• Title/Summary/Keyword: Immune deficiency

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Dosage Adjustment of Zinc (아연의 투여용량설정)

  • Jung, So Young;Shin, Wan Gyoon;Kim, Ho Soon;Cho, Nam Choon
    • Korean Journal of Clinical Pharmacy
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    • v.7 no.2
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    • pp.64-66
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    • 1997
  • Zinc is employed in body cell growth and immune function. Zinc deficiency causes growth retardation, night blindness, delay of wound healing, skin disorders, alopecia, et al. Pharmacokinetic study of zinc in Korean has not yet been proceeded to apply to patient. In this study, we investigated to adjust zinc dosage for maintaining constant zinc optimum serum level. Five NPO inpatients (3 males, 2 females) in Seoul National University of Hospital were evaluated, retrospectively. Zinc was mixed with parenteral nutrition solution and administrated intravenously in 24 hour-continuous infusion, and zinc dosage range was 0.17-0.45 mg/kg/day. AUC to zinc dose (AUC/Dose) was $2.421\pm1.007\;kg{\cdot}min/ml.$ 0.5 mg/kg/day zinc administration may achieve the plasma zinc concentration of $120\;{\mu}g/dl.$(Kor. J. Clin. Pharm. 1997; 7: 64-66)

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TRIF Deficiency does not Affect Severity of Ovalbumin-induced Airway Inflammation in Mice

  • Kim, Tae-Hyoun;Kim, Dong-Jae;Park, Jae-Hak;Park, Jong-Hwan
    • IMMUNE NETWORK
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    • v.14 no.5
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    • pp.249-254
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    • 2014
  • Allergic asthma is a chronic pulmonary inflammatory disease characterized by reversible airway obstruction, hyperresponsiveness and eosinophils infiltration. Toll-like receptors (TLRs) signaling are closely associated with asthma and have emerged as a novel therapeutic target in allergic disease. The functions of TLR3 and TLR4 in allergic airway inflammation have been studied; however, the precise role of TIR-domain-containing adapter-inducing interferon-${\beta}$ (TRIF), the adaptor molecule for both TLR3 and TLR4, is not yet fully understood. To investigate this, we developed a mouse model of OVA-induced allergic airway inflammation and compared the severity of allergic airway inflammation in WT and $TRIF^-/^-$ mice. Histopathological assessment revealed that the severity of inflammation in airway inflammation in TRIF-deficient mice was comparable to that in WT mice. The total number of cells recovered from bronchoalveolar lavage fluid did not differ between WT and TRIF-deficient mice. Moreover, TRIF deficiency did not affect Th1 and Th2 cytokine production in lung tissue nor the level of serum OVA-specific IgE, $IgG_1$ and $IgG_{2c}$. These findings suggest that TRIF-mediated signaling may not be critical for the development of allergic airway inflammation.

Sepsis Mortality in CIITA Deficient Mice is Associated with Excessive Release of High-mobility Group Box 1

  • Kim, Ji-Young;Kim, Ju-Hyun;Seo, Jae-Nam;Oh, Kwon-Ik
    • IMMUNE NETWORK
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    • v.8 no.2
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    • pp.39-45
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    • 2008
  • Background: Down regulation of major histocompatibility complex class II transactivator (CIITA) has been identified as a major factor of immunosuppression in sepsis and the level of CIITA expression inversely correlates with the degree of severity. However, it has not been fully elucidated whether the lower expression of CIITA is a cause of disease process or a just associated sign. Here we determined whether the CIITA deficiency decreased survival rate using murine sepsis model. Methods: Major histocompatibility complex class II (MHC-II) deficient, CIITA deficient and wild type B6 mice were subjected to cecal ligation puncture (CLP) surgery. CIITA and recombination activation gene (RAG)-1 double deficient mice were generated to test the role of lymphocytes in CIITA-associated sepsis progression. Results: Sepsis mortality was enhanced in CIITA deficient mice, not by impaired bacterial clearance resulted from CD4 T cell depletion, but hyper-inflammatory response such as excessive release of a pro-inflammatory cytokine, high-mobility group box 1 (HMGB1). Conclusion: Our results demonstrate that CIITA deficiency affects the course of sepsis via the unexpected function of CIITA, regulation of cytokine release.

Antibody response to pneumococcal vaccination in children with chronic or recurrent rhinosinusitis

  • Baek, Ji Hyeon;Seo, Hyun Kyong;Jee, Hye Mi;Shin, Youn Ho;Han, Man Yong;Oh, Eun Sang;Lee, Hyun Ju;Kim, Kyung Hyo
    • Clinical and Experimental Pediatrics
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    • v.56 no.7
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    • pp.286-290
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    • 2013
  • Purpose: Although chronic and recurrent rhinosinusitis is prevalent in children, little is known about its causes. Here, we investigated the humoral immunity in children with chronic or recurrent rhinosinusitis. Methods: We examined 16 children attending the outpatient clinic at the CHA Bundang Medical Center including 11 boys and 5 girls, aged 3-11 years (mean age, 5.6 years), who had rhinosinusitis for >3 months or >3 times per year. The complete blood count with differential and total serum concentrations of Immunoglobulin (Ig) E, IgA, IgD, IgM, IgG, and IgG subclasses ($IgG_1$, $IgG_2$, $IgG_3$, and $IgG_4$) of all children were measured. All subjects received 23-polysaccharide pneumococcal vaccination (PPV), and the levels of antibodies to 5 serologic types (4, 6B, 14, 18C, and 23F) of pneumococcal capsular polysaccharide antigens were measured before and after vaccination. Post-PPV antibody titers ${\geq}0.35{\mu}g/mL$ or with a ${\geq}4$-fold increase were considered as positive responses. Results: The titers of IgG, IgA, IgD, and IgM were within normal range in all 16 children, whereas the total IgE concentration was higher than normal in 2 children. $IgG_1$ deficiency was observed in 1 patient and $IgG_3$ deficiency in 3. After PPV, 1 patient failed to respond to all 5 serologic types, 2 failed to respond to 4 serologic types, and 2 failed to respond to 3 serologic types. Conclusion: Clinicians should consider the evaluation of humoral immune functions in children with chronic or recurrent rhinosinusitis who do not respond to prolonged antibiotic treatment.

Anti-proliferative Activity of T-bet

  • Oh, Yeon Ji;Shin, Ji Hyun;Won, Hee Yeon;Hwang, Eun Sook
    • IMMUNE NETWORK
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    • v.15 no.4
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    • pp.199-205
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    • 2015
  • T-bet is a critical transcription factor that regulates differentiation of Th1 cells from $CD4^+$ precursor cells. Since T-bet directly binds to the promoter of the IFN-${\gamma}$ gene and activates its transcription, T-bet deficiency impairs IFN-${\gamma}$ production in Th1 cells. Interestingly, T-bet-deficient Th cells also display substantially augmented the production of IL-2, a T cell growth factor. Exogenous expression of T-bet in T-bet deficient Th cells rescued the IFN-${\gamma}$ production and suppressed IL-2 expression. IFN-${\gamma}$ and IL-2 reciprocally regulate Th cell proliferation following TCR stimulation. Therefore, we examined the effect of T-bet on Th cell proliferation and found that T-bet deficiency significantly enhanced Th cell proliferation under non-skewing, Th1-skewing, and Th2-skewing conditions. By using IFN-${\gamma}$-null mice to eliminate the anti-proliferative effect of IFN-${\gamma}$, T-bet deficiency still enhanced Th cell proliferation under both Th1- and Th2-skewing conditions. Since the anti-proliferative activity of T-bet may be influenced by IL-2 suppression in Th cells, we examined whether T-bet modulates IL-2-independent cell proliferation in a non-T cell population. We demonstrated that T-bet expression induced by ecdysone treatment in human embryonic kidney (HEK) cells increased IFN-${\gamma}$ promoter activity in a dose dependent manner, and sustained T-bet expression considerably decreased cell proliferation in HEK cells. Although the molecular mechanisms underlying anti-proliferative activity of T-bet remain to be elucidated, T-bet may directly suppress cell proliferation in an IFN-${\gamma}$- or an IL-2-independent manner.

EXPERIMENTAL STUDY ABOUT ESTROGEN EFFECT OF BONE MARROW AND SPLEEN OF OVARIECTOMIZED RATS (에스트로겐 투여가 난소절제 백서의 골수와 비장에 미치는 효과에 관한 실험적 연구)

  • Park, Young-Sun;Lee, Jae-Hun
    • Maxillofacial Plastic and Reconstructive Surgery
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    • v.18 no.3
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    • pp.515-527
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    • 1996
  • The most serious problem resulting from estrogen deficiency induce osteo porosis. Recently, they make efforts to inquire a relation between hematopoietic organ and bone loss due to estrogen deficiency. Estrogen have an effect on growth and formation of skeletal system, and inhibit bone resorption under the influence of osteoblast and osteoclast, and basically inhibit the increase of hematopoietic progenitor and immune factor connected with bone resorption and prevent the osteoid formation. The purpose of this article was to observe the change of spleen and effect on hematopoietic function following estrogen administration. In this study, female rats of 150g weight was ovariectomized, after 70 days, experimental group was injected estrogen at interval of a week and sacrificed on 1, 2, 3, 4, 6 weeks. Control group was sacrificed after ovariectomy on 11, 12, 13, 14, 16 weeks without estrogen injection, and normal rats were sacrificed for harvest of spleen and femur. Paraffin sections and H&E stain was performed, and observed under light microscope. The obtained results were as follows. 1. From 11 to 12 weeks at bone marrow of control group, hematopoietic cells were decreased in comparison with normal group, and lipid infiltration was seen, and irregular bone remodelling was seen after 13 weeks. From 14 to 16 weeks, there were more decreased hematopoietic cells and lipid degeneration, and lipid degeneration of hematopoietic cells appeared. 2. All the bone marrow of experimental group, the structure of hematopoietic cells with decreased lipid infiltration was recovered from 2 weeks of estrogen adminstration and maintained to 6 weeks. 3. At spleen of control group, borders of white and red pulp was not well demarcated, and size of white pulp was decreased. 4. At spleen of experimental group, borders between white and red pulp have been well demarcated from 3 weeks of estrogen adminstration relatively, and white pulp was increased with distinct border. From above findings, we could regarded that estrogen deficiency due to ovariectomy influenced on hematopoietic cells of bone marrow and spleen, and histologic recovery of hematopoietic cells were observed after 3 weeks of estrogen adminstration even if it was not reach to normal group.

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C1qa deficiency in mice increases susceptibility to mouse hepatitis virus A59 infection

  • Kim, Han-Woong;Seo, Sun-Min;Kim, Jun-Young;Lee, Jae Hoon;Lee, Han-Woong;Choi, Yang-Kyu
    • Journal of Veterinary Science
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    • v.22 no.3
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    • pp.36.1-36.12
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    • 2021
  • Background: Mouse hepatitis virus (MHV) A59 is a highly infectious pathogen and starts in the respiratory tract and progresses to systemic infection in laboratory mice. The complement system is an important part of the host immune response to viral infection. It is not clear the role of the classical complement pathway in MHV infection. Objectives: The purpose of this study was to determine the importance of the classical pathway in coronavirus pathogenesis by comparing C1qa KO mice and wild-type mice. Methods: We generated a C1qa KO mouse using CRISPR/Cas9 technology and compared the susceptibility to MHV A59 infection between C1qa KO and wild-type mice. Histopathological and immunohistochemical changes, viral loads, and chemokine expressions in both mice were measured. Results: MHV A59-infected C1qa KO mice showed severe histopathological changes, such as hepatocellular necrosis and interstitial pneumonia, compared to MHV A59-infected wild-type mice. Virus copy numbers in the olfactory bulb, liver, and lungs of C1qa KO mice were significantly higher than those of wild-type mice. The increase in viral copy numbers in C1qa KO mice was consistent with the histopathologic changes in organs. These results indicate that C1qa deficiency enhances susceptibility to MHV A59 systemic infection in mice. In addition, this enhanced susceptibility effect is associated with dramatic elevations in spleen IFN-γ, MIP-1 α, and MCP-1 in C1qa KO mice. Conclusions: These data suggest that C1qa deficiency enhances susceptibility to MHV A59 systemic infection, and activation of the classical complement pathway may be important for protecting the host against MHV A59 infection.

A case of lethal kwashiorkor caused by feeding only with cereal grain (미음 수유만으로 발생한 치명적인 Kwashiorkor 1례)

  • Lee, Hyun Ju;Km, Kyung Hye;Park, Hye Jin;Lee, Kye Hyang;Lee, Gyeong Hoon;Choi, Eun Jin;Kim, Jin Kyung;Chung, Hai Lee;Kim, Woo Taek
    • Clinical and Experimental Pediatrics
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    • v.51 no.3
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    • pp.329-334
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    • 2008
  • Kwashiorkor is a syndrome of severe protein malnutrition, which manifests itself in hypoalbuminemia, diarrhea, dermatitis, and edema. It can be life-threatening due to associated immune deficiency and an increased susceptibility to infections. Kwashiorkor should be treated early with nutritional support and the control of infection. Dilated cardiomyopathy may develop during the treatment and in such cases a poor prognosis is expected. Kwashiorkor has been known as a common disease of poor countries. To date, in fact, there has been no report of kwashiorkor leading to death in technically advanced countries. We here report a fatal case of a baby girl admitted with kwashiorkor. She had been fed only with cereal grain mixed with juice, without any protein supplement, for 2 months. This diet was deficient not because of poverty, but due to the illiteracy of her parents. The patient suffered from diarrhea, whole body edema, hypothermia, and dermatitis. Laboratory findings revealed an immune-deficient state featuring leukopenia and decreased immunoglobulin. Blood and urine cultures revealed Alcaligenes Xylosoxidans growth. The patient was fed frequent small amounts of protein-containing formula and intravenous albumin and micronutrients were administered for nutritional support. She was also treated with intravenous immunoglobulin and antibiotics in order to control infection. Nevertheless, she developed dilated cardiomyopathy and multi-organ failure and died. We review this case in light of the literature.

Immunomodulatory Effects of an Extract from Pinus koraiensis Cone Peel in LP-BM5 Murine Leukemia Viruses-Induced Murine Acquired Immune Deficiency Syndrome (면역 결핍 동물모델에서 잣피 추출물의 면역조절 효과)

  • Kim, Seong Pil;Kwon, Han Ol;Ha, Yejin;Heo, Seok Hyun;Lee, Jeongmin
    • Journal of the Korean Society of Food Science and Nutrition
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    • v.46 no.9
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    • pp.1027-1034
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    • 2017
  • The immune system is a complex process within the body that protects against disease. Recently, many studies have attempted to discover immunomodulative compounds from natural sources. Pinus koraiensis (PK) cone shell is a by-product of PK. One of the major compounds of PK cone shell is dehydroabietic acid, which has bioactivity, including antiulcer and anti-inflammatory activities. Therefore, this study was performed to examine the immunomodulative effects of PK cone shell. The immunomodulatory effects of PK cone shell extracted with 20% ethanol (EtOH) in vivo were examined initially by measuring the natural killer (NK) cell activity, phagocytic activity, Th1/Th2 cytokines release, serum immunoglobulin, and T/B cell proliferation. The NK cell activity and phagocytic activity were increased significantly by a treatment with a 20% EtOH extract of PK cone shell. Th1 type cytokine and T cell proliferation increased and Th2 type cytokine, B cell proliferation and serum immunoglobulin A, G, and E decreased after a treatment with PK cone shell extract. The 20% EtOH extract of the PK cone shell normalized the unbalanced production of Th1/Th2 type cytokine. This suggests that a 20% EtOH extract of PK cone shell has great potential as a health food.

Association Study of Glutathione-S-Transferase M1/T1 Gene Polymorphism with Deficiency-Excess Differentiation-syndrome in Korean Bronchial Asthmatics (한국인 기관지 천식 환자에서 허설변증과 Glutathione-S-Transferase 유전자의 다형성 연구)

  • Yu, Seung-Ryeol;Jeong, Seung-Yeon;Jung, Ju-Ho;Kim, Jin-Ju;Jung, Sung-Ki
    • The Journal of Internal Korean Medicine
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    • v.28 no.3
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    • pp.453-463
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    • 2007
  • Backgrounds : Glutathione-s-transferase (GST) is a kind of phase II metabolism enzyme and plays an important role in the detoxification of various toxic chemicals. It was reported that the genetic polymorphism of GSTM1 and GSTT1 genes may be responsible for asthma development and susceptibility to allergy. Traditional oriental medicine uses a unique diagnostic technique. differentiation-syndrome. to analyze signs and symptoms of patients synthetically. Through differentiation-syndrome. asthma patients can be divided into two groups: the deficiency syndrome group (DSG) and the excess syndrome group (ESG). Objectives : The purpose of this study was to investigate the possible association of GST gene polymorphism with clinical phenotype by differentiation-syndrome of bronchial asthma patients. Materials and Methods : One hundred and ten participants were evaluated by pulmonary function test. Patients with 53 DSG and 31 ESG by differentiation-syndrome were assessed for genetic analysis. GSTM1 and GSTT1 deletion polymorphism was performed by polymerase chain reaction (PCR). Results : GSTM1 gene deletion was detected in 43.4% of individuals in the DSG and in 38.71 % in the ESG. The distribution of GSTM1 polymorphism between DSG and ESG was not significantly different [$x^2$=0.1767, p=0.6742; OR(95% CI)=1.2139(0.4915-2.9979)]. The proportion of GSTT1 null genotypes was 41.51% in the DGS and 45.16% in the ESG. The distribution of GSTT1 polymorphism between DSG and ESG was also not significantly different [$x^2$=0.1065, p=0.7442; OR(95% CI)=0.8618(0.3525-2.1065)]. In the combined analysis of GSTM1 and GSTT1 genes, the frequency of both null type of GSTM1/GSTT1 genes was not significantly different from both positive type of GSTM1/GSTT1 genes[$x^2$=0.0768, p=0.7817; OR(95% CI)=1.2000(0.3303-4.3602)] Conclusions : These results indicate that polymorphism of the GST gene might not be associated with the symptomatic classification of DSG and ESG by differentiation-syndrome in Korean asthmatics.

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