Xiaoling Qiang

Feinstein Institute for Medical Research

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Ping Wang

Northwell Health

Haichao Wang

Inner Mongolia Agricultural University

Jianhua Li

Feinstein Institute for Medical Research

Kevin J. Tracey

Feinstein Institute for Medical Research

Shu Zhu

Feinstein Institute for Medical Research

Rongqian Wu

Zhujiang Hospital

Mian Zhou

Macau University of Science and Technology

Youxin Ji

Qingdao University

Takayoshi Toyota

Tohoku University

Mikio Sagara

National Institutes for Quantum and Radiological Science and Technology

Cooperative Institutions

Feinstein Institute for Medical Research

Northwell Health

Tohoku University

Hofstra University

North Shore University Hospital

Donald & Barbara Zucker School of Medicine at Hofstra/Northwell

Qingdao University

Wayne State University

Long Island Jewish Medical Center

Sun Yat-sen University

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New melanocortin-like peptide of E. coli can suppress inflammation via the mammalian melanocortin-1 receptor (MC1R): possible endocrine-like function for microbes of the gut

npj Biofilms and Microbiomes (2017)

Xiaoling Qiang Anthony S. Liotta Joseph Shiloach Joanne Gutierrez Haichao Wang

Abstract E. coli releases a 33 amino acid peptide melanocortin-like peptide of E. coli (MECO-1) that is identical to the C-terminus of the E. coli elongation factor-G (EF-G) and has interesting similarities to two prominent mammalian melanocortin hormones, alpha-melanocyte-stimulating hormone (alpha-MSH) and adrenocorticotropin (ACTH). Note that MECO-1 lacks HFRW, the common pharmacophore of the known mammalian melanocortin peptides. MECO-1 and the two hormones were equally effective in severely blunting release of cytokines (HMGB1 and TNF) from macrophage-like cells in response to (i) endotoxin (lipopolysaccharide) or (ii) pro-inflammatory cytokine HMGB-1. The in vitro anti-inflammatoty effects of MECO-1 and of alpha-MSH were abrogated by (i) antibody against melanocortin-1 receptor (MC1R) and by (ii) agouti, an endogenous inverse agonist of MC1R. In vivo MECO-1 was even more potent than alpha-MSH in rescuing mice from death due to (i) lethal doses of LPS endotoxin or (ii) cecal ligation and puncture, models of sterile and infectious sepsis, respectively.

Melanocortins

Melanocortin 1 receptor

10.1038/s41522-017-0039-9

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Molecular basis for the insulinomimetic effects of C-peptide

Diabetologia (2001)

George Grunberger Xiaoling Qiang Z. Li Suresh T. Mathews Diego Sbrissa

Wortmannin

Insulin receptor substrate

10.1007/s001250100632

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Citations (144)

[Inhibited effect of phosphorylated insulin-like growth factor binding protein-1 on hepatoma cells in vitro].

PubMed (1999)

Xiaoling Qiang Huijun Li Yu J

To elucidate the inhibited effect and regulated mechanism of IGFBp-1 on the carcinoma cells.The recombinant human IGF II (rhIGF II), phosphorylated and nonphosphorylated binding protein-1(pBp-1 and npBp-1) that were purified from pregnant woman's amnoitic fluid were used to cultivate cancer cells from 15 cases with hepatocellular carcinoma and ascites. The cell counting and MTT methods were used for determining the dynamics change of proliferation on HCC, and the in situ or dot hybridization with Digoxin label used for the expression of IGF II mRNA qualitatively and quantitatively at different times.The cells grew more slowly, in pBp-1 group, than in control group at the same time, which began to decrease at two days(P < 0.05) by MTT. In situ hybridization showed that there are hybridization signal of IGF II mRNA in all groups during the culture, and scanning dot hybridization showed the OPTMD of IGF II mRNA in pBp-1 group was statistically different from control and other groups (P < 0.01), while in npBp-1 group there was no significant effect compared with other groups (P > 0.05).The pBp-1 can inhibit the growth of hepatoma cells and the expression of IGF II mRNA, which may be regulated and inhibited by pBp-1.

MTT assay

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Reconstruction of bandlimited signal from its non-uniform integral samples

Applicable Analysis (2005)

Xiaoling Qiang

In this article, we discuss the problem of reconstructing a bandlimited signal f from the samples of the integral of the signal. We first apply the trigonometric polynomials to approximate the integral of the signal and then reconstruct instantaneous samples from the signal integral.

Bandlimiting

SIGNAL (programming language)

10.1080/00036810500048137

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Coated Carbon Nanotubes at Nano Copper Modified GCE for Simultaneous Determination of Dopamine and Uric Acid

Advanced materials research (2012)

Xiaoling Qiang Jian Fei Xia Zong Hua Wang Yan Xia Fei Fei Zhang

Copper (Cu) nanoparticles have been electrochemically deposited onto the glassy carbon electrode (GCE) surface by potentiostatic deposition method and then carbon nanotubes (CNTs) was dropped on the nano-Cu modified electrode surface to get a CNTs/nano-Cu/GCE electrode. The CNTs/nano-Cu/GCE has shown much higher electrocatalytic activity than the CNTs/GCE towards the oxidation of dopamine (DA) and uric acid (UA) in a phosphate buffer solution (pH 6.9). It can be applied to determine DA and UA with satisfactory results.

Phosphate buffered saline

10.4028/www.scientific.net/amr.600.238

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Bacterial endotoxin stimulates macrophages to release HMGB1 partly through CD14- and TNF-dependent mechanisms

Journal of Leukocyte Biology (2004)

Chen Guo-qian Jianhua Li Mahendar Ochani B. Rendon-Mitchell Xiaoling Qiang

Abstract Bacterial endotoxin [lipopolysaccharide (LPS)] stimulates macrophages to sequentially release early [tumor necrosis factor (TNF)] and late [high mobility group box 1 (HMGB1)] proinflammatory cytokines. The requirement of CD14 and mitogen-activated protein kinases [MAPK; e.g., p38 and extracellular signal-regulated kinase (ERK)1/2] for endotoxin-induced TNF production has been demonstrated previously, but little is known about their involvement in endotoxin-mediated HMGB1 release. Here, we demonstrated that genetic disruption of CD14 expression abrogated LPS-induced TNF production but only partially attenuated LPS-induced HMGB1 release in cultures of primary murine peritoneal macrophages. Pharmacological suppression of p38 or ERK1/2 MAPK with specific inhibitors (SB203580, SB202190, U0126, or PD98059) significantly attenuated LPS-induced TNF production but failed to inhibit LPS-induced HMGB1 release. Consistently, an endogenous, immunosuppressive molecule, spermine, failed to inhibit LPS-induced activation of p38 MAPK and yet, still significantly attenuated LPS-mediated HMGB1 release. Direct suppression of TNF activity with neutralizing antibodies or genetic disruption of TNF expression partially attenuated HMGB1 release from macrophages induced by LPS at lower concentrations (e.g., 10 ng/ml). Taken together, these data suggest that LPS stimulates macrophages to release HMGB1 partly through CD14- and TNF-dependent mechanisms.

HMGB1

Proinflammatory cytokine

10.1189/jlb.0404242

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Citations (185)

Clinical Observation of Compound Cholinicytidine Diphosphate Associated with Fructose Diphosphate in Treating Neonatal Hypoxic-ischemic Encephalopathy

Hebei yixue (2013)

Xiaoling Qiang

Objective: To evaluate the efficacy and safty of compound cholinicytidine diphosphate associated with fructose diphosphate in treating neonatal hypoxic-ischemic encephalopathy(HIE).Method: 80 cases with HIE were divided into experimental group(40 cases) and control group(40 cases) randomly.All of them were treated by the traditional therapy,and children were treated by cholinicytidine diphosphate added in control group,while those were treated by cholinicytidine diphosphate associated with fructose diphosphate added in experimental group.Result: The disturbance of consciousness,convulsion,convulsion,muscle tonus in experimental group were improved more quickly than those in control group(P0.05),and total effective rate was 95% in experimental group,which was higher than that in control group(P0.05),and the value of NBNA was much more improved in experimental group,and the difference between the two groups showed statistical significance(P0.05).Conclusion: Cholinicytidine diphosphate associated with fructose diphosphate in treating neonatal hypoxic-ischemic encephalopathy is safe and effective.It is worthy to be recommended.

Convulsion

Hypoxic-Ischemic Encephalopathy

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Polymer-assisted in Situ Growth of Copper Nanoparticles on Graphene Surface for Non-Enzymatic Electrochemical Sensing of Glucose

International Journal of Electrochemical Science (2013)

Zonghua Wang Jianfei Xia Xiaoling Qiang Yanzhi Xia Guoyu Shi

10.1016/s1452-3981(23)14819-x

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Development of Procathepsin L (pCTS-L)-Inhibiting Lanosterol-Carrying Liposome Nanoparticles to Treat Lethal Sepsis

International Journal of Molecular Sciences (2023)

Weiqiang Chen Shu Zhu Xiaoling Qiang Shujin Chen Jianhua Li

The pathogenesis of microbial infections and sepsis is partly attributable to dysregulated innate immune responses propagated by late-acting proinflammatory mediators such as procathepsin L (pCTS-L). It was previously not known whether any natural product could inhibit pCTS-L-mediated inflammation or could be strategically developed into a potential sepsis therapy. Here, we report that systemic screening of a NatProduct Collection of 800 natural products led to the identification of a lipophilic sterol, lanosterol (LAN), as a selective inhibitor of pCTS-L-induced production of cytokines [e.g., Tumor Necrosis Factor (TNF) and Interleukin-6 (IL-6)] and chemokines [e.g., Monocyte Chemoattractant Protein-1 (MCP-1) and Epithelial Neutrophil-Activating Peptide (ENA-78)] in innate immune cells. To improve its bioavailability, we generated LAN-carrying liposome nanoparticles and found that these LAN-containing liposomes (LAN-L) similarly inhibited pCTS-L-induced production of several chemokines [e.g., MCP-1, Regulated upon Activation, Normal T Cell Expressed and Presumably Secreted (RANTES) and Macrophage Inflammatory Protein-2 (MIP-2)] in human blood mononuclear cells (PBMCs). In vivo, these LAN-carrying liposomes effectively rescued mice from lethal sepsis even when the first dose was given at 24 h post the onset of this disease. This protection was associated with a significant attenuation of sepsis-induced tissue injury and systemic accumulation of serval surrogate biomarkers [e.g., IL-6, Keratinocyte-derived Chemokine (KC), and Soluble Tumor Necrosis Factor Receptor I (sTNFRI)]. These findings support an exciting possibility to develop liposome nanoparticles carrying anti-inflammatory sterols as potential therapies for human sepsis and other inflammatory diseases.

Proinflammatory cytokine

10.3390/ijms24108649

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Citations (4)

Monoclonal Antibodies Capable of Binding SARS-CoV-2 Spike Protein Receptor Binding Motif Specifically Prevent GM-CSF Induction

bioRxiv (Cold Spring Harbor Laboratory) (2020)

Xiaoling Qiang Shu Zhu Jianhua Li Ping Wang Kevin J. Tracey

A severe acute respiratory syndrome (SARS)-like coronavirus (SARS-CoV-2) has recently caused a pandemic COVID-19 disease that infected more than 25.6 million and killed 852,000 people worldwide. Like the SARS-CoV, SARS-CoV-2 also employs a receptor-binding motif (RBM) of its envelope spike protein for binding the host angiotensin-converting enzyme 2 (ACE2) to gain viral entry. Currently, extensive efforts are being made to produce vaccines against a surface fragment of a SARS-CoV-2, such as the spike protein, in order to boost protective antibody responses. It was previously unknown how spike protein-targeting antibodies would affect innate inflammatory responses to SARS-CoV-2 infections. Here we generated a highly purified recombinant protein corresponding to the RBM of SARS-CoV-2, and used it to screen for cross-reactive monoclonal antibodies (mAbs). We found two RBM-binding mAbs that competitively inhibited its interaction with human ACE2, and specifically blocked the RBM-induced GM-CSF secretion in both human monocyte and murine macrophage cultures. Our findings have suggested a possible strategy to prevent SARS-CoV-2-elicited "cytokine storm", and provided a potentially useful criteria for future assessment of innate immune-modulating properties of various SARS-CoV-2 vaccines. RBM-binding Antibodies Inhibit GM-CSF Induction.

Cytokine Storm

Coronavirus

10.1101/2020.09.04.280081

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Citations (3)