Xueting Liu

Dr. Xueting Liu

Second Affiliated Hospital of Guangzhou Medical University, Guangzhou, Guangdong, China
orcid

Research Focus & Metrics

Academic Career Length

16Years (2011-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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6 July 2022 in Toxins
Verified
Journal Article
Open access
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Huanquan ChenHuanquan Chen
Huanquan Chen
JZJunyan Zhang
Junyan Zhang
YHYing He
Ying He
Zhuoyi LvZhuoyi Lv
Zhuoyi Lv
Zhengtong LiangZhengtong Liang
Zhengtong Liang
Xueting LiuXueting Liu
Xueting Liu
Staphylococcus aureus is a very common Gram-positive bacterium, and S. aureus infections play an extremely important role in a variety of diseases. This paper describes the types of virulence factors involved, the inflammatory cells activated, the process of host cell death, and the associated diseases caused by S. aureus. S. aureus can secrete a variety of enterotoxins and other toxins to trigger inflammatory responses and activate inflammatory cells, such as keratinocytes, helper T cells, innate lymphoid cells, macrophages, dendritic cells, mast cells, neutrophils, eosinophils, and basophils. Activated inflammatory cells can express various cytokines and induce an inflammatory response. S. aureus can also induce host cell death through pyroptosis, apoptosis, necroptosis, autophagy, etc. This article discusses S. aureus and MRSA (methicillin-resistant S. aureus) in atopic dermatitis, psoriasis, pulmonary cystic fibrosis, allergic asthma, food poisoning, sarcoidosis, multiple sclerosis, and osteomyelitis. Summarizing the pathogenic mechanism of Staphylococcus aureus provides a basis for the targeted treatment of Staphylococcus aureus infection.

10 March 2017 in Science
Verified
Journal Article
Closed access
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YYYao-Qing Yu
Yao-Qing Yu
DBDevin M. Barry
Devin M. Barry
YHYan Hao
Yan Hao
Xueting LiuXueting Liu
Xueting Liu
ZCZhou-Feng Chen
Zhou-Feng Chen
To scratch or not to scratch: Observing someone else scratching themselves can make you want to do so. This contagious itching has been observed in monkeys and humans, but what about rodents? Yu et al. found that mice do imitate scratching when they observe it in other mice. The authors identified a brain area called the suprachiasmatic nucleus as a key circuit for mediating contagious itch. Gastrin-releasing peptide and its receptor in the suprachiasmatic nucleus were necessary and sufficient to transmit this contagious behavior. Science , this issue p. 1072

1 August 2019 in Brain, Behavior, and Immunity
Verified
Journal Article
Closed access
SLSisi Liu
Sisi Liu
Xueting LiuXueting Liu
Xueting Liu
HXHui Xiong
Hui Xiong
WWWen Wang
Wen Wang
YLYutong Liu
Yutong Liu
ZMZhinan Mei
Zhinan Mei

13 March 2020 in Nature Communications
Verified
Journal Article
Open access
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DBDevin M. Barry
Devin M. Barry
Xueting LiuXueting Liu
Xueting Liu
BLBenlong Liu
Benlong Liu
XLXian-Yu Liu
Xian-Yu Liu
FGFang Gao
Fang Gao
ZCZhou-Feng Chen
Zhou-Feng Chen
Gastrin-releasing peptide (GRP) functions as a neurotransmitter for non-histaminergic itch, but its site of action (sensory neurons vs spinal cord) remains controversial. To determine the role of GRP in sensory neurons, we generated a floxed Grp mouse line. We found that conditional knockout of Grp in sensory neurons results in attenuated non-histaminergic itch, without impairing histamine-induced itch. Using a Grp-Cre knock-in mouse line, we show that the upper epidermis of the skin is exclusively innervated by GRP fibers, whose activation via optogeneics and chemogenetics in the skin evokes itch- but not pain-related scratching or wiping behaviors. In contrast, intersectional genetic ablation of spinal Grp neurons does not affect itch nor pain transmission, demonstrating that spinal Grp neurons are dispensable for itch transmission. These data indicate that GRP is a neuropeptide in sensory neurons for non-histaminergic itch, and GRP sensory neurons are dedicated to itch transmission.

17 July 2017 in Cell Death Discovery
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Journal Article
Open access
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PHPeide Huang
Peide Huang
ACAnan Chen
Anan Chen
WHWeiyi He
Weiyi He
ZLZhen Li
Zhen Li
GZGuanglin Zhang
Guanglin Zhang
JWJu Wang
Ju Wang
Bone morphogenetic protein 2 (BMP-2) has been reported to facilitate epithelial-to-mesenchymal transition (EMT) and bone metastasis in breast cancer xenograft models. To investigate the role of BMP-2 in the development of breast cancer stem cells (BCSCs), and to further elucidate the mechanisms underlying its influence on breast cancer metastasis, we conducted a comprehensive molecular study using breast cancer cell lines and clinical samples. Our results showed that downregulation of Rb by BMP-2 was associated with ubiquitin-mediated degradation activated by phosphorylation of Rb via the PI3K/AKT signal pathway. In addition, the Smad signaling pathways are implicated in upregulation of CD44 protein expression by BMP-2. It was suggested that cross-talk exists between Rb and CD44 signaling pathways, as recombinant human BMP-2 (rhBMP-2) was found to regulate CD44 expression partly through Rb signals. In clinical tissues, BMP-2 was positively and negatively correlated with CD44 and Rb expression, respectively. Based on the in vitro and in vivo results, we have established an integrated mechanism by which rhBMP-2 induces EMT and stemness of breast cancer cells via the Rb and CD44 signaling pathways, which then contribute to breast cancer metastasis. These findings may be helpful for developing new strategies for the treatment and prognosis of advanced breast cancer.

13 November 2017 in Scientific Reports
Verified
Journal Article
Open access
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LWLi Wan
Li Wan
HJHua Jin
Hua Jin
XLXian-Yu Liu
Xian-Yu Liu
JJJoseph Jeffry
Joseph Jeffry
DBDevin M. Barry
Devin M. Barry
ZCZhou-Feng Chen
Zhou-Feng Chen
A key question in our understanding of itch coding mechanisms is whether itch is relayed by dedicated molecular and neuronal pathways. Previous studies suggested that gastrin-releasing peptide (GRP) is an itch-specific neurotransmitter. Neuromedin B (NMB) is a mammalian member of the bombesin family of peptides closely related to GRP, but its role in itch is unclear. Here, we show that itch deficits in mice lacking NMB or GRP are non-redundant andNmb/Grpdouble KO (DKO) mice displayed additive deficits. Furthermore, bothNmb/GrpandNmbr/GrprDKO mice responded normally to a wide array of noxious stimuli. Ablation of NMBR neurons partially attenuated peripherally induced itch without compromising nociceptive processing. Importantly, electrophysiological studies suggested that GRPR neurons receive glutamatergic input from NMBR neurons. Thus, we propose that NMB and GRP may transmit discrete itch information and NMBR neurons are an integral part of neural circuits for itch in the spinal cord.