• 한국응용곤충학회지
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• 제50권1호
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• pp.39-46
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• 2011

본 연구는 상이한 음파 처리에 따라 파밤나방(Spodoptera exigua) 유충의 소화와 면역 생리반응에 대한 교란 효과를 분석하였다. 조사한 모든 주파수의 음파 처리가 파밤나방 산란에는 뚜렷한 효과를 주지 않았지만, 95 dB 소리세기에서 100-5,000 Hz 주파수의 음파 처리는 유충의 섭식량을 저하시키고, 중장의 소화효소 활성을 억제시켰다. 이 스트레스 음파 처리에 따른 중장 내강에 존재하는 단백질을 이차원전기영동으로 분리하였으며, 무처리구와 상이한 단백질 패턴을 발견하였다. 또한 가장 스트레스 효과를 크게 주는 95 dB의 5,000 Hz 주파수 음파 처리를 받은 유충은 곰팡이 감염에 대해서 혈구의 소낭형성이 억제되었다. 이 음파 처리 받은 유충의 혈구와 혈장에서 인지질분해효소(phospholipase $A_2$: $PLA_2$)의 활성은 현격하게 감소하였다. 스트레스 음파 처리에 따라 파밤나방 유충은 살충제에 대한 감수성이 증가했다. 이러한 상이한 주파수에 따른 생리교란 효과는 소리세기의 차이에 따라 뚜렷하게 차등을 보였다. 이러한 결과는 음파처리가 파밤나방의 생리과정에 스트레스를 주어 비화학적 해충 방제 관리 기술 개발에 적용될 수 있다고 본 연구는 제시한다.

• 동의생리병리학회지
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• 제23권5호
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• pp.1106-1115
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• 2009

Mori Ramulus has multiple applications in Korean traditional medicine prescription because it has antioxidant and anti-inflammatory effects by reducing macrophage activities. Yet, no studies on the anti-arthritic activity of EMR (extract of Mori Ramulus) have been reported in vitro and in vivo. Rheumatoid arthritis (RA) is a systemic autoimmune disease with chronic inflammation characterized by hyperplasia of synovial cells in affected joints, which ultimately leads to the destruction of cartilage and bone. Because collagen-induced arthritis (CIA) is similar to RA in pathological symptoms and immune reactions, there have been several reports concerning RA using CIA mouse model. Here, we investigated the effects of Mori Ramulus on RA using CIA mice. The importance of CD4+ Th1 cells in RA progress was previously indicated and studies further showed that Th17 cells play a prime role in severity of disease. Accordingly, the present study was focused on CIA associated with CD4+ Th1 cells and Th1 7 cells. DBA/1OlaHsd mice were immunized with bovine type II collagen (CII). After a second collagen immunization, mice were treated with EMR once a day for 4 weeks. The severity of arthritis within the paw joints was evaluated by histological assessment of cartilage destruction and pannus formation. Immune cells in peripheral blood mononuclear cells (PBMC), draining lymph node (DLN) and paw joints, cytokine production and gene expression were assessed from CIA mouse using ELISA, FACS and real-time PCR analysis. Administration of EMR significantly suppressed the progression of CIA and inhibited the production of TNF-$\alpha$, IL-6 and IL-17 in the serum. The erosion of cartilage was dramatically reduced in mouse knees after treatment with EMR. In conclusion, our results demonstrate that EMR significantly suppressed the progression of CIA and that this action was mediated by the decreased production of TNF-$\alpha$, IL-6, IL-17 and collagen II-specific antibody in the serum. EMR suppressed Th17 cells and reduced level of IL-6 via B cell suppression, and thus, the levels of autoantibodies produced from B cells were decreased. Furthermore, EMR suppressed NKT cells which directly stimulate B cells and develop imbalance of Th1/Th2 cell. Oral administration of EMR (100 mg/kg or 200 mg/kg) significantly suppressed the progression of CIA, which is comparable to that of methotrexate (MTX, 0.3 mg/kg) used as a positive control. We are currently studying the mechanism underlying the therapeutic role for EMR in CIA mice.

• 대한미생물학회지
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• 제13권1호
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• pp.17-24
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• 1978

Modulating effects of Candida albicans on the immune responses of mice immunized with sheep red blood cells(SRBC) were assessed both by footpad tests for anaphylactic, Arthus and delayed type hypersensitivity rections against homologous and heterologous antigenic challenges and by serum antibody titrations for hemagglutinin and hemolysin against SRBC. The results are summarized as follows: 1. In the mice simultaneously immunzed with C. albicans and SRBC, anaphylactic type and Arthus type footpad reactions to C. albicans challenge were enhanced, and extents of the enhancements were proportional to the concentration of SRBC administered for immunization, reaching peak in mice immunized with 0.2ml($10^8$) of 5% SRBC suspension. Although a little enhancement of delayed type hypersensitivity to C. albicans was observed in those mice, there was no significant difference between the mice groups immunized either with SRBC alone or SRBC and C. albicans simultaneously. 2. Simultaneous immunization of mice with C. albicans and SRBC resulted in the suppression of both anaphylactic type and Arthus type footpad reactions to SRBC, and the extent of such suppressions was inversly proportional to the numbers of C. albicans administered for immunization. Delayed type reaction of the mice to SRBC varied little in regards to the different numbers of C. albicans injected. 3. Hemagglutinin titers differed little between the mice groups immunized with SRBC alone or with SRBC and C. albicans simultaneously. Hewever, hemolysin titers were lower in the mice immunized simultaneously with SRBC and C. albicans. 4. In the peripheral blood of mice immunized simultaneously with SRBC and C. albicnas. there observed increases in the percents of monocyte and polymorphonuclear leukocytes and decrease in the numbers of lymphocytes and pyroninophilic lymphocytes. These results indicated that C. albicans is an immunosuppressant of the mice to SRBC when both anteigns were administered simultaneously for immunization, and that SRBC acted as an enhancer of anaphylactic type and Arthus type reaction of mice to C. albicans when administered simultaneously.

• Archives of Pharmacal Research
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• 제22권5호
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• pp.437-447
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• 1999

Type I diabetes, also known as insulin-dependent diabetes mellitus (IDDM) results from the destruction of insulin-producing pancreatic $\beta$ cells by a progressive $\beta$ cell-specific autoimmune process. The pathogenesis of autoimmune IDDM has been extensively studied for the past two decades using animal models such as the non-obese diabetic (NOD) mouse and the Bio-Breeding (BB) rat. However, the initial events that trigger the immune responses leading to the selective destruction of the $\beta$ cells are poorly understood. It is thought that $\beta$ cell auto-antigens are involved in the triggering of $\beta$ cell-specific autoimmunity. Among a dozen putative $\beta$ cell autoantigens, glutamic acid decarboxylase (GAD) has bee proposed as perhaps the strongest candidate in both humans and the NOD mouse. In the NOD mouse, GAD, as compared with other $\beta$ cell autoantigens, provokes the earliest T cell proliferative response. The suppression of GAD expression in the $\beta$ cells results in the prevention of autoimmune diabetes in NOD mice. In addition, the major populations of cells infiltrating the iselts during the early stage of insulitis in BB rats and NOD mice are macrophages and dendritic cells. The inactivation of macrophages in NOD mice results in the prevention of T cell mediated autoimmune diabetes. Macrophages are primary contributors to the creation of the immune environment conducive to the development and activation of $\beta$cell-specific Th1-type CD4+ T cells and CD8+ cytotoxic T cells that cause autoimmune diabetes in NOD mice. CD4+ and CD8+ T cells are both believed to be important for the destruction of $\beta$ cells. These cells, as final effectors, can kill the insulin-producing $\beta$ cells by the induction of apoptosis. In addition, CD8+ cytotoxic T cells release granzyme and cytolysin (perforin), which are also toxic to $\beta$ cells. In this way, macrophages, CD4+ T cells and CD8+ T cells act synergistically to kill the $\beta$ cells in conjunction with $\beta$ cell autoantigens and MHC class I and II antigens, resulting in the onset of autoimmune type I diabetes.

• 생명과학회지
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• 제25권6호
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• pp.686-692
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• 2015

암조직에 대한 면역반응은 종양의 성장을 억제하거나 유도한다. Foxp3 양성 T 림프구는 종양에 대한 면역억제 반응을 유도하여 종양의 성장을 유도하는 반면 CD8 양성 T 림프구는 종양의 성장을 억제한다. 본 연구에서는 피부에서 발생한 편평세포암종, 편평세포 암종의 전암병변인 광선각화증과 보웬병 그리고 기저세포암종 조직에 면역조직화학염색을 시행하여 CD8 양성 T 림프구 및 Foxp3 양성 T 림프구의 분포 그리고 두 종류의 림프구의 비(CD8/Foxp3)를 조사하여 다음과 같은 결과를 얻었다. CD8 양성 T 림프구와 Foxp3 양성 T 림프구는 보웬병과 평평세포암종의 침습부위에서 광선각화증과 기저세포암종의 침습부위에 비하여 더 많이 침윤하였으며 CD8/Foxp3는 보웬병에서 광선각화증과 기저세포암종의 침습부위에 비하여 낮았다. CD8 양성 T 림프구와 Foxp3 양성 T 림프구의 침윤 정도 및 CD8/Foxp3는 보웬병과 편평세포암종의 침습부위에서 유의한 차이가 없었다. 기저세포암종과 편평세포암종에서 CD8 양성 T 림프구와 Foxp3 양성 T 림프구는 침습부위에서 종양의 중심부위에 비하여 더 많이 침윤하였다. 이러한 결과로 보아 편평세포종양과 기저세포암종은 서로 다른 면역반응을 보이며 종양내에서도 부위에 따라 상이한 면역반응을 보인다고 생각된다.

• Journal of Ginseng Research
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• 제31권4호
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• pp.175-180
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• 2007

고려홍삼이 HIV-1 감염자에게서 바이러스의 활발한 증식으로 유발된 면역계의 과활성화를 장기간에 걸쳐 억제하는지 살펴보기 위해 면역 활성화 지표인 soluble CD8항원(sCD8)을 측정하였다. HIV-1 감염 대조군 49명, zidovudine (ZDV) 복용군 22명, KRG 복용군 48명, KRG와 ZDV 병용군(49명)을 대상으로 하였다. HIV-1 감염 대조군에서는 혈청 sCD8 농도가 31-48개월 동안 33% 증가하였으며(P < 0.05), sCD8/CD8+T 림프구 비도 $21{\pm}13$개월동안 54% 증가하였다(P < 0.001). ZDV 복용군에서는 혈청 sCD8농도가 초기 6개월 동안은 감소하였으나 그 이후로는 서서히 증가하였으며, sCD8/CD8+T 림프구 비도 증가하였다. KRG 복용군은 sCD8 농도가 31-48개월 동안 45% 감소하였으며(P < 0.01), sCD8/CD8+T 림프구 비도 $19\;{\pm}\;11$개월 동안 19% 감소하였다(P < 0.05). 병용군에서는 sCD8 농도가 31-48개월 동안 29%(P < 0.01) 감소하였다. 추적관찰 기간 동안 각 군간의 sCD8 농도 변화가 명확한 차이를 보였으며, KRG 복용군에서는 ZDV 복용군에서 관찰된 'rebound현상'(sCD8이 초기에 감소하다가 다시 증가하는 경향)이 없었다. 결론적으로 본 연구에서는 HIV-1 감염환자에서 KRG를 장기간 복용시켰을 경우 sCD8 농도가 지속적으로 감소하여, KRG가 면역계의 소모적인 과활성화 상태를 방지함을 알 수 있었다.

• Journal of Photoscience
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• 제9권2호
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• pp.197-200
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• 2002

UVR-induced immunosuppression contributes to skin cancer. The aim was to construct accurate dose response curves for primary and secondary contact sensitivity for solar-simulated UVR (ssUVR; 290-400nm), UVA and UVB as the role of UVA in immunosuppression is controversial. We used a xenon arc source. The mice were immobilised, enabling accurate dosing. C57BL/6 mice were immunosuppressed at half the dose of ssUVR required to cause sunburn but not by higher doses (up to the sunburn dose). Thus, ssUVR causes systemic immunosuppression only over a narrow, low dose range. UVA caused suppression at low but not high doses whereas UVB induced immunosuppression at all doses tested. 8 weeks later the mice were resensitised to assess tolerance. Mice exposed to the minimum immunosuppressive dose of ssUVR prior to primary sensitisation were tolerant to re-sensitisation. However, at higher doses of ssUVR, these mice were protected from tolerance. Interestingly, while low doses of UV A caused immunosuppression, even lower doses enhanced the response to the second sensitisation. Higher doses of UVA had no affect. UVB induced tolerance in a dose related manner. Thus, ssUVR only induces immunosuppression and tolerance over a narrow dose range. Both UVA and UVB are immunosuppressive at this dose, while higher doses of UVA protect from the suppressive effects of UVB. Surprisingly very low doses of UVA enhanced memory development. Thus UVR has complex effects on the immune system depending on dose and spectrum.

• Asian-Australasian Journal of Animal Sciences
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• 제19권11호
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• pp.1665-1670
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• 2006

The objective of this research was to provide the characterization and method for producing anti-E. coli O157:H7 antibodies in egg-laying hens and to determine if the antibody can restrain the proliferation of E. coli O157:H7 in-vitro. Selected antigenic fractions (whole cell, outer membrane protein and lipopolysaccharide (LPS)) from E. coli O157:H7 were injected to hens in order to produce anti-E. coli O157:H7 antibodies. The immune response and the egg yolk antibodies of laying hens against the whole cell, outer membrane protein and LPS antigens were monitored by ELISA. The level of antibodies against whole cell antigen monitored through ELISA sharply increased after the initial immunization, and it was found to be maximum on day 49 however, the level was maintained up to day 70. Antibodies (5 mg/ml) directed against the whole cell inhibited E. coli proliferation 10-13 times more than outer membrane protein or LPS. The antibody response against the whole cell antigens appeared to have higher activity in restraining the proliferation of E. coli O157:H7 than antibody against outer membrane protein or LPS. Results reflected that increasing the IgY's in the egg yolk could prevent greater economic losses due to human and animal health from pathogenic bacteria i.e. E. coli O157:H7.

• IMMUNE NETWORK
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• 제15권4호
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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.

• IMMUNE NETWORK
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• 제13권4호
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• pp.123-132
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• 2013

Obesity is consistently increasing in prevalence and can trigger insulin resistance and type 2 diabetes. Many lines of evidence have shown that macrophages play a major role in inflammation associated with obesity. This study was conducted to determine metformin, a widely prescribed drug for type 2 diabetes, would regulate inflammation through down-regulation of scavenger receptors in macrophages from obesity-induced type 2 diabetes. RAW 264.7 cells and peritoneal macrophages were stimulated with LPS to induce inflammation, and C57BL/6N mice were fed a high-fat diet to generate obesity-induced type 2 diabetes mice. Metformin reduced the production of NO, $PGE_2$ and pro-inflammatory cytokines ($IL-1{\beta}$, IL-6 and $TNF-{\alpha}$) through down-regulation of $NF-{\kappa}B$ translocation in macrophages in a dose-dependent manner. On the other hand, the protein expressions of anti-inflammatory cytokines, IL-4 and IL-10, were enhanced or maintained by metformin. Also, metformin suppressed secretion of $TNF-{\alpha}$ and reduced the protein and mRNA expression of $TNF-{\alpha}$ in obese mice as well as in macrophages. The expression of scavenger receptors, CD36 and SR-A, were attenuated by metformin in macrophages and obese mice. These results suggest that metformin may attenuate inflammatory responses by suppressing the production of $TNF-{\alpha}$ and the expressions of scavenger receptors.