• 제목/요약/키워드: interleukin 17A

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Fidelity of Transgene Transmission and Expression in the Transgenic Mice

  • Zheng, Z. Y.;Y. M. Han;Y. K. Kang;K. B. Oh;W. J. Shin;Lee, K. K.
    • 한국동물번식학회:학술대회논문집
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    • 한국동물번식학회 2002년도 춘계학술발표대회 발표논문초록집
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    • pp.89-89
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    • 2002
  • In this study, we examined transmission efficiency and expression level of the transgenes in the transgenic mice. The transgenic lines secreting a considerable amount of human lactoferrin(LF) thrombopoietin(TPO), interleukin-10(IL-10) into their milk were subjected to access the inheritance and maintenance of transgenic phenotype. They were bred through three generations. The transmission frequency for each generations(F9, F10, F11) of 3 lines was 38.03±10.43%(13/35), 48.33±3.76%(19/39) and 31.83±8.88%(9/28) in the LF line, 51.33±18.98%(20/38), 63.70±35.71%(12/20) and 29.57± 15.05%(8/26) in the TPO line, 38.27±17.74%(15/37), 47.47±29.88%(14/28) and 50.87±5.85%(14/28) in the IL-10 line, respectively. (omitted)

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Release of Newcastle Disease Virus Vaccine from Chitosan Microspheres In vitro and In vivo

  • Park, I.K.;Jiang, H.L.;Yun, C.H.;Choi, Y.J.;Kim, S.J.;Akaike, T.;Kim, S.I.;Cho, C.S.
    • Asian-Australasian Journal of Animal Sciences
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    • 제17권4호
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    • pp.543-547
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    • 2004
  • Newcastle disease vaccine (NDV)-loaded chitosan microspheres (NDV-CM) were prepared. Stimulatory effects of these NDV-CM on antibody response compared to free NDV were examined in vitro and in vivo. In vitro stimulation of macrophages with virus vaccine resulted in higher number of cells compared to saline-treated control. Both NDV and NDV-CM induced secretion of interleukin-1 (IL-1) in dose dependent manner and the secretion of IL-1 by NDV-CM was delayed compared to free NDV. Irrespective of vaccine formulation, NDV subunit antigen was not effective in preventing mortality of the birds after challenge. However, CM loaded with NDV made of whole viron had antibody responses and protection similar to those shown by ND-K, a commercial inactivated oilemulsion vaccine.

Effect of Cordycepin on the Expression of the Inflammatory Cytokines TNF-alpha, IL-6, and IL-17A in C57BL/6 Mice

  • Seo, Min Jeong;Kim, Min Jeong;Lee, Hye Hyeon;Park, Jeong Uck;Kang, Byoung Won;Kim, Gi-Young;Rhu, En Ju;Kim, Jung-In;Kim, Kwang Hyuk;Jeong, Yong Kee
    • Journal of Microbiology and Biotechnology
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    • 제23권2호
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    • pp.156-160
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    • 2013
  • Culture supernatants of splenocytes from C57BL/6 mice were exposed to 0.3, 1.0, and 3.0 ${\mu}g/ml$ cordycepin plus 3.0 ${\mu}g/ml$ lipopolysaccharide (LPS) to investigate the effects of cordycepin (3'-deoxyadenosine) on the production of inflammatory cytokines. Coadministration of 3.0 ${\mu}g/ml$ cordycepin with LPS in cultured murine spleen cells significantly diminished expression of the inflammatory cytokines tumor necrosis factor-${\alpha}$ and interleukin-6 (IL-6) in a time-dependent manner. Expression of the inflammatory cytokine IL-17A was substantially downregulated in a timeand concentration-dependent manner at all cordycepin concentrations. These findings suggest that cordycepin downregulates the immediate hypersensitivity reaction stimulated by LPS.

Inverse behavior of IL-23R and IL-17RA in chronic and aggressive periodontitis

  • Ruiz-Gutierrez, Alondra del Carmen;Rodriguez-Montano, Ruth;Pita-Lopez, Maria Luisa;Zamora-Perez, Ana Lourdes;Guerrero-Velazquez, Celia
    • Journal of Periodontal and Implant Science
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    • 제51권4호
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    • pp.254-263
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    • 2021
  • Purpose: Periodontitis is associated with a dysbiosis of periodontopathic bacteria, which stimulate the interleukin (IL)-23/IL-17 axis that plays an essential role in the immunopathogenesis of this disease, leading to alveolar bone destruction through receptor activator of nuclear factor κB ligand (RANKL). IL-23 receptor mRNA (IL-23R) has been identified in periodontitis, and IL-17 receptor A mRNA (IL-17RA) and its protein have not yet been evaluated in patients with periodontitis. In this study was measure IL-23R and IL-17RA in gingival tissue (GT) from patients with generalized chronic periodontitis (GCP) and generalized aggressive periodontitis (GAP) and to explore correlations with clinical parameters. Methods: We included 16 healthy subjects (HS), 18 patients with GCP, and 14 with GAP. GT samples were collected during periodontal surgery. Both IL-23R and IL-17RA were detected by enzyme-linked immunosorbent assay. Results: The results were analyzed with Mann-Whitney U test and Spearman' rank correlation coefficients using SPSS version 25.0. We found lower IL-23R levels in patients with GCP and GAP than in HS. Contrarily, we observed higher IL-17RA levels in GCP and GAP patients than in HS. Moreover, we found negative correlations between IL-23R in GT and probing depth and clinical attachment loss (CAL). Likewise, a positive correlation of IL-17RA in GT with CAL was found. Conclusions: The results of these findings suggest that the reverse behavior between IL-23R and IL-17RA in periodontitis patients may also be involved with the activation of RANKL, which promotes alveolar bone loss.

Ginsenoside F2 attenuates chronic-binge ethanol-induced liver injury by increasing regulatory T cells and decreasing Th17 cells

  • Kim, Myung-Ho;Kim, Hee-Hoon;Jeong, Jong-Min;Shim, Young-Ri;Lee, Jun-Hee;Kim, Ye Eun;Ryu, Tom;Yang, Keungmo;Kim, Kyu-Rae;Jeon, Byeong-Min;Kim, Sun Chang;Jung, Jae-Kwang;Choi, Jae-Kap;Lee, Young-Sun;Byun, Jin-Seok;Jeong, Won-Il
    • Journal of Ginseng Research
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    • 제44권6호
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    • pp.815-822
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    • 2020
  • Background: Recently, beneficial roles of ginsenoside F2 (GF2), a minor constituent of Panax ginseng, have been demonstrated in diverse inflammatory diseases. However, its roles in alcoholic liver inflammation and injury have not been clearly understood. Here, we investigated the underlying mechanism by which GF2 ameliorated alcoholic liver injury. Methods: To induce alcoholic liver injury, C57BL/6J wild type (WT) or interleukin (IL)-10 knockout (KO) mice were orally administered with ethanol (3 g/kg) or ethanol-containing GF2 (50 mg/kg) for 2 wk. Liver injury and infiltration of macrophages and neutrophils were evaluated by serum biochemistry and immunohistochemistry, respectively. The changes of hepatic immune cells were assessed by flow cytometry and polymerase chain reaction analysis. In vitro differentiation of naïve T cells was performed. Results: GF2 treatment significantly attenuated alcoholic liver injury, in which infiltrations of inflammatory macrophages and neutrophils were decreased. Moreover, the frequencies of Foxp3+ regulatory T cells (Tregs) increased but IL-17-producing T (Th17) cells decreased in GF2-treated mice compared to controls. Furthermore, the mRNA expression of IL-10 and Foxp3 was significantly increased, whereas IL-17 mRNA expression was suppressed in GF2-treated mice. However, these beneficial roles of GF2 were not observed in GF2-treated IL-10 KO mice, suggesting a critical role of IL-10. Similarly, GF2 treatment suppressed differentiation of naïve T cells into Th17 cells by inhibiting RORgt expression and stimulating Foxp3 expression. Conclusion: The present study suggests that GF2 treatment attenuates alcoholic liver injury by increasing IL-10 expression and Tregs and decreasing IL-17 expression and Th17 cells.

A Clinical Study on Juheli (Recombinant Human Interleukin - 11) in the Second Prevention of Chemotherapy Induced Thrombocytopenia

  • Xiao, Yang;Liu, Jun;Huang, Xin-En;Guo, Jian-Xiong;Fu, Peng-Chao;Huang, Xiao-Hong;Zhou, Juan;Ye, Ai-Qin
    • Asian Pacific Journal of Cancer Prevention
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    • 제17권2호
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    • pp.485-489
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    • 2016
  • Objective: to investigate the effect and side effects of recombinant human interleukin - 11 (rhIL - 11, in Chinese Juheli, produced by Qi Lu Biotechnology CO., LTD) in the second prevention of chemotherapy induced thrombocytopenia (CIT). Methods: Cancer patients with CIT were recruited and were treated with rhIL - 11 (treatment phase, TP), and in the following cycle, all these patients administered with rhIL - 11 24 hours immediately after chemotherapy (preventive treatment phase, PTP). Duration and severity of thrombocytopenia between two phases were compared. Results: for patients in TP or PTP, nadir values of platelet were ($29.28{\pm}20.08){\times}10^9/L$ and ($45.24{\pm}19.66){\times}10^9/L$, duration of thrombocytopenia in TP and PTP was ($11.52{\pm}4.33$) and ($8.20{\pm}+2.77$)days, recovery time was ($19.40{\pm}3.89$)and ($13.44{\pm}3.02$)days, duration of rhIL - 11 administration was ($10.68{\pm}2.46$)and ($6.28{\pm}1.77$)days, number of patients needing platelet infusion was 16and4 respectively, all differences were statistically significant (p value were 0.007, 0.002, 0.000, 0.000, 0.034 respectively). For TP and PTP, number of patients with hemorrhage was 8 and 4, duration of bleeding was ($5.00{\pm}0.82$) and ($4.50{\pm}0.71$) days respectively, with no statistically significant difference. Adverse reactions mainly included fever, edema, arrhythmia, joint pain, fatigue, skin rash, headache, dizziness, etc., all were not statistically significant between TP and PTP. Conclusion: rhIL - 11 could be well tolerated and is effective that could reduce the duration, severity of CIT, platelet transfusion, and incidence of bleeding, as well as shorten the recovery time, duration of rhIL - 11 administration. Thus, rhIL - 11 could be commended in the second prevention of CIT for patients with cancer.

IL-17 and IL-17C Signaling Protects the Intestinal Epithelium against Diisopropyl Fluorophosphate Exposure in an Acute Model of Gulf War Veterans' Illnesses

  • Kristen M. Patterson;Tyler G. Vajdic;Gustavo J. Martinez;Axel G. Feller;Joseph M. Reynolds
    • IMMUNE NETWORK
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    • 제21권5호
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    • pp.35.1-35.16
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    • 2021
  • Gulf War Veterans' Illnesses (GWI) encompasses a broad range of unexplained symptomology specific to Veterans of the Persian Gulf War. Gastrointestinal (GI) distress is prominent in veterans with GWI and often presents as irritable bowel syndrome (IBS). Neurotoxins, including organophosphorus pesticides and sarin gas, are believed to have contributed to the development of GWI, at least in a subset of Veterans. However, the effects of such agents have not been extensively studied for their potential impact to GI disorders and immunological stability. Here we utilized an established murine model of GWI to investigate deleterious effects of diisopropyl fluorophosphate (DFP) exposure on the mucosal epithelium in vivo and in vitro. In vivo, acute DFP exposure negatively impacts the mucosal epithelium by reducing tight junction proteins and antimicrobial peptides as well as altering intestinal microbiome composition. Furthermore, DFP treatment reduced the expression of IL-17 in the colonic epithelium. Conversely, both IL-17 and IL-17C treatment could combat the negative effects of DFP and other cholinesterase inhibitors in murine intestinal organoid cells. Our findings demonstrate that acute exposure to DFP can result in rapid deterioration of mechanisms protecting the GI tract from disease. These results are relevant to suspected GWI exposures and could help explain the propensity for GI disorders in GWI Veterans.

기관지 천식환자에서 CD62L의 발현 및 싸이토카인의 변화 (Activity of Cytokines and Expression of CD62L in Patients with Bronchial Asthma)

  • 송광선;이원연;홍애라;김희선;용석중;신계철
    • Tuberculosis and Respiratory Diseases
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    • 제45권1호
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    • pp.90-98
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    • 1998
  • 연구배경: 외인성 천식은 TH2세포에 의한 매개체의 주요 원인중 하나임이 밝혀지고 있다. 연구자 등은 증상 악화로 내원한 기관지천식 환자와 만성기관지염 환자 사이에 T 림프구 아형의 변화와 싸어토카인 (cytokine)들의 변화에 차이가 있는지 연구하고자 하였다. 방 법: 기관지 천식으로 치료중인 환자 중에서 천식 악화로 내원한 외인성 천식 15예와 만성기관지염 환자 12예, 그리고 정상인 5예를 대상으로 하였다. 환자의 병력과 임상소견, 피부반응검사, 그리고 특이 IgE 측정을 시행하고 단일항체인 CD62L를 이용하여 flow cytometer로 림프구아형을 분석하고 ELISA kit(Quantikine IL-4, IFN-$\gamma$)를 이용하여 IL-4, IFN-$\gamma$을 측정하였다. 결 과: CD4+ T 림프구는 기관지천식환자에서 $40{\pm}7.2%$ 만성기관지염 환자 $43{\pm}19.8%$, 정상인에서 $41{\pm}14%$로 기관지 천식환자와 다른 군간에 의미있는 차이는 없었다(p=0.49, p=0.75). CD62L(L-selectin) 양성 T 림프구의 세포 백분율은 기관지천식환자(n=7) 에서 $24.8{\pm}23.6%$였고, 만성기관지염환자(n=5) $17.0{\pm}16.9%$, 정상인(n=5) $16.7{\pm}16.4%$으로 기관지천식환자와 다른 군간에 의미있는 차이는 없었다(p=0.32, p=0.22). 혈청 IL-4 의 활성도는 기관지천식환자에서 $3.6{\pm}0.9pg/ml$ 만성기관지염 환자 $2.0{\pm}1.2pg/ml$, 정상인에서 $0.7{\pm}1.1pg/ml$로 기관지 천식환자에서 만성기관지염 환자군에 비하여 증가되어 있었으며 (p=0.02) 정상인보다 증가되어 있었다(p=0.006)(Fig. 4). 혈청 INF-$\gamma$의 활성도는 증가되지 않았다. 결 론: 결론적으로 CD62L 양성 T 림프구의 세포 백분율은 기관지천식환자에서 증가되어 있지 않았으며 혈청 IL-4의 활성도는 기관지천식환자에서 증가되어 있었다.

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Immunological mechanism of postherpetic neuralgia and effect of pregabalin treatment on the mechanism: a prospective single-arm observational study

  • Mercan, Aysel;Uzun, Sema Tuncer;Keles, Sevgi;Hacibeyoglu, Gulcin;Yilmaz, Resul;Reisli, Ruhiye
    • The Korean Journal of Pain
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    • 제34권4호
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    • pp.463-470
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    • 2021
  • Background: Although neuropathic pain is a severe and common pain, its pathophysiology has not been elucidated yet. Studies in recent years have focused on the immune system's role in the pathogenesis of neuropathic pain. The aim of this study was to investigate the role of immunological mechanisms in neuropathic pain and the effect of pregabalin by measuring immunological marker levels in peripheral blood before and after pregabalin treatment in postherpetic neuralgia (PHN) patients with neuropathic pain. Methods: Forty patients diagnosed with PHN were included in the study. CD4, T follicular cells (Tfh: CD4+CXCR5+PD1+), Th17 (CD4+CCR6+ and CD4+IL17A+), regulatory T cells (Treg: CD4+ CD25+foxp3+), Th1 (CD4+ CXCR3+ and CD4+ IFN-γ+) and Th2 (CD4+ IL-4+) cell ratios were measured in peripheral blood samples before treatment and after 3 months of treatment. Results: When immunological marker and inflammation parameter levels were compared before and after treatment, the helper T cell ratio (CD3+, CD4+) was 30.28 ± 12.27% before treatment and 34.93 ± 11.70% after treatment, so there was a statistically significant increase (P = 0.028). Th17 was 4.75 ± 5.02% before treatment and 5.80 ± 3.13% after treatment, and there was a statistically significant increase (P = 0.036). Conclusions: Immunological mechanisms play an essential role in the pathogenesis of neuropathic pain, immunologically based treatment approach will be the critical point of treatment.

Cigarette Smoke Extract Enhances IL-17A-Induced IL-8 Production via Up-Regulation of IL-17R in Human Bronchial Epithelial Cells

  • Lee, Kyoung-Hee;Lee, Chang-Hoon;Woo, Jisu;Jeong, Jiyeong;Jang, An-Hee;Yoo, Chul-Gyu
    • Molecules and Cells
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    • 제41권4호
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    • pp.282-289
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    • 2018
  • Interleukin-17A (IL-17A) is a pro-inflammatory cytokine mainly derived from T helper 17 cells and is known to be involved in the pathogenesis of chronic obstructive pulmonary disease (COPD). Cigarette smoke (CS) has been considered as a primary risk factor of COPD. However, the interaction between CS and IL-17A and the underlying molecular mechanisms have not been clarified. In the current study, we investigated the effects of cigarette smoke extract (CSE) on IL-17A-induced IL-8 production in human bronchial epithelial cells, and sought to identify the underlying molecular mechanisms. IL-8 production was significantly enhanced following treatment with both IL-17A and CSE, while treatment with either IL-17A or CSE alone caused only a slight increase in IL-8 production. CSE increased the transcription of IL-17RA/RC and surface membrane expression of IL-17R, which was suppressed by an inhibitor of the phosphoinositide 3-kinase (PI3K)/Akt pathway (LY294002). CSE caused inactivation of glycogen synthase $kinase-3{\beta}$ ($GSK-3{\beta}$) via the PI3K/Akt pathway. Blockade of $GSK-3{\beta}$ inactivation by overexpression of constitutively active $GSK-3{\beta}$ (S9A) completely suppressed the CSE-induced up-regulation of IL-17R expression and the CSE-induced enhancement of IL-8 secretion. In conclusion, inactivation of $GSK-3{\beta}$ via the PI3K/Akt pathway mediates CSE-induced up-regulation of IL-17R, which contributes to the enhancement of IL-17A-induced IL-8 production.