• 생명과학회지
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• 제17권1호
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• pp.31-38
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• 2007

사람의 장티푸스 연구는 생쥐에 감염되는 Salmonella typhimurium를 모델로 연구되고 있으며, 생쥐에 있어서 S. typhimurium의 감염은 이자세포의 증식반응을 감소시키는 것으로 알려져 있다. S. typhimurium lipid A의 처리가 T세포 mitogen에 의한 이자 세포의 증식에 어떤 영향을 주는 가를 in vitro와 ex vivo조건에서 알아 보았다. Lipid A 단독 처리는 이자 세포의 증식을 보였으나, lipid A 처리 후 T 세포 mitogen인 concanavalin A (Con A)와 phytohemagglutinin (PHA)에 의한 in vitro와 ex vivo 조건에서의 이차 처리는 오히려 세포증식이 억제되었다. Lipid A를 주사한 생쥐로부터 분리한 이자 세포에서 대식세포를 제거하였을 조건에서는 T 세포 mitogen에 의한 증식 효과가 유지되었으나 대식세포를 제거하지 않았을 경우에는 T세포 mitogen에 의한 증식 효과가 억제되었다. Lipid A를 주사한 생쥐에서 얻은 대식세포를 포함한 이자세포의 숫자를 증가하면서 Lipid A를 주사하지 않은 생쥐에서 얻은 이자세포와 혼합 배양하였을 때 Lipid A를 주사한 생쥐에서 얻은 대식세포를 포함한 이자세포의 숫자가 높을수록 Con A와 PHA에 의한 증식억제가 높게 측정되었다. 이러한 결과는 Con A와 PHA의 이자세포 증식 기능이 lipid A의 전처리에 의해 활성화된 대식세포의 직접적인 접촉 작용으로 억제된 것으로 생각된다. 본 연구의 결과를 바탕으로 억제에 관여하는 대식세포 표면분자를 밝히는 것이 사람의 장티푸스 연구에 도움이 되리라 생각된다.

• Molecules and Cells
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• 제26권1호
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• pp.67-73
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• 2008

Herpetic stromal keratitis (HSK) is an inflammatory disorder induced by HSV-1 infection and characterized by T cell-dependent destruction of corneal tissues. It is not known what triggers $CD4^+$ T cell migration into the stroma of HSV-1-infected corneas. The keratocyte is a fibroblast-like cell that can function as an antigen-presenting cell in the mouse cornea by expressing MHC class II and costimulatory molecules after HSV-1 infection. We hypothesized that chemokines produced by stromal keratocytes are involved in $CD4^+$ T cell infiltration into the cornea. We found that keratocytes produce several cytokines and chemokines, including MCP-1, RANTES, and T cell activation (TCA)-3. HSV-1 infection increased the production of MCP-1 and RANTES by keratocytes, and these acted as chemoattractants for HSV-1-primed $CD4^+$ T cells expressing CCR2 and CCR5. ExpreHerpetic stromal keratitis (HSK) is an inflammatory disorder induced by HSV-1 infection and characterized by T cell-dependent destruction of corneal tissues. It is not known what triggers $CD4^+$ T cell migration into the stroma of HSV-1-infected corneas. The keratocyte is a fibroblast-like cell that can function as an antigen-presenting cell in the mouse cornea by expressing MHC class II and costimulatory molecules after HSV-1 infection. We hypothesized that chemokines produced by stromal keratocytes are involved in $CD4^+$ T cell infiltration into the cornea. We found that keratocytes produce several cytokines and chemokines, including MCP-1, RANTES, and T cell activation (TCA)-3. HSV-1 infection increased the production of MCP-1 and RANTES by keratocytes, and these acted as chemoattractants for HSV-1-primed $CD4^+$ T cells expressing CCR2 and CCR5. Expression of MCP-1 in the corneal stroma was confirmed in vivo. Finally, when HSV-1-primed $CD4^+$ T cells were adoptively transferred into wild type and MCP-1-deficient mice that had been sublethally irradiated to minimize chemokine production from immune cells, infiltration of $CD4^+$ T cells was markedly reduced in the MCP-1-deficient mice, suggesting that it is the MCP-1 from HSV-1-infected keratocytes that attracts $CD4^+$ T cells into the cornea.

• Journal of Photoscience
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• 제9권2호
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• pp.194-196
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• 2002

While ultraviolet radiation alters various cutaneous cell functions, little is known about photo-immunological and photobiological effects of infrared radiation (IR) on the skin except its local thermal effects. The fIrst part of this study demonstrated that single exposure of mouse skin to near IR (0.7 - 1.3 $\mu$m) reversibly suppressed the proliferating activity of the epidermis, the density of Langerhans cells, and the ability of skin to induce contact hypersensitivity reaction. The second part demonstrated that the rate of wound closure was significantly accelerated by repeated exposures in animal models. The production of transforming growth factor-$\beta$l and matrix metalloproteinase-2, which are responsible for the wound healing processes, was significantly upregulated by irradiation, as shown by enzyme immunoassay, zymography, and reverse transcription polymerase chain reaction. Thermal controls were negative. The results suggest that near-IR irradiation can modulate the epidermal proliferation and part of the skin immune system, and stimulate the wound healing processes, presumably by non-thermal effects.

• Childhood Kidney Diseases
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• 제19권2호
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• pp.79-88
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• 2015

Neutrophil gelatinase-associated lipocalin (NGAL) has emerged as one of the most promising biomarkers of renal epithelial injury. Numerous studies have presented the diagnostic and prognostic utility of urinary and plasma NGAL in patients with acute kidney injury, chronic kidney disease, renal injury after kidney transplantation, and other renal diseases. NGAL is a member of the lipocalin family that is abundantly expressed in neutrophils and monocytes/macrophages and is a mediator of the innate immune response. The biological significance of NGAL to hamper bacterial growth by sequestering iron-binding siderophores has been studied in a knock-out mouse model. Besides neutrophils, NGAL is detectable in most tissues normally encountered by microorganisms, and its expression is upregulated in epithelial cells during inflammation. A growing number of studies have supported the clinical utility of NAGL for detecting invasive bacterial infections. Several investigators including our group have reported that measuring NGAL can be used to help predict and manage urinary tract infections and acute pyelonephritis. This article summarizes the biology and pathophysiology of NGAL and reviews studies on the implications of NGAL in various renal diseases from acute kidney injury to acute pyelonephritis.

• Journal of Microbiology and Biotechnology
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• 제15권2호
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• pp.265-268
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• 2005

To study the effect of bifidobacteria on preventing allergy response, levels of IFN-$\gamma$, IgG2a, IL-4, and IgG1 were investigated in splenocytes isolated from ovalbumin (OVA)­sensitized allergic mice and BGN4-administered allergy­suppressed mice in the presence of various bifidobacterial strains. Most of the bifidobacteria, except 2A, increased production of Th I-associated immune markers, IFN -$\gamma$ and IgG2a. In addition, most of the bifidobacteria, except 2A and 19A, decreased production of IL-4, whereas the differences in the production of IgG1 were less pronounced. These results suggest that some strains of bifidobacteria may have the potential to prevent the occurrence of allergy by switching Th1/Th2-type antibodies and/or related cytokines.

• 한방안이비인후피부과학회지
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• 제8권1호
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• pp.1-19
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• 1995

Seungmagalgeuntang-gamibang has long been known to have anti-allergic effect. However, the mechanism of action of Seungmagalgeuntang-gamibang is not well investigated. The author analysed the effects of Seungmagalgeuntang-gamibang on the vascular permeability, delayed-type and contact hypersensitivities, and phagocytic function, the results obtained are as follows: 1. Administration of Seungmagalgeungtang-gamibang decreased the vascular permeability induced by serotonin in the mouse. 2. Administration of Seungmagalgeuntang-gamibang decreased the vascular permeability induced by histamine without statistical significant. 3. Administration of Seungmagalgeuntang-gamibang decreased the delayed-type hypersensitivity induced by sheep red blood cells. 4. Administration of Seungmagalgeungtang-gamibang decreased the contact hypersensitivity induced by dinitrochlorobenzene. 5. Seungmagalgeungtang-gamibang increased the phagocytic-activities of macrophages in vitro and in vivo. 6. Seungmagalgeungtang-gamibang enhanced the formation of reactive oxygen intermediates in vitro and in vivo. The above results demonstrate that Seungmagalgeuntang-gamibang suppresses the hypersensitivity reactions with increasing the phagocytic functions and formations of reactive oxygen intermediates from macrophages.

• 대한의생명과학회지
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• 제24권4호
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• pp.305-310
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• 2018

Microglia are emerging as critical regulators of innate immune responses in AD and other neurodegenerative disorders, highlighting the importance of understanding their molecular and cellular mechanisms. We attempted to determine the role of crosstalk signaling between $IFN-{\gamma}$ and $TGF-{\beta}$ in $A{\beta}$ clearance by microglia cells. We used in vitro and in vivo mouse models that recapitulated acute and chronic aspects of microglial responses to $A{\beta}$ peptides. We showed that crosstalk signaling between $TGF-{\beta}$ and Smad2 was an important mediator of neuro-inflammation. These findings suggest that microglial $TGF-{\beta}$ activity enhances the pathological progression to AD. As $TGF-{\beta}$ displays broad regulatory effects on beneficial microglial functions, the activation of inflammatory crosstalk signaling between $TGF-{\beta}$ and Smad2 may be a promising strategy to restore microglial functions, halt the progression of $A{\beta}$-driven pathology, and prevent AD development.

• 대한약학회:학술대회논문집
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• 대한약학회 2002년도 Proceedings of the Convention of the Pharmaceutical Society of Korea Vol.2
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• pp.308.2-308.2
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• 2002

Tissue macrophages produce at least two groups of protein mediators of inflammation. interleukin 1(IL-1) and tumor necrosis factor (TNF) when they were activated. Recent studies have emphasized that TNF and IL-1modulate the inflammatory function of endothelial cells. leukocytes. and fibroblasts, Aloe vera has been claimed to have several important therapeutic properties including acceleration of wound healing, immune stimulation, anti-cancer and anti-viral effects. (omitted)

• 한국동물생명공학회지
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• 제38권1호
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• pp.17-25
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• 2023

Brassica oleracea var. italica (broccoli) is a type of cabbage that contains vitamins, minerals, and phytochemicals. Consequently, it is used as a potential nutraceutical source for improving human health by reducing oxidative stress and inflammatory responses. Here, the effects of broccoli sprout extract (BSE) on the inflammatory response were investigated through lipopolysaccharide (LPS)-induced inflammatory mouse models. First, we found that the BSE obviously reduce NO production in RAW 264.7 cells in response to LPS stimulation in in vitro study. Pretreatment with BSE administration improved sperm motility and testicular cell survivability in LPS-induced endotoxemic mice. Additionally, BSE treatment decreased the levels of the pro-inflammatory cytokines TNF-a, IL-1β, and IL-6, and COX-2 in testis of LPS-induced endotoxemic mice models. In conclusion, BSE could be a potential nutraceutical for preventing the excessive immune related infertility.

• IMMUNE NETWORK
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• 제13권5호
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• pp.213-217
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• 2013

Enterotoxigenic Bacteroides fragilis (ETBF) is a human gut commensal bacteria that causes inflammatory diarrhea and colitis. ETBF also promotes colorectal tumorigenesis in the Min mouse model. The key virulence factor is a secreted metalloprotease called B. fragilis toxin (BFT). BFT induces E-cadherin cleavage, cell rounding, activation of the ${\beta}$-catenin pathway and secretion of IL-8 in colonic epithelial cells. However, the precise mechanism by which these processes occur and how these processes are interrelated is still unclear. E-cadherin form homophilic interactions which tethers adjacent cells. Loss of E-cadherin results in detachment of adjacent cells. Prior studies have suggested that BFT induces IL-8 expression by inducing E-cadherin cleavage; cells that do not express E-cadherin do not secrete IL-8 in response to BFT. In the current study, we found that HT29/C1cells treated with dilute trypsin solution induced E-cadherin degradation and IL-8 secretion, consistent with the hypothesis that E-cadherin cleavage causes IL-8 secretion. However, physical damage to the cell monolayer did not induce IL-8 secretion. We also show that EDTA-mediated disruption of E-cadherin interactions without E-cadherin degradation was sufficient to induce IL-8 secretion. Finally, we determined that HT29/C1 cells treated with LiCl (${\beta}$-catenin activator) induced IL-8 secretion in a dose-dependent and time-dependent manner. Taken together, our results suggest that BFT induced IL-8 secretion may occur by the following process: E-cadherin cleavage, disruption of cellular interactions, activation of the ${\beta}$-catenin pathway and IL-8 expression. However, we further propose that E-cadherin cleavage per se may not be required for BFT induced IL-8 secretion.