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Your search keyword '"Tian, Shifu"' showing total 13 results
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13 results on '"Tian, Shifu"'

3. Costimulation of γδTCR and TLR7/8 promotes Vδ2 T-cell antitumor activity by modulating mTOR pathway and APC function

Author

Wang, Huaishan, primary, Chen, Hui, additional, Liu, Shujing, additional, Zhang, Jie, additional, Lu, Hezhe, additional, Somasundaram, Rajasekharan, additional, Choi, Robin, additional, Zhang, Gao, additional, Ou, Lingling, additional, Scholler, John, additional, Tian, Shifu, additional, Dong, Liyun, additional, Yeye, Guo, additional, Huang, Lili, additional, Connelly, Thomas, additional, Li, Ling, additional, Huang, Alexander, additional, Mitchell, Tara C, additional, Fan, Yi, additional, June, Carl H, additional, Mills, Gordon B, additional, Guo, Wei, additional, Herlyn, Meenhard, additional, and Xu, Xiaowei, additional

Published
2021
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8. Filifactor alocis modulates human neutrophil antimicrobial functional responses.

Author

Edmisson, Jacob S., Tian, Shifu, Armstrong, Cortney L., Vashishta, Aruna, Klaes, Christopher K., Miralda, Irina, Jimenez‐Flores, Emeri, Le, Junyi, Wang, Qian, Lamont, Richard J., and Uriarte, Silvia M.

Subjects
*NEUTROPHILS, *ANTI-infective agents, *PHAGOSOMES, *STAPHYLOCOCCUS aureus, *RESPIRATORY diseases
Abstract

Filifactor alocis is a newly appreciated pathogen in periodontal diseases. Neutrophils are the predominant innate immune cell in the gingival crevice. In this study, we examined modulation of human neutrophil antimicrobial functions by F. alocis. Both non-opsonised and serum-opsonised F. alocis were engulfed by neutrophils but were not efficiently eliminated. Challenge of neutrophils with either non-opsonised or serum-opsonised F. alocis induced a minimal intracellular as well as extracellular respiratory burst response compared to opsonised Staphylococcus aureus and fMLF, respectively. However, pretreatment or simultaneous challenge of neutrophils with F. alocis did not affect the subsequent oxidative response to a particulate stimulus, suggesting that the inability to trigger the respiratory response was only localised to F. alocis phagosomes. In addition, although neutrophils engulfed live or heat-killed F. alocis with the same efficiency, heat-killed F. alocis elicited a higher intracellular respiratory burst response compared to viable organisms, along with decreased surface expression of CD35, a marker of secretory vesicles. F. alocis phagosomes remained immature by delayed and reduced recruitment of specific and azurophil granules, respectively. These results suggest that F. alocis withstands neutrophil antimicrobial responses by preventing intracellular ROS production, along with specific and azurophil granule recruitment to the bacterial phagosome. [ABSTRACT FROM AUTHOR]

Published
2018
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13. Filifactor alocisPromotes Neutrophil Degranulation and Chemotactic Activity

Author

Armstrong, Cortney L., Miralda, Irina, Neff, Adam C., Tian, Shifu, Vashishta, Aruna, Perez, Lisandra, Le, Junyi, Lamont, Richard J., and Uriarte, Silvia M.

Abstract

ABSTRACTFilifactor alocisis a recently recognized periodontal pathogen; however, little is known regarding its interactions with the immune system. As the first-responder phagocytic cells, neutrophils are recruited in large numbers to the periodontal pocket, where they play a crucial role in the innate defense of the periodontium. Thus, in order to colonize, successful periodontal pathogens must devise means to interfere with neutrophil chemotaxis and activation. In this study, we assessed major neutrophil functions, including degranulation and cell migration, associated with the p38 mitogen-activated protein kinase (MAPK) signaling pathway upon challenge with F. alocis.Under conditions lacking a chemotactic gradient, F. alocis-challenged neutrophils had increased migration compared to uninfected cells, indicating that F. alocisincreases chemokinesis in human neutrophils. In addition, neutrophil chemotaxis induced by interleukin-8 was significantly enhanced when cells were challenged with F. alocis, compared to noninfected cells. Similar to live bacteria, heat-killed F. alocisinduced both random and directed migration of human neutrophils. The interaction of F. alociswith Toll-like receptor 2 induced granule exocytosis along with a transient ERK1/2 and sustained p38 MAPK activation. Moreover, F. alocis-induced secretory vesicle and specific granule exocytosis were p38 MAPK dependent. Blocking neutrophil degranulation with TAT-SNAP23 fusion protein significantly reduced the chemotactic and random migration induced by F. alocis. Therefore, we propose that induction of random migration by F. alociswill prolong neutrophil traffic time in the gingival tissue, and subsequent degranulation will contribute to tissue damage.

Published
2016
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