| Summary: | 碩士 === 國立交通大學 === 生物醫學研究所 === 96 === Heat shock protein 60 of Helicobacter pylori has been found that it can induce interleukin-8 (IL-8) secretion in human monocytic cells and gastric epithelium cells. In this study, we further found that the IL-6, IL-8, TNF-���nand IL-1���nwere induced in THP-1 cells after H. pylori HSP60 stimulation. The kinetic of cytokine expression showed that TNF-���nwas earliest secreted at 2 h, and reached a maximum at 4 h. This result consisted with the kinetic of TNF-�� mRNA expression analyzed by quantitative real-time PCR. TNF-�� may have a great effect on THP-1 cells activation. Dissimilarly, IL-1��, IL-6, and IL-8 were later produced by THP-1 cells. We further examined THP-1 cells activation by detecting its enodocytosis activity and surface marker expression. Surprisingly, the endocytosis ability of THP-1 cells was weakened after rHpHSP60 stimulation. However, the co-stimulatory molecules (CD40, CD80, and CD86) were up-regulated, whereas MHC class II which plays a central in presenting the foreign antigen to T helper cells was significantly down-regulated. MHC I expression was not influenced by rHpHSP60. Interestingly, the rhTNF-�� mimicry experiments indicated that the endocytosis activity of THP-1 cells was diminished by rhTNF-�� in�na�ndoes-dependent manner. However, it can promote CD40 expression on THP-1 cells surface. To mimic the chronic inflammation area of H. pylori-infected patients, rhTNF-�� and TGF-��1 were used to treat THP-1 cells. The inhibitory effect on endocytotic activity of THP-1 cells was observed by rhTNF-�� and TGF-��1 synergy treatment. TNF-�� seemed to synergize with TGF-��1 to decrease the engulf ability of cells. However TGF-��1 further inhibited TNF-��-mediated CD40 expression. This study suggested rHpHSP60 induced TNF-��, IL-1��, IL-6, and IL-8 secretion in THP-1 cells. Among these cytokines, TNF-�� was earliest secreted. Even through the endocytosis ability of THP-1 cells was inhibited and the MHC class II was significantly decreased after rHpHSP60 stimulation. The role of TNF-���nin our study was not an “effector” on THP-1 cells activation but diminished its activity. In the chronic inflammation, the inhibition effect of TNF-���ncombining with TGF-��1 on monocytes activation was more critical.
|
|---|
