Interleukin-18 Receptor α Modulates the T Cell Response in Food Allergy

Kim Eun Gyul,Leem Ji Su,Baek Seung Min,Kim Hye Rin,Kim Kyung Won,Kim Mi Na,손명현 대한천식알레르기학회 2022 Allergy, Asthma & Immunology Research Vol.14 No.4

Purpose: The prevalence of food allergy, triggered by T-helper type 2 (Th2) cell-mediated inflammation, is increasing worldwide. Interleukin (IL)-18 plays an important role in inflammatory diseases by binding with the IL-18 receptor. IL-18/IL-18 receptor α (IL-18Rα) is a cofactor for immunoglobulin E (IgE) production and Th2 cell development. Studies have not investigated the association between the IL-18/IL-18Rα signaling pathway and food allergy. Here, we investigated the role of IL-18Rα in food allergy induction and development. Methods: Wild-type (WT) and IL-18Rα-null mutant (IL-18Rα−/−) C57BL/6 mice were sensitized and challenged using ovalbumin (OVA) for food allergy induction. Food allergy symptoms, T cell-mediated immune responses, and signal transducer and activator of transcription (STAT)/suppressors of cytokine signaling (SOCS) pathways were analyzed in mice. Results: IL-18Rα expression was increased in WT mouse intestines after OVA treatment. Food allergy-induced IL-18Rα−/− mice showed attenuated systemic food allergic reactions, OVA-specific IgE and mouse mast cell protease-1 production, inflammatory cell infiltration, and T cell activation. Ex vivo experiments showed that cell proliferation and Th2 cytokine production were lower in IL-18Rα−/− mouse splenocytes than in WT mouse splenocytes. IL-18Rα blockade in WT splenocytes attenuated cell proliferation and Th2 cytokine production. Moreover, STAT3 phosphorylation was reduced in IL-18Rα−/− mice, and SOCS3 and SOCS1 activation were diminished in IL-18Rα−/− intestinal T cells. Conclusions: IL-18Rα regulates allergic reactions and immune responses by regulating T cell responses in food allergies. Moreover, IL-18Rα is involved in the STAT/SOCS signaling pathways. Targeting IL-18Rα signaling might be a novel therapeutic strategy for food allergy.

Chitinase 3-Like 1 Contributes to Food Allergy via M2 Macrophage Polarization

Eun Gyul Kim,김미나,홍정연,Jae Woo Lee,Soo Yeon Kim,김경원,이춘근,Jack A Elias,송태원,손명현 대한천식알레르기학회 2020 Allergy, Asthma & Immunology Research Vol.12 No.6

Purpose: Food allergy is a hypersensitive immune response to specific food proteins. Chitinase 3-like 1 (CHI3L1, also known as YKL-40 in humans or BRP-39 in mice) is associated with various chronic diseases, such as cancer, rheumatoid arthritis, and allergic disease. CHI3L1 is involved in allergen sensitization and type 2 helper T (Th2) inflammation, but the role of CHI3L1 in food allergy remains unclear. In this study, we sought to investigate the role of CHI3L1 in the development of food allergy. Methods: We measured serum levels of CHI3L1 in food allergic patients. Food allergy was induced in wild-type (WT) and CHI3L1 null mutant (CHI3L1−/−) BALB/c mice with ovalbumin (OVA). We investigated Th2 immune responses, M2 macrophage polarization, and mitogen-activated protein kinase (MAPK)/phosphoinositide 3-kinase (PI3K) signaling pathways, and also performed transcriptome analysis. Results: Serum levels of CHI3L1 were significantly higher in children with food allergy compared with those in healthy controls. Furthermore, CHI3L1 expression levels were elevated in WT mice after OVA treatment. Food allergy symptoms, immunoglobulin E levels, Th2 cytokine production, and histological injury were attenuated in food allergy-induced CHI3L1−/− mice compared with those in food allergy-induced WT mice. CHI3L1 expression was increased in OVA-treated WT intestinal macrophages and caused M2 macrophage polarization. Furthermore, CHI3L1 was involved in the extracellular signal-regulated kinases (ERK) and AKT signaling pathways and was associated with immune response and lipid metabolism as determined through transcriptome analysis. Conclusions: CHI3L1 plays a pivotal role in Th2 inflammation and M2 macrophage polarization through MAPK/ERK and PI3K/AKT phosphorylation in food allergy.

온도 데이터 기반 스마트 냉동컨테이너 전력량 소비 추정 연구

김은결(Eun Gyul Kim),최지호(Ji Ho Choi),강병오(Byung O Kang) 대한전기학회 2023 대한전기학회 학술대회 논문집 Vol.2023 No.7

온도 데이터 기반 스마트 냉동컨테이너 전력량 소비 추정 연구

김은결(Eun Gyul Kim),최지호(Ji Ho Choi),강병오(Byung O Kang) 대한전기학회 2023 대한전기학회 학술대회 논문집 Vol.2023 No.7

Deletion of activated leukocyte cell adhesion molecule (ALCAM/CD166) aggravates pulmonary fibrosis

( Mi Na Kim ),( Jung Yeon Hong ),( Eun Gyul Kim ),( Jae Woo Lee ),( Kyung Won Kim ),( Myung Hyun Sohn ) 대한결핵 및 호흡기학회 2019 대한결핵 및 호흡기학회 추계학술대회 초록집 Vol.127 No.-

Rationale: Idiopathic pulmonary fibrosis is a chronic, progressive lung disease characterized by fibroproliferative matrix molecule accumulation, collagen deposition and apoptosis. Activated leukocyte cell-adhesion molecule (ALCAM; CD166) is a cell adhesion molecule that has been implicated in adhesive and migratory attribution including leukocyte homing and trafficking and the cancer metastasis. We investigated the involvement of ALCAM on development of bleomycin-induced pulmonary fibrosis in murine model. Methods: Bleomycin-induced pulmonary fibrosis model was established with wild type and ALCAM-/- mice. Pulmonary fibrosis was also induced in TGF- β1 transgenic mice that conditionally overexpress TGF-β1 upon doxycycline administration. Levels of ALCAM were measured in lung tissue and bronchial alveolar lavage fluid (BALF). Histopathologic investigation was assessed by hematoxylin and eosin stain and masson trichrome stain. Terminal deoxynucleotidyl transferase dUTP nick end labeling assay, enzyme-linked immunosorbent assay, Western blot and real-time PCR were evaluated. Result: The protein and mRNA levels of ALCAM were decreased in the BALF and lung tissue of bleomycin-treated wild type mice. Reduced ALCAM levels were also observed in BALF and lung tissue of doxycycline administered TGF-β transgenic mice relative to those of control mice. ALCAM-/- mice showed aggravated lung fibrosis response compared with wild type mice upon bleomycin treatment. Doxycycline administration derived fibrosis also exacerbated in ALCAM-/- TGF- β transgenic mice compared to wild type TGF- β transgenic mice. ALCAM-/- mice showed aggravated cell death through PI3K and ERK signaling pathways in bleomycin-induced fibrosis. Conclusion: ALCAM contributes to bleomycin-induced pulmonary fibrosis associated with TGF-β response via PI3K and ERK signaling pathway.

An aptamer-antibody complex (oligobody) as a novel delivery platform for targeted cancer therapies

Heo, Kyun,Min, Sung-Won,Sung, Ho Jin,Kim, Han Gyul,Kim, Hyun Jung,Kim, Yun Hee,Choi, Beom Kyu,Han, Sewoon,Chung, Seok,Lee, Eun Sook,Chung, Junho,Kim, In-Hoo Elsevier 2016 Journal of controlled release Vol.229 No.-

<P><B>Abstract</B></P> <P>Aptamers have recently emerged as reliable and promising targeting agents in the field of biology. However, their therapeutic potential has yet to be completely assessed due to their poor pharmacokinetics for systemic administration. Here, we describe a novel aptamer-antibody complex, designated an “oligobody” (<U>oligo</U>mer+anti<U>body</U>) that may overcome the therapeutic limitations of aptamers. To provide proof-of-principle study, we investigated the druggability of oligobody <I>in vivo</I> using cotinine conjugated t44-OMe aptamer, which is specific for the sequence of pegaptanib, and an anti-cotinine antibody. The antibody part of oligobody resulted in extended <I>in vivo</I> pharmacokinetics of the aptamer without influencing its binding affinity. Moreover, the aptamer of oligobody penetrated deeply into the tumor tissues whereas the anti-VEGF antibody did not. Finally, the systemic administration of this oligobody reduced the tumor burden in a xenograft mouse model. Together, these results suggested that our oligobody strategy may represent a novel platform for rapid, low-cost and high-throughput cancer therapy.</P> <P><B>Graphical abstract</B></P> <P> <B>Aptamer-antibody hybrid complex</B>: Because the oligobody requires only a single antibody and utilizes a simple antigen–antibody reaction, it could offer the benefits of aptamers and antibodies, and may be a potentially valuable tool for cancer therapeutics.</P> <P>[DISPLAY OMISSION]</P>

Incidence and risk factors of incisional hernia after laparoendoscopic single-site (LESS) surgery in gynecology

( Gyul Jung ),( Hee Jin Kang ),( Yoo Hyun Chung ),( Ji Geun Yoo ),( Su Mi Kim ),( Eun Young Ki ),( In Cheol Jeong ) 대한산부인과학회 2021 대한산부인과학회 학술대회 Vol.107 No.-

Delayed Absorption of Subretinal Fluid after Retinal Reattachment Surgery and Associated Choroidal Features

Jong Min Kim,Eun Jung Lee,Ga Eun Cho,Kunho Bae,Ju Yeun Lee,Gyule Han,Se Woong Kang 대한안과학회 2017 Korean Journal of Ophthalmology Vol.31 No.5

Purpose: The aim of this study was to investigate the incidence and associated clinical factors of delayed absorption of subretinal fluid (SRF) after surgery for rhegmatogenous retinal detachment. Methods: This study involved 36 eyes of 36 consecutive patients who underwent successful surgery for rhegmatogenous retinal detachment. A complete ophthalmologic evaluation, including clinical fundus examination, optical coherence tomography, and indocyanine green angiography, was conducted before and after surgery. Delayed absorption was defined as the presence of residual concave SRF or an SRF bleb at 6 months after surgery. Clinical factors and choroidal features on indocyanine green angiography were compared according to the presence and absence of delayed absorption. Results: Eighteen of 36 eyes (50%) showed delayed absorption. Macular involvement and worse preoperative visual acuity were significantly related to the presence of delayed absorption (p = 0.001 and p = 0.034, respectively). On indocyanine green angiography, preoperative choroidal vascular hyperpermeability was noted in 70% of eyes with delayed absorption and in 14% of eyes without it (p = 0.010). Conclusions: Delayed absorption of SRF after retinal reattachment surgery was not rare, with a 50% of incidence in this study. Macula-off status was significantly related to the incidence of delayed SRF absorption, and choroidal features such as choroidal vascular hyperpermeability might be responsible in part, possibly through the resultant exudative property of choroid.

군 병사의 학교 폭력 피해 경험이 부대 내 부정적 대인관계에 미치는 영향 : 자기효능감의 매개효과 검증

곽주연(Juyeon Kwak),김재엽(Jae Yop Kim),오은영(Eun Young Oh),황성결(Sung Gyul Hwang) 한국군사회복지학회 2023 한국군사회복지학 Vol.16 No.1

본 연구의 목적은 군 병사의 학교 폭력 피해 경험이 부대 내 부정적 대인관계에 미치는 영향을 파악하고 자기효능감의 매개효과를 검증하는 것이다. 특히 학교 폭력 유형에 따른 피해 영향이 다를 수 있다는 점에서 학교 폭력 세 가지 유형(언어폭력, 따돌림, 신체적·물리적 폭력)에 따른 피해 경험이 부대 내 부정적 대인관계에 어떠한 영향을 미치는지 확인하였다. 이를 위해 2016년에 연세대학교 가족청소년복지 연구팀에서 진행한 「한국군 장병의 정신건강 실태조사」에서 수집된 자료를 통해 총 988명을 SPSS 29.0의 Process Macro 4.2로 분석하였다. 본 연구의 주요 결과는 군 병사의 학교 폭력 피해 경험과 부대 내 부정적 대인관계 사이에서 자기효능감이 완전매개하는 것으로 나타났다. 학교 폭력 피해 경험의 유형에 따라 살펴보면, 언어폭력 피해 경험과 부대 내 부정적 대인관계에서 자기효능감이 완전매개하는 것으로 나타났다. 이와 같은 연구 결과를 바탕으로 군 병사의 군대 내 부정적 대인관계와 자기효능감 증진을 위한 함의를 제시하고자 한다. The purpose of this study is to understand the influence of military soldiers' experience of school violence on negative interpersonal relationships within the unit and to verify the mediating effect of self-efficacy. Specifically, the study explores the association between experiences of victimization from three types of school violence(verbal violence, bullying, and physical violence) and negative interpersonal dynamics. To achieve this, data from the 'Survey on Mental Health of Korean Soldiers' conducted in 2016 by the Family and Youth Welfare Research Team at Yonsei University were analyzed using Process Macro 4.2 of SPSS 29.0, involving a total of 988 participants. The main findings of this study indicated that self-efficacy completely mediated the relationship between military soldiers' experiences of school violence and negative interpersonal relationships within the unit. When examining the specific types of school violence experiences, it was found that the experience of verbal violence was fully mediated by the sense of self-efficacy in relation to negative interpersonal dynamics within the unit. Based on these research results, implications for addressing negative interpersonal relationships within the military and enhancing self-efficacy among military personnel will be discussed.

Role of clusterin in protection against hyperoxic lung injury in mice

( Jung Yeon Hong ),( Mi Na Kim ),( Eun Gyul Kim ),( Jae Woo Lee ),( Kyung Won Kim ),( Myung Hyun Sohn ) 대한결핵 및 호흡기학회 2019 대한결핵 및 호흡기학회 추계학술대회 초록집 Vol.127 No.-

Purpose: Clusterin (CLU) is a highly conserved glycoprotein whose gene expression is ubiquitous and attribute to many cellular physiologic functions, including cell-cell interactions, complement inhibition, lipid transportation, cell survival, and apoptosis. We hypothesized that CLU might be important in hyperoxic acute lung injury. Methods: CLU expression and signaling was determined in airway epithelial cells after in vitro hyperoxia challenge. Using a murine model of hyperoxia-induced lung injury, the role of CLU was determined using CLU-deficient mice. CLU and cell death was detected by immunohistochemistry, real-time PCR, ELISA and Western blotting. Results: Increased CLU expression was observed in tracheal aspirates from babies with bronchopulmonary dysplasia or death. After hyperoxic exposure, CLU-/- mice exhibited more acute lung injury and activation of apoptotic cascades compared with wild-type (WT) mice. Further, hyperoxic conditions were a major stimulus for increased CLU expression and apoptosis in cultured human airway epithelial cells. We also observed that CLU overexpression attenuated hyperoxia- induced apoptosis in human airway epithelial cells. Conclusion: CLU has a significant protective role against pulmonary hyperoxic injury and their expression is related to the cell survival or protection of oxidant injury and cell death.