Journal of Yeungnam Medical Science

Original Articles

Effect of on Aerosolized Vitamin E Pretreatment on Interleukin-1 Induced Acute Lung Injury in Rats: Jin Hong Chung, Kyeong-Cheol Shin; Yeungnam Univ J Med. 2007;24(2 Suppl):S365-372. Published online December 31, 2007; DOI: https://doi.org/10.12701/yujm.2007.24.2S.S365

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Abstract PDF: Background
：Interleukin-1 (IL-1) and neutrophil appear to contribute to the pathogenesis of acute respiratory distress syndrome (ARDS). Reactive oxygen species, as well as elastase released from activated neutrophil, are thought to play pivotal roles in the experimental models of acute lung leak. This study investigated whether aerosolized vitamin E can attenuate acute lung injury induced by IL-1 in rats. Materials and Methods：We intratracheally instilled either saline or IL-1 with and without pretreatment with aerosolized vitamin E in rats. After 5 hours of intratracheal instillation, lung lavage neutrophils, lung lavage protein concentration, lung myeloperoxidase(MPO) activity and lung wet weight to dry weight ratio(WW/DW) were measured in rat.
Results
：In rats given IL-1 intratracheally, lung lavage neutrophils, lung lavage protein concentration, lung MPO activity and WW/DW were higher. Pretreatment with aerosolized vitamin E decreased lung lavage neutrophils, lung MPO activity and WW/DW in rats given IL-1 intratracheally.
Conclusion
：These results suggest that direct pulmonary supplement of vitamin E decreases lung inflammation and leak in rats given IL-1 intratracheally.

Upregulation of IP-10(CXCL10) mRNA Expression by Interleukin-18.: Hyo Young Kim, Hee Sun Kim; Yeungnam Univ J Med. 2007;24(1):67-78. Published online June 30, 2007; DOI: https://doi.org/10.12701/yujm.2007.24.1.67

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Abstract PDF: BACKGROUND
Interleukin-18 (IL-18) is one of the principal inducers of interferon-gamma (IFN-gamma) in lymphocytes. MATERIALS AND METHODS: The effect of IL-18 on the expression of chemokine IP-10(CXCL10) mRNA in C57BL/6 mouse peritoneal macrophages was studied by using Northern blot analysis, enzyme linked immunosobent assay and electrophoretic mobility shift assay. RESULTS: IL-18 was determined to exert no direct effect on the expression of IP-10(CXCL10) mRNA. However, IL-18 pretreatment was determined to play a cooperative role in the synergistic induction of LPS-induced IP-10(CXCL10) mRNA expression. The effect associated with IL-18 pretreatment with regard to the synergistic induction of LPS-induced IP-10 (CXCL10) mRNA expression was detected after 16 hr of IL-18 pretreatment, administered prior to LPS stimulation. The pattern of NF-kB binding activity during IL-18 pretreatment with LPS stimulation was found to coincide with the expression of IP-10(CXCL10) mRNA. CONCLUSION: Although IL-18 alone exerts no direct effect on the expression of chemokine IP-10(CXCL10), a definite period of IL-18 pretreatment induces the synergistic expression of LPS-induced IP-10(CXCL10) mRNA. NF-kB activation is a component of this synergistic effect of IL-18 pretreatment. These results provide useful information, which may facilitate the elucidation of the action mechanisms underlying IL-18 effect on the expression of IP-10(CXCL10) mRNA.

Review

Identification of Interleukin 1-Responsive Genes in Human Chondrosarcoma SW1354 cells by cDNA Microarray Technology.: Jun Ha Jeon, Yong Wook Jung, Dae Young Yun, Hyun Do Kim, Chang Mo Kwon, Young Hoon Hong, Jae Ryong Kim, Choong Ki Lee; Yeungnam Univ J Med. 2007;24(1):24-40. Published online June 30, 2007; DOI: https://doi.org/10.12701/yujm.2007.24.1.24

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Abstract PDF: BACKGROUND
Accumulating evidence shows that interleukin(IL)-1 plays a critical role in inflammation and connective tissue destruction observed in both osteoarthritis and rheumatoid arthritis. IL-1 induces gene expression related to cytokines, chemokines and matrix metalloproteinases by activation of many different transcription factors. MATERIALS AND METHODS: The chondrosarcoma cell line, SW1353, is known to be a valuable in vitro system for investigating catabolic gene regulation by IL-1beta in chondrocytic cells. To explore and analyze the changes in gene expression by IL-1 responsible for arthritis, SW1353 was treated with IL-1 for 1, 6 and 24 h and then total RNAs were purified for each time. The changes in gene expression were analyzed with 17k human cDNA microarrays and validated by semi-quantitative RT-PCR. RESULTS: Greater than a two-fold change was observed in 1,200 genes including metallothioneins, matrix metalloproteinases, extracellular matrix proteins, antioxidant proteins, cytoskeleton proteins, cell cycle regulatory proteins, proteins for cell growth and apoptosis, signaling proteins and transcription factors. These changes appeared to be correlate with the pathophysiological changes observed in early osteoarthritis. CONCLUSION: cDNA microarray analysis revealed a marked variability in gene expression, and provided insight into the overall molecular changes. The result of this study provide initial information for further studies to identify therapeutic targets in osteoarthritis pathogenesis.

Original Articles

Effect of Neutrophil Elastase inhibitor, ICI 200,355, on Interleukin-1 Induced acute lung injury in rats.: Jin Hong Chung, Yeung Chul Mun, Hye Jung Park, Kyeong Cheol Shin, Kwan Ho Lee; Yeungnam Univ J Med. 2002;19(1):55-62. Published online June 30, 2002; DOI: https://doi.org/10.12701/yujm.2002.19.1.55

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Abstract PDF: BACKGROUND
Interleukin-1 (IL-1) and neutrophil appear to contribute to the pathogenesis of acute respiratory distress syndrome (ARDS). Elastase, as well as reactive oxygen species released from activated neutrophil, are thought to play pivotal roles in the experimental models of acute lung leak. This study investigated whether ICI 200,355, a synthetic elastase inhibitor, can attenuate acute lung injury induced by IL-1 in rats. MATERIALS AND METHODS: We intratracheally instilled either saline or IL-1 with and without treatment of ICI 200,355 in rats. Lung lavage neutrophils, lung lavage cytokine-induced neutrophil chemoattractant(CINC) concentration, lung lavage protein concentration, lung myeloperoxidase(MPO) activity and lung leak index were measured at 5 hours of intratracheal treatment. RESULTS: In rats given IL-1 intratracheally, lung lavage neutrophils, lung lavage CINC concentration, lung lavage protein concentration, lung MPO activity and lung leak index were higher. Intratracheal ICI 200,355 administration decreased lung lavage neutrophils, lung MPO activity and lung leak index, respectively, but did not decreased lung lavage CINC concentration. CONCLUSION: These results suggest that ICI 200,355 decreases lung inflammation and leak without decreasing lung lavage CINC concentration in rats given IL-1 intratracheally.

The effect of interleukin-10 on KC gene expression in mouse peritoneal macrophages.: Hee Sun Kim; Yeungnam Univ J Med. 1998;15(1):47-54. Published online June 30, 1998; DOI: https://doi.org/10.12701/yujm.1998.15.1.47

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Abstract PDF: Interleukin-10(IL-10) inhibits production of a wide range of cytokines in various cell types and transcriptionally inhibits lipopolysaccharide(LPS)-induced expression of proinflammatory mediators. Cytokine expression by macrophages is an important aspect to ochestrate inflammatory responses. As an approach to identify mechanistic targets of IL-10, it was examined the time course for expression of KC(murine homologue of Gro) gene in murine peritoneal macrophages stimulated with LPS with or without IL-10. The effect of IL-10 on LPS induced KC mRNA expression was delayed and only seen after 1 hour treatment. Pretreatment with IL-10 did not eliminate the delayed inhibitory response nor increase the magnitude of suppression. These effects did not depend upon time of IL-10 treatment but the time of LPS treatment. LPS-induced KC mRNA expression by inhibitoy action of IL-10 was not controlled at the level of transcription. The result indicates that IL-10 acts late in the process of KC gene expression and that the prominant site of action may be mRNA stability or translation.

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