Ji Hye Kim

Publications (3)11.25 Total impact

• Article: Particle-induced expression of SF20/IL25 is mediated by reactive oxygen species and NF-κB in alveolar macrophages

  Ji-Hye Kim, An-Soo Jang, Eun Kyong Shin, Chun-Mi Kang, Jung Seok, Eun Hee Lee, Myung Ok Kim, Sung Woo Park, SooTaek Uh, Choon-Sik Park
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  ABSTRACT: Bone marrow stroma-derived growth factor (SF20/IL25) regulates proliferation of lymphoid cells. We previously observed the upregulation of SF20/IL25 in alveolar macrophages treated with fine TiO2 particles and in a TiO2 particle-treated animal model. To identify the mechanism behind TiO2 particle-induced expression of SF20/IL25, we examined the dependence of the induction process on reactive oxygen species and on cytokine-mediated signaling transduction. For in vivo studies, TiO2 particles were intratracheally instilled in Sprague-Dawley rats. For in vitro studies, alveolar macrophages obtained from rat bronchoalveolar lavage cells were cultured in the presence of TiO2 particles. The antioxidant N-acetyl-L-cysteine (NAC) was used to block the formation of reactive oxygen species both in vivo and in vitro, and TPCK, SB203580, and GF10923X were used to inhibit signal transduction mediated by nuclear factor (NF)-κB, p38 MAP kinase, and protein kinase C, respectively, in vitro. In TiO2 particle-treated rats, intraperitoneal administration of NAC significantly decreased lung inflammation and attenuated the production of SF20/IL25 mRNA and protein. In TiO2 particle-stimulated alveolar macrophages, the upregulation of SF20/IL25 mRNA expression was abolished by NAC in a dose-dependent manner. The expression of SF20/IL25 mRNA in the stimulated macrophages was dose-dependently attenuated by TPCK, but not by SB203580 or GF10923X. Fine TiO2 particles stimulate alveolar macrophages to produce SF20/IL25 via the NF-κB-dependent generation of reactive oxygen species. KeywordsMacrophages-NF-κB-Reactive oxygen species-SF20/IL25-Particulate matter
  Molecular and Cellular Toxicology 04/2012; 6(3):305-312. · 0.88 Impact Factor
• Article: Association of IL-17RB gene polymorphism with asthma.

  Ji-Sun Jung, Byung Lae Park, Hyun Sub Cheong, Joon Seol Bae, Ji-Hye Kim, Hun Soo Chang, Taiyoun Rhim, Jong-Sook Park, An-Soo Jang, Young-Mok Lee, Ki-Up Kim, Soo-Taek Uh, Ju Ock Na, Yong-Hoon Kim, Choon-Sik Park, Hyoung Doo Shin
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  ABSTRACT: Interleukin (IL)-17E is a member of the IL-17 family, which induces IL-4, IL-5, IL-13, and eotaxin in experimental animals via IL-17 receptor B (IL-17RB). The activation of IL-17RB amplifies allergic-type inflammatory responses by inducing Jun kinase (or JNK), p38 mitogen-activated protein kinase (or MAPK), and nuclear factor-kappaB. We examined the association of polymorphisms in the IL-17RB gene with asthma susceptibility and investigated the effects of those polymorphisms on the transcription of various IL-17RB isoforms. In total, 954 asthmatic patients or 265 healthy control subjects were screened for polymorphisms in IL-17RB by single-base extension. The messenger RNA expression IL-17RB in B-cell lines derived from patients was also measured by reverse transcription-polymerase chain reaction. Direct sequencing of 24 unrelated Korean DNA samples revealed 18 genetic variants, including four insertion/deletions and 14 single-nucleotide polymorphisms (SNPs). Six of the SNPs (-1465G>A, +5661G>A, +6297T>C [Y123Y], +13797C>T, +18661C>T, and +18965G>A) were used to screen a larger group of subjects. Intronic polymorphism +5661G>A was significantly associated with the development of asthma (p = 0.001); moreover, a minor allele of IL-17RB +5661G>A appeared at a lower frequency in the asthmatic patients than in the healthy control subjects (0.13 vs 0.19, respectively). The IL-17RB messenger RNA expression in B cells homozygous for IL-17RB+ 5661GG was significantly higher than that in B cells homozygous for IL-17RB+5661AA (p = 0.002). A rare allele of IL-17RB +5661G>A may have a protective role against the development of asthma via regulation at the level of transcription. The SNPs identified in this study may be used to develop markers to assess the risk of asthma.
  Chest 01/2009; 135(5):1173-80. · 5.25 Impact Factor
• Article: Interleukin-25 and interleukin-13 production by alveolar macrophages in response to particles.

  Chun-Mi Kang, An-Soo Jang, Mi-Hyun Ahn, Jeong-Ah Shin, Ji-Hye Kim, Yun-Sung Choi, Tai-Youn Rhim, Choon-Sik Park
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  ABSTRACT: Particle inhalation-induced lung inflammation acts as an adjuvant to allergens or respiratory viral infection in a process that is mediated by macrophages and epitheliums. The production of interleukin (IL)-4 and IL-13 by activated T cells is involved in the augmentation of Th2-type immune responses to particles, and IL-25 induces the synthesis of IL-4 and IL-13. However, whether IL-13 and IL-25 are directly regulated by particle instillation in the lung has not been studied. The aim of this study was to reveal particle induction of IL-13 and IL-25 in the lung. TiO(2) instillation potently induced the mRNA expression for IL-25 and IL-13 in lung tissue extracts 24 h after treatment, as compared with the sham group. Immunostaining for IL-25 and IL-13 showed strong positivity for macrophages in the inflammatory lung lesions of TiO(2)-treated rats. The alveolar macrophages expressed IL-25 and IL-13 24 h after in vitro stimulation with TiO(2) particles in dose- and time-dependent manners, with maximal induction at 24 and 48 h after stimulation, respectively. The sequence of the rat IL-25 gene is 95% homologous with the mouse IL-25 gene. These findings indicate that alveolar macrophages play an important role in particle-induced lung inflammation via direct induction of IL-13 and IL-25 production.
  American Journal of Respiratory Cell and Molecular Biology 10/2005; 33(3):290-6. · 5.13 Impact Factor