• Title/Summary/Keyword: Immune response

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Regulation of Innate Immune Response to Fungal Infection in Caenorhabditis elegans by SHN-1/SHANK

  • Sun, Lingmei;Li, Huirong;Zhao, Li;Liao, Kai
    • Journal of Microbiology and Biotechnology
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    • v.30 no.11
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    • pp.1626-1639
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    • 2020
  • In Caenorhabditis elegans, SHN-1 is the homologue of SHANK, a scaffolding protein. In this study, we determined the molecular basis for SHN-1/SHANK in the regulation of innate immune response to fungal infection. Mutation of shn-1 increased the susceptibility to Candida albicans infection and suppressed the innate immune response. After C. albicans infection for 6, 12, or 24 h, both transcriptional expression of shn-1 and SHN-1::GFP expression were increased, implying that the activated SHN-1 may mediate a protection mechanism for C. elegans against the adverse effects from fungal infection. SHN-1 acted in both the neurons and the intestine to regulate the innate immune response to fungal infection. In the neurons, GLR-1, an AMPA ionotropic glutamate receptor, was identified as the downstream target in the regulation of innate immune response to fungal infection. GLR-1 further positively affected the function of SER-7-mediated serotonin signaling and antagonized the function of DAT-1-mediated dopamine signaling in the regulation of innate immune response to fungal infection. Our study suggests the novel function of SHN-1/SHANK in the regulation of innate immune response to fungal infection. Moreover, our results also denote the crucial role of neurotransmitter signals in mediating the function of SHN-1/SHANK in regulating innate immune response to fungal infection.

Transcriptome Analysis to Characterize the Immune Response of NecroX-7 in Mouse CD4+ T Cells

  • Kim, Eun-Jung
    • Biomedical Science Letters
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    • v.21 no.2
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    • pp.60-68
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    • 2015
  • NecroX-7 is a novel small compound of the NecroX series based on the indole moiety, which has potent cytoprotective and antioxidant properties. We previously detected potential immune regulatory effects of NecroX-7 in immune related diseases like Graft-versus-Host Disease. However, the function and the underlying mechanisms of immunological effects of NecroX-7 in the immune system have not been well established. In this study, we investigated the immune response characterization of differentially expressed genes of NecroX-7 administration in $CD4^+$ T cells by microarray analysis. $CD4^+$ T cells stimulated with NecroX-7 ($40{\mu}M$) or vehicle for 72 hours resulted in the identification of 337 differentially expressed genes (1.5 fold, P<0.05) by expression profiling analysis. Twenty eight of the explored NecroX-7-regulated genes were related to immune system processes. These genes were validated by quantitative real-time PCR. The most significant genes were glutathione reductase, eukaryotic translation elongation factor 1, lymphotoxin-alpha, heat shock protein 9 and chloride intracellular channel protein 4. These findings demonstrate the strongly immune response of NecroX-7 in $CD4^+$ T cells, suggesting that cytoprotection and immune regulation may underlie the critical aspects of NecroX-7 exposure.

Effect of Aconitine and Heated Aconitine on the Immune Response in Mice (Aconitine 및 가열처리한 Aconitine이 Mouse의 면역반응에 미치는 영향)

  • 안영근;김정훈;정동환
    • Environmental Analysis Health and Toxicology
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    • v.3 no.1_2
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    • pp.33-42
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    • 1988
  • Dose-dependent, immune modulatory effects of aconitine and heated aconitine were studied in mice. Mice, administered aconitine and heated aconitine intraperitoneally every other day for 4 weeks, were sensitized and challenged with sheep red blood cells. Serum antibody titer, foot pad swelling and rosette forming cell number were measured to evaluate hurmoral and cell mediated immune responses. The results show that Humoral immune response was suppressed by aconitine 0.05 mg/kg and heated aconitine but increased by aconitine 0.10 mg/kg administration. Cell mediated immune response was suppressed in all groups. Especially heated aconitine administration significantly suppressed the cell mediated immune response. The number of peripheral circulating white blood cell was reduced by aconitine but was not affected by heated aconitine.

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Aging of Immune System (면역 반응체계의 노화)

  • Chung, Kyung Tae
    • Journal of Life Science
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    • v.29 no.7
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    • pp.817-823
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    • 2019
  • Immune system provides defense integrity of body against external invaders. In order to accomplish the important defending role immune system is composed of many different components which are regenerated continuously during lifespan. The key components are professional killing cells such as macrophage, neutrophil, natural killer cell, and cytotoxic T cell and professional blocking molecule, antibody, which is produced by plasma cell, the terminal differentiated B cell. Immune response is orchestrated harmoniously by all these components mediated through antigen presenting cells such as dendritic cells. Immune responses can be divided into two ways: innate immune response and adaptive immune response depending on induction mechanism. Aging is a broad spectrum of physiological changes. Likewise other physiological changes, the immune components and responses are wane as aging is progressing. Immune responses become decline and dysregulating, which is called immunosenescense. Immune components of both innate and adaptive immune response are affected as aging progresses leading to increased vulnerability to infectious diseases. Numbers of immune cells and amounts of soluble immune factors were decreased in aged animal models and human and also functional and structural alterations in immune system were reduced and declined. Cellular intrinsic changes were discovered as well. Recent researches focusing on aging have been enormously growing. Many advanced tools were developed to bisect aging process in multi-directions including immune system area. This review will provide a broad overview of aging-associated changes of key components of immunity.

Effects of Methidathion on Humoral Immune Response in Mice (Methidathion이 체액성 면역 반응에 미치는 영향)

  • 정혜주;김형수;박재현;박현애;김진호;정승태;한형미;조대현;김주일
    • Toxicological Research
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    • v.15 no.1
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    • pp.47-53
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    • 1999
  • The effects of methidathion on humoral immune response were studied in BALB/c mice. 0.5 or 5.0 mg/kg/day methidathion were administered orally for 14 days. The parameters examined to assess apparent toxicity of methidathion included changes of body weight, relative weight of spleen, thymus, sidney and liver, and viable spllenic cell numbers. To evaluate the humoral immune response, thymus, kidney and liver, and viable splenic cell numbers. To evaluate the humoral immune resopnse, the plaque forming cell(PFC) responses sheep the red blood cells (SRBC) and the lovels of serum IgG to hen egg lysozyme (HEL) were determined. No alterations were observed in changes of body weights, relative organ weights and the numbers of viable splenocytes by exposure to any dose of methidathion. At the dose of 0.5mg/kg only PFC response was decreased, whereas both PFC response and the level of serum IgG were decreased significantly at the dose of 5.0 mg/kg. These results indicate that exposure to methidathion may cause sup[pression of humoral immune reponse in mice without overt changed in lymphoid organ weight or viability of splenocytes.

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Effect of Sound Stress on Immune Response (소음 스트레스가 면역반응에 미치는 영향에 관한 실험적 연구)

  • 김금재
    • Journal of Korean Academy of Nursing
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    • v.19 no.2
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    • pp.135-146
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    • 1989
  • This study was undertaken to assess the effect of sound stress on humoral and cellular immune responses to thymus-dependent and independent antigens in mice. After mice were exposed to 4 hr daily sound stessors(83㏈) for 4 days before or after immunization, the primary and / or secondary immune response to sheep red blood cells(SRBC), polyvinylpyrroridone(PVP) or picry1 chloride(TNCB) were assayed. When mice were exposed to sound stressor before or after immunization, delayed-type hypersensitivity reaction and contact sensitivity to TNCB was remarkably depressed compared with those of the unstressed control mice. However, the primary and secondary hemagglutinin response of the stresed mice to SRBC showed a pronounced increase compared with that of the unstressed mice, In contrast to antibody response to SRBC, the primary antibody response of the stressed mic to PVP was almost not detected. surprisingly, the secondary antibody response to PVP of the mice receiving the secondary sound stress was markedly increased when the immune-depressed mice received the secondary immunization with PVP at 46 days after the primary immunization. The susceptibility of mice to intraven-oulsy infected Candida albicans was not changed by the sound stress.

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Effect of Progressive Muscle Relaxation using Biofeedback on Perceived Stress, Stress Response, Immune Response and Climacteric Symptoms of Middle-Aged Women (바이오피드백을 이용한 점진적 근육이완이 중년여성의 지각된 스트레스, 스트레스반응, 면역반응 및 갱년기 증상에 미치는 효과)

  • 정인숙
    • Journal of Korean Academy of Nursing
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    • v.34 no.2
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    • pp.213-224
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    • 2004
  • Purpose: This study was aimed to evaluate the effect of progressive muscle relaxation training using biofeedback on perceived stress, stress response, immune response and climacteric symptoms, Method: This was a crossover, pre-post test design, The study subjects are 36 middle-aged women who were selected at 2 public health centers, The independent variable was Biofeedback training for 4 weeks, twice a week and home training for 4 weeks, Dependent variables were perceived stress, stress response, immune response, and climacteric symptoms measured with Hildtch's scale (1996), Result: Progressive muscle relaxation training using biofeedback was not effective in reducing perceived stress, but it was shown to be effective in reducing physiological stress responses such as pulse rate and EMG, Though blood pressure and skin conductance were repeatedly down, and skin temperature slowly increased, there were no statistically significant differences. Progressive muscle relaxation training using biofeedback was not effective in reducing serum cortisol, enhancing immune responses, or decreasing climacteric symptoms. Conclusion: The findings point to a pressing need for further, well-controlled and designed research with consideration in selection of subjects and instruments, frequency of measurements, the sampling method, and intervention modalities.

Effect of Ethanol on the Immunotoxicity of Ampicillin in Mice (Ampicillin의 면역독성에 미치는 Ethanol의 영향)

  • 안영근;김정훈;나헌진
    • Environmental Analysis Health and Toxicology
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    • v.3 no.1_2
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    • pp.55-64
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    • 1988
  • Experiments were performed on mice to investigate the influences of ampicillin and ethanol on the immune response. Ampicillin was injected intraperitoneally and ethanol was administered in the drinking water. Mice were sensitized and challenged with sheep red blood cells. Immune responses were evaluated by humoral immunity, cellular immunity, peripheral circulating white blood cell and phagocyte activity. 1. The combined administration of ampicillin and ethanol as compared to ampicillin had not influence on the weight of spleen, but increased the weight of thymus. 2. Humoral immune response was slightly reduced by ampicillin. Especially, the combined administration of ampicillin and ethanol significantly reduced hemclysin production. 3. Cellural immune response was reduced by ampicillin. The combine administration of ampicillin and ethanol significantly reduced cellural immune response. 4. Peripheral circulating white blood cell was reduced by the combined administration of ampicillin and ethanol as compared to ampicillin. 5. The combined administration of ampicillin and ethanol as compared to ampicillin had not influence on the phagocyte activity.

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Innate immune response to oral bacteria and the immune evasive characteristics of periodontal pathogens

  • Ji, Suk;Choi, Youngnim
    • Journal of Periodontal and Implant Science
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    • v.43 no.1
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    • pp.3-11
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    • 2013
  • Periodontitis is a chronic inflammation of periodontal tissue caused by subgingival plaque-associated bacteria. Periodontitis has long been understood to be the result of an excessive host response to plaque bacteria. In addition, periodontal pathogens have been regarded as the causative agents that induce a hyperinflammatory response from the host. In this brief review, host-microbe interaction of nonperiodontopathic versus periodontopathic bacteria with innate immune components encountered in the gingival sulcus will be described. In particular, we will describe the susceptibility of these microbes to antimicrobial peptides (AMPs) and phagocytosis by neutrophils, the induction of tissue-destructive mediators from neutrophils, the induction of AMPs and interleukin (IL)-8 from gingival epithelial cells, and the pattern recognition receptors that mediate the regulation of AMPs and IL-8 in gingival epithelial cells. This review indicates that true periodontal pathogens are poor activators/suppressors of a host immune response, and they evade host defense mechanisms.

Cochlin-cleaved LCCL is a dual-armed regulator of the innate immune response in the cochlea during inflammation

  • Rhyu, Hyeong-Jun;Bae, Seong Hoon;Jung, Jinsei;Hyun, Young-Min
    • BMB Reports
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    • v.53 no.9
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    • pp.449-452
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    • 2020
  • The inner ear is a complex and delicate structure composed of the cochlea and the vestibular system. To maintain normal auditory function, strict homeostasis of the inner ear is needed. A proper immune response against infection, thus, is crucial. Also, since excessive immune reaction can easily damage the normal architecture within the inner ear, the immune response should be fine regulated. The exact mechanism how the inner ear's immune response, specifically the innate immunity, is regulated was unknown. Recently, we reported a protein selectively localized in the inner ear during bacterial infection, named cochlin, as a possible mediator of such regulation. In this review, the immunological function of cochlin and the mechanism behind its role within inner ear immunity is summarized. Cochlin regulates innate immunity by physically entrapping pathogens within scala tympani and recruiting innate immune cells. Such mechanism enables efficient removal of pathogen while preserving the normal inner ear structure from inflammatory damage.