종의 혼합감염군을 대상으로 폐와 림프절에서 cytokine의 발현의 변화를 조사한 결과에서는, IL-6을 제외한 조사된 모든 cytokine들이 2종 및 3종 복합 감염군에서 대조군에 비해 감소되었다.

Possible Mechanism Underlying the Antiherpetic Activity of a Proteoglycan Isolated from the Mycelia of Ganoderma lucidum in Vitro

  • Li, Zubing;Liu, Jing;Zhao, Yifang
    • BMB Reports
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    • 제38권1호
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    • pp.34-40
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    • 2005
  • GLPG (Ganoderma lucidum proteoglycan) was a bioactive fraction obtained by the liquid fermentation of the mycelia of Ganoderma lucidum, EtOH precipitation, and DEAE-cellulose column chromatography. GLPG was a proteoglycan with a carbohydrate: protein ratio of 10.4: 1. Its antiviral activities against herpes simplex virus type 1 (HSV-1) and type 2 (HSV-2) were investigated using a cytopathic inhibition assay. GLPG inhibited cell death in a dose-dependent manner in HSV-infected cells. In addition, it had no cytotoxic effect even at 2 mg/ml. In order to study the mode of action of the antiviral activity of GLPG, cells were treated with GLPG before, during, and after infection, and viral titer in the supernatant of cell culture 48 h post-infection was determined using a $TCID_{50}$ assay. The antiviral effects of GLPG were more remarkable before viral treatment than after treatment. Although the precise mechanism has yet to be defined, our work suggests that GLPG inhibits viral replication by interfering with the early events of viral adsorption and entry into target cells. Thus, this proteoglycan appears to be a candidate anti-HSV agent.

Role of HIV Vpr as a Regulator of Apoptosis and an Effector on Bystander Cells

  • Moon, Ho Suck;Yang, Joo-Sung
    • Molecules and Cells
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    • 제21권1호
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    • pp.7-20
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    • 2006
  • The major event in human immunodeficiency virus type 1 (HIV-1) infection is the death of many cells related to host immune response. The demise of these cells is normally explained by cell suicide mechanism, apoptosis. Interestingly, the decrease in the number of immune cells, such as non-CD4+ cells as well as CD4+ T cells, in HIV infection usually occurs in uninfected bystander cells, not in directly infected cells. It has, therefore, been suggested that several soluble factors, including viral protein R (Vpr), are released from the infected cells and induce the death of bystander cells. Some studies show that Vpr interacts directly with adenine nucleotide translocator (ANT) to induce mitochondrial membrane permeabilization (MMP). The MMP results in release of some apoptogenic factors such as cytochrome-c (cyt-c) and apoptosis-inducing factor (AIF). Vpr also has indirect effect on mitochondria through enhancing the level of caspase-9 transcription and suppressing nuclear factor-kappa B (NF-${\kappa}B$). The involvement of p53 in Vpr-induced apoptosis remains to be studied. On the other hand, low level of Vpr expression has anti-apoptotic effect, whereas it's high level of expression induces apoptosis. Extracellular Vpr also exhibits cytotoxicity to uninfected bystander cells through apoptotic or necrotic mechanism. The facts that Vpr has cytotoxic effect on both infected cells and bystander cells, and that it exhibits both proand anti-apoptotic activity may explain its role in viral survival and disease progression.

Genome Wide Analysis of the Potato Soft Rot Pathogen Pectobacterium carotovorum Strain ICMP 5702 to Predict Novel Insights into Its Genetic Features

  • Mallick, Tista;Mishra, Rukmini;Mohanty, Sasmita;Joshi, Raj Kumar
    • The Plant Pathology Journal
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    • 제38권2호
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    • pp.102-114
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    • 2022
  • Pectobacterium carotovorum subsp. carotovorum (Pcc) is a gram-negative, broad host range bacterial pathogen which causes soft rot disease in potatoes as well as other vegetables worldwide. While Pectobacterium infection relies on the production of major cell wall degrading enzymes, other virulence factors and the mechanism of genetic adaptation of this pathogen is not yet clear. In the present study, we have performed an in-depth genome-wide characterization of Pcc strain ICMP5702 isolated from potato and compared it with other pathogenic bacteria from the Pectobacterium genus to identify key virulent determinants. The draft genome of Pcc ICMP5702 contains 4,774,457 bp with a G + C content of 51.90% and 4,520 open reading frames. Genome annotation revealed prominent genes encoding key virulence factors such as plant cell wall degrading enzymes, flagella-based motility, phage proteins, cell membrane structures, and secretion systems. Whereas, a majority of determinants were conserved among the Pectobacterium strains, few notable genes encoding AvrE-family type III secretion system effectors, pectate lyase and metalloprotease in addition to the CRISPR-Cas based adaptive immune system were uniquely represented. Overall, the information generated through this study will contribute to decipher the mechanism of infection and adaptive immunity in Pcc.

Negative evidence on the transgenerational inheritance of defense priming in Arabidopsis thaliana

  • Yun, Se-Hun;Noh, Bosl;Noh, Yoo-Sun
    • BMB Reports
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    • 제55권7호
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    • pp.342-347
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    • 2022
  • Defense priming allows plants to enhance their immune responses to subsequent pathogen challenges. Recent reports suggested that acquired resistances in parental generation can be inherited into descendants. Although epigenetic mechanisms are plausible tools enabling the transmission of information or phenotypic traits induced by environmental cues across generations, the mechanism for the transgenerational inheritance of defense priming in plants has yet to be elucidated. With the initial aim to elucidate an epigenetic mechanism for the defense priming in plants, we reassessed the transgenerational inheritance of plant defense, however, could not observe any evidence supporting it. By using the same dipping method with previous reports, Arabidopsis was exposed repeatedly to Pseudomonas syringae pv tomato DC3000 (Pst DC3000) during vegetative or reproductive stages. Irrespective of the developmental stages of parental plants that received pathogen infection, the descendants did not exhibit primed resistance phenotypes, defense marker gene (PR1) expression, or elevated histone acetylation within PR1 chromatin. In assays using the pressure-infiltration method for infection, we obtained the same results as above. Thus, our results suggest that the previous observations on the transgenerational inheritance of defense priming in plants should be more extensively and carefully reassessed.