Browsing by Author "Lin, Ching-Yi"

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Characterizing the polymeric status of Helicobacter pylori heat shock protein 60
(2009-10-16)
Lin, Ching-Yi
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Huang, Yu-Shan
;
Li, Chi-Han
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Hsieh, Yuan-Ting
;
Tsai, Nu-Man
Helicobacter pylori heat shock protein 60 (HpHsp60) was first identified as an adhesion molecule associated with H. pylori infection. Here we have analyzed the structure of HpHsp60 via amino acid BLAST, circular dichroism, and electrophoresis and the results indicate that most recombinant HpHsp60 molecules exist as dimers or tetramers, which is quite different from Escherichia coli Hsp60. Treatment of human monocytic cells THP-1 with HpHsp60 was found to up-regulate a panel of cytokines including IL-1 alpha, IL-8, IL-10, IFN-gamma, TNF-alpha, TGF-beta, GRO, and RANTES. Carboxymethylated HpHsp60 molecules with a switched oligomeric status were able to further enhance NF-kappa B-mediated IL-8 and TNF-alpha secretion in THP-1 cells compared to unmodified HpHsp60 molecules. These results indicated that the oligomeric status of HpHsp60s might have an important role in regulating host inflammation and thus help facilitate H. pylori persistent infection. (C) 2009 Elsevier Inc. All rights reserved.
Combined immunogene therapy of IL-6 and IL-15 enhances anti-tumor activity through augmented NK cytotoxicity
(2008-12-18)
Lin, Ching-Yi
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Chuang, Tien-Fu
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Liao, Kuang-Wen
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Huang, Yi-Jun
;
Pai, Chien-Chun
Many tumors evade host immunity by lowering expression of major histocompatibility complex (MHC) molecules. Theoretically, low MHC expression should activate natural killer (NK) cells and in some cases suppress tumor growth; nevertheless, some tumors also produce high concentrations of immunosuppressive cytokines, such as transforming growth factor (TGF)-beta, to inhibit the activity of NK cells. Using a canine transmissible venereal tumor (CTVT) model, we have previously demonstrated that IL-6 is a strong antagonist for TGF-beta. Herein, we found that IL-6 alone was unable to significantly promote TGF-beta-inhibited NK activities. Conversely, IL-15 alone strongly promoted NK activities; however, NK activities were inhibited to baseline levels following the addition of TGF-beta. Therefore, a new strategy using combined immunogene therapy of both IL-6 and IL-15 mediated by electroporation was used in this study. This combined IL-6 and IL-15 treatment effectively relieved the inhibitory effect of TGF-beta and activated NK cell cytotoxicity of lymphokine-activated killer (LAK) cells. Similarly, in isolated DX5(+) NK cells, only IL-6 and IL-15 in combination significantly overcame the inhibitory effect of TGF-beta and promoted NK cytotoxicity. The group of BALB/c mice injected with plasmids with IL-6 and IL-15 genes (pIL-6/pIL-15) had the highest percentages of DX5(+) NK cells as compared with either the pIL-6 or pIL-15 groups. Further, in SCID mice inoculated with CTVT, electroporation-mediated delivery of pIL-6/pIL-15 was significantly more efficient in suppressing both tumor establishment and tumor growth as compared with pIL-6 or pIL-15 inoculation alone. In addition, the anti-asialo GM-1 antibody abolished NK activities in SCID mice and resulted in outgrowth of the tumors. Together, these results suggest that the TGF-beta-associated inhibition of NK cytotoxicity cannot be adequately restored by simply antagonizing TGF-beta with IL-6: the co-existence of NK activating factors such as IL-15 is also important in restoring TGF-beta-inhibited cytotoxicity. This study highlights the therapeutic potential of the pIL-6/pIL-15 combination by inhibiting TGF-beta activity and enhancing NK cytotoxicity. (c) 2008 Elsevier Ireland Ltd. All rights reserved.
Helpful or unhelpful? Self-affirmation on challenge-confronting tendencies for students who fear being laughed at
(2016-01)
Liu, Cheng-Hong
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Huang, Po-Sheng
;
Chang, Jen-Ho
;
Lin, Ching-Yi
;
Huang, Ching-Chun
Studies suggest that self-affirmation interventions may help increase students\' tendencies to confront challenges. However, we posited that self-affirmation cannot help students with higher levels of fear of being laughed at (gelotophobia) confront challenges because it may lead them to accept negative information (feelings of threat) about their ability and decrease their perceptions of self-ability. In support of this hypothesis, Experiment 1 found that being attribute-affirmed enhanced the tendencies to confront a challenging task for junior high school students with low gelotophobia, but not for those with high gelotophobia. Experiment 2 revealed that being value-affirmed increased challenge-confronting tendencies for senior high school students with low gelotophobia. However, it decreased high gelotophobia students\' challenge-confronting tendencies because it caused them to feel less capable of performing the task. Thus, self-affirmation, which may decrease high gelotophobia students\' self-perceived ability in challenging situations, may be unhelpful or even harmful in motivating them to confront challenges. (C) 2015 Elsevier Inc. All rights reserved.
Preferential induction of transforming growth factor-beta production in gastric epithelial cells and monocytes by Helicobacter pylori soluble proteins
(2007-11-01)
Wu, Ming-Shiang
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Lin, Jaw-Town
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Hsu, Ping-Ning
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Lin, Ching-Yi
;
Hsieh, Yuan-Ting
Background. The cytokines induced by Helicobacter pylori, as well as the intricate balance of proinflammatory and anti-inflammatory cytokines, are relevant to the outcomes of H. pylori infection. Transforming growth factor (TGF)-beta and interleukin (IL)-10 are 2 vital anti-inflammatory cytokines that regulate mucosal immunity in various inflammatory and infectious diseases. Methods. To elucidate whether host-bacteria interaction can influence TGF-beta and IL-10 production, we investigated the expression of TGF-beta and IL-10 in various mammalian cell lines preincubated with H. pylori and other enteric bacteria. Results. The amount of TGF-beta protein, but not IL-10, was significantly increased after stimulation with H. pylori, but other enteric bacteria did not induce TGF-beta production. Different H. pylori strains isolated from patients with gastritis, peptic ulcer, gastric cancer and strains with cagA or vacA isogenic mutations showed similar effects on TGF-beta induction, indicating that this effect was a constitutional characteristic of H. pylori and independent of cagA and vacA status. Conclusion. The results imply the presence of a protein factor ( termed "TGF-beta-inducing protein") that induces production of TGF-beta. In view of the multiple effects of TGF-beta, we conclude the TGF-beta-inducing protein of H. pylori might mediate the immune response and contribute to the pathogenesis of H. pylori infection.