• Tuberculosis and Respiratory Diseases
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• 제73권4호
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• pp.219-223
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• 2012

Background: We investigated the prevalence of latent tuberculosis infection (LTBI) among medical students in South Korea. Methods: Students from one medical school, who were in second- or third-year classes before clerkship course, were enrolled for three consecutive years in the study. A standard questionnaire was given to each participant, and tuberculin skin test (TST), QuantiFERON-TB GOLD In-Tube (QFT-GIT) assay, and chest radiography were performed. Results: A total of 153 participants were enrolled in the study. The mean age of the subjects was $21.9{\pm}0.9$ years, 105 (68.6%) were male, and 132 (86.3%) had been vaccinated with Bacille Calmette-Gu$\acute{e}$rin (BCG). Four students (2.6%) had a history of contact with tuberculosis (TB) patients during medical practice. No abnormal chest radiograph findings were found for any of the subjects. Of the 153 subjects, 23 (15.0%) tested positive for the TST, and 8 (5.2%) tested positive for the QFT-GIT. The agreement between the two tests was determined to be 0.34 using kappa coefficients. Of the four students who had a history of contact with TB patients, only one subject tested positive for both tests, and the other three students tested negative for both tests. Conclusion: A low prevalence of LTBI was found among medical students before clerkship course in South Korea.

• 보건행정학회지
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• 제23권4호
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• pp.349-357
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• 2013

Background: Although interferon-gamma release assay (IGRA) is now available alternatives to tuberculin skin test (TST) for detection of latent tuberculosis infection (LTBI), the cost of IGRA test is much higher than TST. So economic analysis of LTBI screening strategies have been done in many countries, but there are few reports in Korea. This study examined cost analysis of LTBI screening strategies in Korea. Methods: The economic outcomes were evaluated by five strategies. These were 1) TST alone, 2) IGRA alone, 3) combination of TST and IGRA (TST followed by IGRA) and 4) no testing no prevention, 5) no testing all prevention. Last two strategies were added to compare with three main LTBI screening strategies. Decision analysis model were used to perform economic analysis. A cohort study of Korean Institute of Tuberculosis and the data of published literatures were used to estimate the cost analysis. Results: In a base-case scenario which was assumed that TST specificity was 80%, TST alone was the least expensive strategy. In a alternative scenario which was assumed that TST specificity was 97%, the combination of TST and IGRA was the least expensive strategy. Sensitivity analysis shows that patients adherent rate to LTBI treatment, TST sensitivity, IGRA sensitivity and IGRA specificity did not have a significant impact on the outcomes. Conclusion: In Korea, for the diagnosis of LTBI at the time of child and adolescent, TST alone reduces medical costs compared with IGRA alone or combination of TST and IGRA.

• Journal of Ginseng Research
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• 제44권4호
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• pp.593-602
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• 2020

Background: Heat stress orchestrates neurodegenerative disorders and results in the formation of reactive oxygen species that leads to cell death. Although the immunomodulatory effects of ginseng are well studied, the mechanism by which ginseng alleviates heat stress in the brain remains elusive. Methods: Rats were exposed to intermittent heat stress for 6 months, and brain samples were examined to elucidate survival and antiinflammatory effect after Korean Red Ginseng (KRG) treatment. Results: Intermittent long-term heat stress (ILTHS) upregulated the expression of cyclooxygenase 2 and inducible nitric oxide synthase, increasing infiltration of inflammatory cells (hematoxylin and eosin staining) and the level of proinflammatory cytokines [tumor necrosis factor α, interferon gamma (IFN-γ), interleukin (IL)-1β, IL-6], leading to cell death (terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling assay) and elevated markers of oxidative stress damage (myeloperoxidase and malondialdehyde), resulting in the downregulation of antiapoptotic markers (Bcl-2 and Bcl-x_L) and expression of estrogen receptor beta and brain-derived neurotrophic factor, key factors in regulating neuronal cell survival. In contrast, KRG mitigated ILTHS-induced release of proinflammatory mediators, upregulated the mRNA level of the antiinflammatory cytokine IL-10, and increased myeloperoxidase and malondialdehyde levels. In addition, KRG significantly decreased the expression of the proapoptotic marker (Bax), did not affect caspase-3 expression, but increased the expression of antiapoptotic markers (Bcl-2 and Bcl-x_L). Furthermore, KRG significantly activated the expression of both estrogen receptor beta and brain-derived neurotrophic factor. Conclusion: ILTHS induced oxidative stress responses and inflammatory molecules, which can lead to impaired neurogenesis and ultimately neuronal death, whereas, KRG, being the antioxidant, inhibited neuronal damage and increased cell viability.

• The Korean Journal of Physiology and Pharmacology
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• 제14권4호
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• pp.235-240
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• 2010

Toll-like receptors (TLRs) functionally expressed in salivary epithelial cells, but their roles remain elusive. Among TLRs family, TLR3 is activated by dsRNA, a byproduct of viral infection. The aim of this study was to investigate the role of TLR3 in the inflammatory immune responses using HSG cells. Reverse transcriptase-polymerase chain reaction (RT-PCR), real-time PCR and ELISA were performed to identify expression of TLRs and TLR3-mediated chemokine inductions. The chemotaxis assay of activated T lymphocytes was also performed. Treatment of HSG cells with polyinosinic: polycytidylic acid (poly(I:C)) significantly increased interferon-$\gamma$-inducible protein 10 (IP-10), interferoninducible T-cell $\alpha$ chemoattractant (I-TAC), and regulated on activation, normal T-cells expressed and secreted (RANTES) gene expressions in a concentration-dependent manner. Anti-TLR3 antibody blocked the increases of IP-10 and I-TAC genes. Poly(I:C)-induced increases of IP-10 and I-TAC were also confirmed at protein levels from cell lysates, but their release into extracellular medium was detected only in IP-10. We found that the culture media from HSG cells stimulated with poly(I:C) significantly increases T lymphocyte migration. Our results suggest that TLR3 plays an important role in chemokine induction, particularly IP-10, in salivary epithelial cells.

• 대한한방내과학회지
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• 제44권5호
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• pp.1011-1016
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• 2023

We have experienced a case in which herbal medicine was administered to treat drug-induced liver damage and would like to introduce it. A 49-year-old man exhibited a positive result in the interferon-gamma release assay. He had never suffered from tuberculosis in the past, and the route and time of infection could not be confirmed. He had no respiratory or systemic symptoms suggestive of active tuberculosis, and a chest X-ray examination showed no active lung lesions, so he was diagnosed with latent tuberculosis infection. He was confirmed to be within the normal range in the liver function test, renal function test, and complete blood cell count test, and started taking rifampin (600 mg qd). In the screening test performed on the 19th day of taking the drug, other test items were normal, but alanine aminotransferase (ALT) increased to 50 U/L (reference value: 4-40 U/L). In a test performed on the 29th day of taking the drug, ALT was clearly elevated to 102 U/L. Ursodeoxycholic acid and Injinho-tang were taken together with rifampin, and the patient's progress was observed. In a test performed 14 days later, ALT decreased to 26 U/L, within the normal range. It is presumed that Injinho-tang may have partially contributed to alleviating liver damage in this case.

• Journal of Acupuncture Research
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• 제19권6호
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• pp.111-124
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• 2002

A line of study reported that electroacupuncture(EA) modulate natural killer cell(NK Cell) activities. One report suggested that EA enhanced splenic interferon-gamma($IFN-{\gamma}$), interleukin-2(IL-2), and NK cell activity in Sprague-Dawley rats. Another study suggested that $IFN-{\gamma}$ mediates the up-regulation of NK cell activity, and endogenous ${\beta}$-endorphin secretion also play a role in the up-regulation of NK cell activity induced by EA stimulation. In order to better understand the molecular regulation underlying the activation of NK cell induced by EA, we have utilized cDNA microarray to elucidate how EA alters program of gene expression of spleen in rats. First, we divided three groups, group I was EA group treated with EA in restriction holder, group II was sham group with only holder stress, and last group III was control group with no treatment. We measured NK cell activity after EA stimulation three times for 2 days using $^{51}Cr$ release assay. Second, Biotin-labeled cDNA probes synthesized from EA group and sham group, were competitively hybridized to the microarray that contained variable genes. Such high-throughput screening has identified a number of EA-responsive gene candidates. Of these, we found that EA induced a subset of genes of genes that functionally could modulatory effects on NK cell activity. Genes(vascular cell adhesion molecule-1, protein-tyrosine kinase, CD94 mRNA) related to boost NK cell activity, were increased by EA And, genes(protein-tyrosine-phospatase mRNA, protein-tyrosine phosphatase(SHP-1) mRNA) related to inhibit NK cell activity, were decreased by EA. These EA-responsive genes may provide key insights from which to understand mechanisms of activation of NK cell induced by EA.

• Tuberculosis and Respiratory Diseases
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• 제75권1호
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• pp.18-24
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• 2013

Background: We investigated the prevalence of latent tuberculosis infection (LTBI) among the health care workers (HCWs) and analyzed its risk factors in South Korea. Methods: A standard questionnaire regarding the baseline demographics and risk factors for LTBI was given to each participant and tuberculin skin test (TST), QuantiFERON-TB GOLD In-Tube (QFT-GIT) assay, and chest radiography were performed. Results: A total of 493 participants, 152 (30.8%) doctors and 341 (69.2%) nurses were enrolled in eight tertiary referral hospitals. The mean age of the subjects was 30.6 years old, and 383 (77.7%) were female. Of the 152 doctors, 63 (41.4%) and 36 (23.7%) were positive by TST and by QTF-GIT, respectively, and among the 341 nurses, 119 (34.9%) and 49 (14.4%) had positive TST and QFT-GIT results, respectively. Overall, the agreement between the two tests was 0.22 by the chance corrected proportional agreement rate (kappa coefficient) in 493 subjects. Experience of working in tuberculosis (TB)-related departments was significantly associated with positive LTBI test results by QFT-GIT assay, not by TST. In multivariate analysis, only age was independently associated with increased risk of a positive TST result, while age and experience of working in TB-related departments (odds ratio, 2.29; 95% confidence interval, 1.01-5.12) were independently associated with increased risk of a positive QFT-GIT result. Conclusion: A high prevalence of LTBI was found among South Korean HCWs. Considering the association between the experience of working in TB-related departments and high risk of LTBI, QFT-GIT may be a better diagnostic test for LTBI than TST in HCWs.

• Pediatric Infection and Vaccine
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• 제23권2호
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• pp.94-101
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• 2016

목적: 대학병원에 근무하던 중 활동성 폐결핵으로 진단된 전공의에게 노출된 의료종사자들에 대하여 실시한 접촉자 조사의 결과를 보고한다. 방법: 활동성 폐결핵 환자와 밀접한 접촉을 한 사람(접촉자) 101명 중 89명이 접촉자 조사에 응하여 조사를 받았다. 1차 접촉자 조사는 지표환자의 증상 개시 후 30일경에, 2차 조사는 1차 조사 10주 후에 기침, 발열, 인후통, 체중 감소와 같은 임상증상 확인 및 단순흉부촬영과 함께 결핵반응검사(Tuberculin skin test, TST)/QuantiFERON-TB Gold (QFT-G) 2단계 검사법을 시행하였다. 결과: 1차 TST 양성자는 34명(38.2%)이었고, TST 양성자 중 35세 이하 접촉자에서 시행한 QFT-G 양성률은 37.5% (6/16)이었다. 1차 TST 음성 대상자 41명에게서 시행한 2차 TST에서 17명(41.5%)이 양전을 보였고 그들 중 시행한 QFT-G 검사에서 3명(17.6%)이 양성이었다. 활동성 결핵으로 진단된 접촉자는 없었으며 지표환자에 노출되어 발생한 결핵 전파율은 2단계 검사법으로는 7.3% (3/41)였고, TST 진단법으로는 41.5% (17/41)였다. 결론: 국내에서 처음 보고되는 병원 내 결핵 접촉자 조사 연구로서 LTBI 발생률이 그 진단 기법에 따라 달랐으며 따라서 앞으로 발생할 수 있는 의료종사자들에 대한 병원 내 결핵 접촉자 조사를 위해 조직적이고 실용적인 가이드라인이 필요할 것이다.

• International Journal of Oral Biology
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• 제33권4호
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• pp.163-177
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• 2008

Periodontal disease, a form of chronic inflammatory bacterial infectious disease, is known to be a risk factor for cardiovascular disease (CVD). Porphyromonas gingivalis has been implicated in periodontal disease and widely studied for its role in the pathogenesis of CVD. A previous study demonstrating that periodontopathic P. gingivalis is involved in CVD showed that invasion of endothelial cells by the bacterium is accompanied by an increase in cytokine production, which may result in vascular atherosclerotic changes. The present study was performed in order to further elucidate the role of P. gingivalis in the process of atherosclerosis and CVD. For this purpose, invasion of human aortic smooth muscle cells (HASMC) by P. gingivalis 381 and its isogenic mutants of KDP150 ($fimA^-$), CW120 ($ppk^-$) and KS7 ($relA^-$) was assessed using a metronidazole protection assay. Wild type P. gingivalis invaded HASMCs with an efficiency of 0.12%. In contrast, KDP150 failed to demonstrate any invasive ability. CW120 and KS7 showed relatively higher invasion efficiencies, but results for these variants were still negligible when compared to the wild type invasiveness. These results suggest that fimbriae are required for invasion and that energy metabolism in association with regulatory genes involved in stress and stringent response may also be important for this process. ELISA assays revealed that the invasive P. gingivalis 381 increased production of the proinflammatory cytokine interleukin (IL)-$1{\beta}$ and the chemotactic cytokines (chemokine) IL (interleukin)-8 and monocyte chemotactic (MCP) protein-1 during the 30-90 min incubation periods (P<0.05). Expression of RANTES (regulation upon activation, normal T cell expressed and secreted) and Toll-like receptor (TLR)-4, a pattern recognition receptor (PRR), was increased in HASMCs infected with P. gingivalis 381 by RT-PCR analysis. P. gingivalis infection did not alter interferon-$\gamma$-inducible protein-10 expression in HASMCs. HASMC nonspecific necrosis and apoptotic cell death were measured by lactate dehydrogenase (LDH) and caspase activity assays, respectively. LDH release from HASMCs and HAMC caspase activity were significantly higher after a 90 min incubation with P. gingivalis 381. Taken together, P. gingivalis invasion of HASMCs induces inflammatory cytokine production, apoptotic cell death, and expression of TLR-4, a PRR which may react with the bacterial molecules and induce the expression of the chemokines IL-8, MCP-1 and RANTES. Overall, these results suggest that invasive P. gingivalis may participate in the pathogenesis of atherosclerosis, leading to CVD.

• Journal of Korean Medical Science
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• 제33권47호
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• pp.292.1-292.10
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• 2018

Background: We investigated the incidence of active tuberculosis among patients with inflammatory bowel disease (IBD) treated with tumor necrosis factor (TNF) inhibitors, with or without latent tuberculosis infection (LTBI). Methods: The study was performed at a Korean tertiary referral center between January 2011 and June 2017. In total, 740 patients with IBD who underwent LTBI screening tests and were followed-up for ${\geq}1$ year after TNF inhibitor treatment initiation were enrolled. LTBI was detected on the basis of tuberculin skin test results, interferon-gamma release assay results, chest X-ray findings, and previous tuberculosis treatment history. The patients were classified into LTBI (n = 84) or non-LTBI (n = 656) group. The risk of developing tuberculosis in each group was assessed on the basis of standardized incidence ratio (SIR) and 95% confidence interval (CI) for active tuberculosis. Results: Mean patient age was 33.1 years, and patients with Crohn's disease were predominant (80.7%). Within 1 year after the initiation of TNF inhibitor treatment, 1 patient in the LTBI group (1/84; 1.2%) and 7 patients in the non-LTBI group (7/656; 1.1%) developed active tuberculosis. The overall 1-year incidence of tuberculosis among the patients was significantly higher than that among the general population (SIR, 14.0; 95% CI, 7.0-28.0), and SIR was not affected by LTBI status (LTBI group: 14.5, 95% CI, 2.0-102.6; non-LTBI group: 14.0, 95% CI, 6.7-29.4). Conclusion: Patients with IBD undergoing TNF inhibitor treatment showed a higher 1-year incidence of tuberculosis than the general population irrespective of LTBI status.