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927 results on '"Tang, Yu‐Ping"'

34. Mast cell-derived factor XIIIA contributes to sexual dimorphic defense against group B streptococcal infections

Author

Piliponsky, Adrian M., Sharma, Kavita, Quach, Phoenicia, Brokaw, Alyssa, Nguyen, Shayla, Orvis, Austyn, Saha, Siddhartha S., Samanas, Nyssa Becker, Seepersaud, Ravin, Tang, Yu Ping, Mackey, Emily, Bhise, Gauri, Gendrin, Claire, Furuta, Anna, Seo, Albert J., Guga, Eric, Miralda, Irina, Coleman, Michelle, Sweeney, Erin L., Bauml, Charlotte A., Imhof, Diana, Snyder, Jessica M., Moeser, Adam J., and Rajagopal, Lakshmi

Subjects
Pneumococcal infections -- Development and progression, Mast cells -- Physiological aspects -- Health aspects, Coagulation -- Health aspects, Blood coagulation factor VIII -- Physiological aspects -- Health aspects, Dimorphism (Biology) -- Health aspects, Health care industry
Abstract

Invasive bacterial infections remain a major cause of human morbidity. Group B streptococcus (GBS) are Gram-positive bacteria that cause invasive infections in humans. Here, we show that factor XIIIA-deficient (FXIIIA-deficient) female mice exhibited significantly increased susceptibility to GBS infections. Additionally, female WT mice had increased levels of FXIIIA and were more resistant to GBS infection compared with isogenic male mice. We observed that administration of exogenous FXIIIA to male mice increased host resistance to GBS infection. Conversely, administration of a FXIIIA transglutaminase inhibitor to female mice decreased host resistance to GBS infection. Interestingly, male gonadectomized mice exhibited decreased sensitivity to GBS infection, suggesting a role for gonadal androgens in host susceptibility. FXIIIA promoted GBS entrapment within fibrin clots by crosslinking fibronectin with ScpB, a fibronectin-binding GBS surface protein. Thus, ScpB- deficient GBS exhibited decreased entrapment within fibrin clots in vitro and increased dissemination during systemic infections. Finally, using mice in which FXIIIA expression was depleted in mast cells, we observed that mast cell-derived FXIIIA contributes to host defense against GBS infection. Our studies provide insights into the effects of sexual dimorphism and mast cells on FXIIIA expression and its interactions with GBS adhesins that mediate bacterial dissemination and pathogenesis., Introduction Invasive bacterial infections are one of the leading causes of human morbidity and mortality. An important cause of invasive infections is group B streptococcus (GBS) or Streptococcus agalactiae. GBS [...]

Published
2022
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42. Comparative analysis of the main active constituents from different parts of Leonurus japonicus Houtt. and from different regions in China by ultra-high performance liquid chromatography with triple quadrupole tandem mass spectrometry

Author

Tan, Ya-Jie, Xu, Ding-Qiao, Yue, Shi-Jun, Tang, Yu-Ping, Guo, Sheng, Yan, Hui, Zhang, Jing, Zhu, Zhen-Hua, Shi, Xu-Qin, Chen, Yan-Yan, Gu, Yao, Ding, Xiao-Rui, Huang, Sheng-Liang, Peng, Guo-Ping, Zhou, Gui-Sheng, and Duan, Jin-Ao

Published
2020
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48. Microbes mediated immunogenic cell death in cancer immunotherapy.

Author

Huang, Jumin, Duan, Fugang, Xie, Chun, Xu, Jiahui, Zhang, Yizhong, Wang, Yuwei, Tang, Yu‐Ping, and Leung, Elaine Lai‐Han

Subjects
CELL death, CANCER cells, IMMUNE checkpoint inhibitors, IMMUNOTHERAPY, MICROORGANISMS
Abstract

Summary: Immunogenic cell death (ICD) is one of the 12 distinct cell death forms, which can trigger immune system to fight against cancer cells. During ICD, a number of cellular changes occur that can stimulate an immune response, including the release of molecules called damage‐associated molecular patterns (DAMPs), signaling to immune cells to recognize and attack cancer cells. By virtue of their pivotal role in immune surveillance, ICD‐based drug development has been a new approach to explore novel therapeutic combinations and personalized strategies in cancer therapy. Several small molecules and microbes can induce ICD‐relevant signals and cause cancer cell death. In this review, we highlighted the role of microbe‐mediate ICD in cancer immunotherapy and described the mechanisms through which microbes might serve as ICD inducers in cancer treatment. We also discussed current attempts to combine microbes with chemotherapy regimens or immune checkpoint inhibitors (ICIs) in the treatment of cancer patients. We surmise that manipulation of microbes may guide personalized therapeutic interventions to facilitate anticancer immune response. [ABSTRACT FROM AUTHOR]

Published
2024
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