• IMMUNE NETWORK
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• 제15권3호
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• pp.135-141
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• 2015

Dysfunction of gut immune regulation is involved in mucosal damage in inflammatory bowel disease (IBD). However, there is still no efficacious immune-regulator for the treatment of IBD. Alloferon is a novel immune-modulatory peptide that was originally isolated from infected insects. It shows anti-inflammatory effects by the regulation of cytokine production by immune cells and their activities. Therefore, we investigated the effect of alloferon in a mouse model of colitis using dextran sulfate sodium (DSS). Colitis was induced by administration of DSS in drinking water for 7 consecutive days. It was confirmed by the presence of weight loss, diarrhea, hematochezia, and colon contraction. Alloferon was injected 4 days after DSS administration. We found that alloferon improved the pathogenesis of IBD based on the reduced disease activity index (DAI) and colon contraction. Edema, epithelial erosion, and immune cell infiltration were found in mice administered DSS, but the phenomena were reduced following alloferon treatment. The plasma level of IL-6, a classical pro-inflammatory cytokine in colitis, was also decreased by alloferon. Moreover, alloferon inhibited the TNF-${\alpha}$-induced degradation and phosphorylation of $I{\kappa}B$ in Colo205 colon cancer cells. Taken together, these results show that alloferon has anti-inflammatory effects and attenuates DSS-induced colitis.

• 한국응용약물학회:학술대회논문집
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• 한국응용약물학회 2001년도 추계학술대회 및 정기총회
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• pp.14-20
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• 2001

Rheumatoid arthritis (RA) is one of the most typical rheumatic diseases, and is characterized by chronic inflammation, cartilage destruction and joint deformity ［1,2］. During this process, profound hypertrophic changes of the synovium with infiltration of immune cells, increased vascularity, and hyperplasia result in the formation of a synovial pannus that invades cartilage and bone ［3］. In early stages of RA, the synovial membrane begins to invade the cartilage. In established RA, the synovial membrane becomes transformed into inflammatory tissue, the pannus (Fig. 1). The cell types that occupy cartilage-pannus junctions include synovial macrophages, fibroblasts, mast cells, polymorphonuclear lymphocytes (PMNs), and displaced, probably differentiated condrocytes ［4-6］. Recent studies of rheumatoid synovial tissue have demonstrated localized accumulations of mast cells and evidence of their activation/degranulation［7］.

• Archives of Reconstructive Microsurgery
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• 제21권1호
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• pp.34-40
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• 2012

Prevention of acute rejection in composite tissue allotransplantation without continuous immunosuppression lacks reports in worldwide literature. Recently dendritic cells (DC) gained considerble attention as antigen presenting cells that are also capable of immunologic tolerance induction. This study assesses the effect of alloantigen-pulsed dendritic cells in induction of survival in a rat hindlimb allograft. We performed hindlimb allotransplantation between donor Sprague-Dawley and recipient Fischer344 rats. Recipient derived dendritic cells were harvested from rat whole blood and cultured with anti-inflammatory cytokine IL-10. Then donor-specific alloantigen pulsed dendritic cells were reinjected into subcutaneous tissue before limb transplantation. Groups: I) untreated (n=6), II) DC injected (n=6), III) Immunosuppressant (FK-506, 2 mg/Kg) injected (n=6), IV) DC and immunouppressant injected (n=6). Graft appearance challenges were assessed postoperatively. Observation of graft appearance, H-E staning, immunohistochemical (IHC) study, and confocal immunofluoreiscece were performed postoperatively. Donor antigen pulsed host dendritic cell combined with short-term immunosuppression showed minimal mononuclear cell infiltration, regulator T cell presence, and could prolong limb allograft survival.

• IMMUNE NETWORK
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• 제8권3호
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• pp.90-97
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• 2008

Background: Hypersensitivity pneumonitis (HP) comprises a group of lung diseases resulting from repeated inhalation of various antigens such as Saccharopolyspora rectivirgula (SR). HP is categorized as a Th1 disease. Therefore, it has been suggested that IL-4, Th2 type cytokine, plays a protective role in the development of HP. However, the functional role of IL-4 in HP has not been extensively investigated in vivo. Therefore, we investigated the functional role of IL-4 in HP using IL-4 knockout (KO) mice. Methods: HP was induced by repeated exposure to SR in C57BL/6 (B6) and IL-4 KO (C57BL/6 background) mice. Results: IL-4 KO mice aggravated HP in terms of histological alteration, SR-specific immune responses, and inflammatory cell infiltration in the lungs compared with B6 mice. IL-4 KO mice produced high levels of IFN-${\gamma}$, TGF-${\beta}$ and TNF-${\alpha}$ in the lungs, whereas B6 mice showed the enhanced production of IL-4. Moreover, chemokines such as MIP-1${\alpha}$, MCP-1, and RANTES were highly expressed in IL-4 KO mice. IFN-${\gamma}$-secreting CD4, CD8 T cells, and neutrophils were enhanced in the bronchoalveolar lavage fluid (BALF) of IL-4 KO mice than those of B6 mice. The administration of recombinant(r) IL-4 restored these immunologic parameters in IL-4 KO mice. Conclusion: These results indicate that IL-4 plays a suppressive role in SR-induced HP by attenuating Th1-dominant immune responses.

• 대한수의학회지
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• 제35권4호
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• pp.843-851
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• 1995

To observe the effect of Demodex canis infection on the cellular immune response and hematological profile, 8 Doberman pinschers experimentally infected with D cains and 4 uninfected control dogs were sensitized with 2, 4-dinitro-chlorobenzene(DNCB) on the skin and were challenged with DNCB 14 days after the initial sensitization to elicit allergic contact dermatitis. Histological and hematological changes of these dogs were then observed. Macroscopic changes of skin challenged with DNCB in D canis-infected dogs included significantly reduced area of allergic reaction(p<0.05) than in uninfected control group. Infiltration of inflammatory cells in the D canis-infected group was also significantly reduced(p<0.05) than in the uninfected control group. These changes indicated that the cell-mediated immune response of the animals was suppressed by the infection with D canis. Total white blood cell count in dogs infected with D canis was increased when dogs were sensitized with DNCB (p<0.01). The result appeared to be caused by stress due to D canis infection, secondary bacterial infection and decreased efficacy of general body defense system. Blood eosionophils were increased in D canis-infected dogs which appreared to be caused by the allergic contact dermatitis. Blood chemistry analysis revealed that total protein and globulin were increased(p<0.05), while albumin level was decreased. This result appeared to be caused by secondary bacterial infection.

• IMMUNE NETWORK
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• 제20권5호
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• pp.39.1-39.13
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• 2020

Sjögren's syndrome (SS) is a chronic and systemic autoimmune disease characterized by lymphocytic infiltration in the exocrine glands. In SS, type I IFN has a pathogenic role, and recently, inflammasome activation has been observed in both immune and non-immune cells. However, the relationship between type I IFN and inflammasome-associated pyroptosis in SS has not been studied. We measured IL-18, caspase-1, and IFN-stimulated gene 15 (ISG15) in saliva and serum, and compared whether the expression levels of inflammasome and pyroptosis components, including absent in melanoma 2 (AIM2), NLR family pyrin domain containing 3 (NLRP3), apoptosis-associated speck-like protein (ASC), caspase-1, gasdermin D (GSDMD), and gasdermin E (GSDME), in minor salivary gland (MSG) are related to the expression levels of type I IFN signature genes. Expression of type I IFN signature genes was correlated with mRNA levels of caspase-1 and GSDMD in MSG. In confocal analysis, the expression of caspase-1 and GSDMD was higher in salivary gland epithelial cells (SGECs) from SS patients. In the type I IFN-treated human salivary gland epithelial cell line, the expression of caspase-1 and GSDMD was increased, and pyroptosis was accelerated in a caspase-dependent manner upon inflammasome activation. In conclusion, we demonstrate that type I IFN may contribute to inflammasome-associated pyroptosis of the SGECs of SS patients, suggesting another pathogenic role of type I IFN in SS in terms of target tissue -SGECs destruction.

• 대한한방내과학회지
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• 제30권4호
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• pp.788-798
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• 2009

목적 : 이 연구는 백련초의 천식마우스 모델에 대한 효과를 조사하기 위해 수행하였다. 방법: 폐 세척액의 전체 세포와 호산구 수 그리고 폐조직으로의 면역세포의 침윤은 헤마톡실린과 에오신 염색으로 관찰 하였다. Interleukin (IL)-4의 발현량은 Enzyme-linked immunosorbent assay을 이용하여 측정하였으며, NO는 Griess roagont을 이용하였다. 결과 : 천식 병리현상의 하나인 Ovalbumin(OVA)에 의한 전체 세포와 호산구 수의 증가는 백련초 추출물 (200 mg/kg)을 처리한 군에서 감소하였다 (respectively, p<0.001 and p<0.01). 또한 OVA에 의한 증가된 면역세포의 침투는 백련초 추출물에 의해 감소하였다 (p < 0.01). 호산구의 침윤증상은 interleukin (IL)-4 그리고 5를 포함한 T helper (Th) 2 반응과 관련있기 때문에 폐세척액에서 IL-4의 발현량을 조사하였다. OVA에 증가한 IL-4는 백련초 추출물에 의해 감소하였다 (p < 0.05). 천식이 염증성 질병이기 때문에, lipopolysaccharide (LPS)로 자극한 RAW 264.7 세포에서 nitrite (NO) 생성을 살펴보았다. LPS에 의해 증가한 NO 생성을 백련초 추출물 (50, 100 and 200 mg/ml)에서 감소하였다 (respectively, p < 0.05, p<0.01 and p<0.05). 결론 : 이런 결과들은 백련초가 천식의 호산구 침윤에 저해효과를 가지고 있다고 나타내며, 백련초 추출물의 천식을 포함한 염증성 질환의 치료에 치료후보물질로 제안할 수 있다.

• Clinical and Experimental Pediatrics
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• 제56권11호
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• pp.482-489
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• 2013

Purpose: The aim of the present study was to investigate the differences in lower airway inflammatory immune responses, including cellular responses and responses in terms of inflammatory mediators in bronchoalveolar lavage fluid (BALF) and the airway, to rhinovirus (RV) infection on asthma exacerbation by comparing a control and a murine asthma model, with or without RV infection. Methods: BALB/c mice were intraperitoneally injected with a crude extract of Dermatophagoides farinae (Df ) or phosphate buffered saline (PBS) and were subsequently intranasally treated with a crude extract of Df or PBS. Airway responsiveness and cell infiltration, differential cell counts in BALF, and cytokine and chemokine concentrations in BALF were measured 24 hours after intranasal RV1B infection. Results: RV infection increased the enhanced pause (Penh) in both the Df sensitized and challenged mice (Df mice) and PBS-treated mice (PBS mice) (P<0.05). Airway eosinophil infiltration increased in Df mice after RV infection (P<0.05). The levels of interleukin (IL) 13, tumor necrosis factor alpha, and regulated on activation, normal T cells expressed and secreted (RANTES) increased in response to RV infection in Df mice, but not in PBS mice (P<0.05). The level of IL-10 significantly decreased following RV infection in Df mice (P<0.05). Conclusion: Our findings suggest that the augmented induction of proinflammatory cytokines, Th2 cytokines, and chemokines that mediate an eosinophil response and the decreased induction of regulatory cytokines after RV infection may be important manifestations leading to airway inflammation with eosinophil infiltration and changes in airway responsiveness in the asthma model.

• 대한본초학회지
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• 제27권1호
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• pp.11-16
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• 2012

Objectives : In the theory of Korean medicine, Pear has long been considered to protect throat, bronchus and lung. Pear has been believed to remove sputum in Korean people. This study was conducted to investigate the effect of pear ethanol extract (PEE) on asthma induced by ovalbumin in mice. Methods : We investigated the effects of PEE on airway hyperresponsiveness to methacholine, production levels of ovalbumin (OVA) specific total immunoglobulin G (IgG), IgG1, IgG2a and IgE in serum and histopathological changes of lung tissues in asthamtic mice. Results : PEE decreased airway hyperresponsiveness to methacholine significantly compared to non-treated asthmatic mice (P<0.05). Level of OVA specific IgE in serum was lowered by oral administration of PEE effectively (P<0.05). In histopathological observation, administration of PEE reduced infiltration of immune cells into lung tissue. Conclusion : These results suggest that pear has anti-asthmaitc action and related mechanims are involved in anti-inflammatory action such as reducing level of OVA specific IgE and immune cell infiltration.

• 동의생리병리학회지
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• 제21권3호
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• pp.714-720
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• 2007

Atopic dermatitis (AD) is a chronic inflammatory skin disease characterized by inflammatory cell infiltration in the skin. This study was performed to assess the therapeutic effects of BHOSB on the DNCB-induced dermatitis in NC/Nga mice, characterized by the onset of AD along with an increase the number of inflammatory cells and dysregulation of inflammatory mediators including cytokines and chemokines. BHOSB administration significantly reduced clinical dermatitis severity including pruritus, edema, eczematous and erythema. Histological findings indicated that the thickening of epidermis/dermis and dermal infiltration of inflammatory cells including mast cells were dramatically reduced. The suppression of dermatitis by BHOSB was accompanied by a decrease in the number of CD11b$^+$/Gr-1$^+$ immune cells in skin but not CD3$^+$/CCR3$^+$ cells. However, the number of CD3$^+$ cells was increased in BHOSB administrated NC/Nga mice. Oral administration of BHOSB significantly reduced the level of IL-6, TNF-a and eotaxin 2 mRNA in skin. These data suggest that BHOSB may be effective therapeutic agents for the treatment of AD.