Xiaojin Liu

Shantou University, Swatow, Guangdong, China

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Publications (6)18.03 Total impact

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    ABSTRACT: Asthma is thought to result from the generation of T helper type 2 (Th2) responses, leading to bronchial inflammation. IFN-λ1 (also known as IL-29) is a recently described member of the IFN-λ family and has been shown to decrease production of Th2 cytokines in vitro. However, the role and mechanism of IFN-λ1 in asthma remain unknown. The aim of this study was to clarify the importance of IFN-λ1 in allergen-induced airway hyperresponsiveness (AHR) and inflammation. We used a murine model for ovalbumin (OVA)-induced asthma to examine the effect of intranasal delivery of recombinant adenovirus expressing human IFN-λ1 (Ad-hIFN-λ1) on AHR and allergic airway inflammation. Intranasal instillation of Ad-hIFN-λ1 before airway antigen challenge in OVA-immunized mice significantly decreased the severity of AHR and numbers of eosinophils and levels of IL-4, IL-5, and IL-13, but not IL-10 and IFN-γ; both in vivo, in the bronchoalveolar lavage fluid and in vitro, following stimulation of lymphocytes from spleens with OVA, compared with administration of a control virus (Ad-mock). Furthermore, Ad-hIFN-λ1 treatment inhibited serum IgE secretion and increased numbers of splenic CD4+CD25+FOXP3+ Treg cells. Histological studies showed that Ad-hIFN-λ1 attenuated OVA-induced lung tissue eosinophilia. These results demonstrate that delivery of the Ad-hIFN-λ1 can mitigate allergic airway inflammation in experimental asthma. The potent immunoregulatory action of IFN-λ1 may offer a novel therapeutic approach to treat allergic asthma.
    No preview · Article · May 2014 · International immunopharmacology
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    Chuan Qiu · Yan Li · Mingcai Li · Min Li · Xiaojin Liu · Charles McSharry · Damo Xu
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    ABSTRACT: The mechanism by which cigarette smoke (CS) causes chronic obstructive pulmonary disease (COPD) is poorly understood. IL-33 is a pleiotropic cytokine predominantly expressed in lung tissue and can elicit airway inflammation in naïve mice. We tested the hypothesis that IL-33 is induced by CS and contributes to CS-mediated airway inflammation in a mouse model of CS-induced COPD. Groups of mice were exposed to CS three times per day for 4 consecutive days. The expression levels of IL-33 and ST2 were markedly enhanced in the lung tissue of mice inhaling CS. CS exposure also induced neutrophil and macrophage infiltration and inflammatory cytokine (IL-1β, TNF-α, IL-17), chemokine (MCP-1) and MUC5AC expression in the airways. More importantly, all these CS-induced pathogenic changes were significantly inhibited by the treatment of neutralizing anti-IL-33 antibody delivered intranasally. Thus, our results suggest that IL-33 plays a critical role in the CS-mediated airway inflammation and may be a therapeutic target in CS-related diseases including COPD. © 2012 The Authors. Immunology © 2012 Blackwell Publishing Ltd.
    Full-text · Article · Oct 2012 · Immunology
  • Mingcai Li · Yan Li · Xiaojin Liu · Xueming Gao · Yaqing Wang
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    ABSTRACT: IL-33 is a recently described member of the IL-1 family that has been reported to have a pathogenic role in several inflammatory diseases. In this study, we evaluated the role of IL-33 in a murine model of multiple sclerosis, experimental autoimmune encephalomyelitis (EAE). We showed that the expression of IL-33 and its receptor, ST2, was markedly elevated in the spinal cord of mice during myelin oligodendrocyte glycoprotein (MOG)(35-55) peptide-induced EAE. Administration of a blocking anti-IL-33 antibody in mice of EAE during the induction phase significantly inhibited the onset and severity of EAE and reduced MOG(35-55)-induced IFN-γ and IL-17 production. In contrast, treatment with recombinant IL-33 worsened the disease course of EAE in association with increased induction of both IFN-γ and IL-17. Furthermore, anti-IL-33 treatment caused a remarkable decrease in expression of IL-17, IFN-γ, T-bet and RORγt, and an upregulation of IL-10 and TGF-β in the spinal cord of EAE mice. These results demonstrate that endogenous IL-33 plays a pivotal role in the pathogenesis of EAE and indicate that blockade of IL-33 has a significant protective effect against EAE.
    No preview · Article · Apr 2012 · Journal of neuroimmunology
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    Xiaojin Liu · Yan Wu · Mingcai Li · Sui Chen · Yanchun Zhou
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    ABSTRACT: Interleukin (IL)-33 is the latest member of IL-1 cytokine family. In this study, the cloning, expression, purification, and polyclonal antibody preparation of mouse IL-33 were described. The coding region of IL-33 mature protein was cloned into the prokaryotic expression vector pET-44. The recombinant protein, IL-33 containing a hexahistidine tag in the C-terminal, was expressed in Escherichia coli. The expressed soluble protein was purified by immobilized metal-ion affinity chromatography using Ni2+-nitrilotriacetic acid agarose. The rabbits were immunized with the purified recombinant protein. The obtained antiserum was precipitated by saturated ammonium sulfate and then purified by Protein A affinity chromatography. The sensitivity and specificity of the antibodies were evaluated by enzyme-linked immunosorbent assay and immunohistochemistry. The high titer (1 : 32000) polyclonal antibodies with high specificity were obtained by immunizing rabbits with the purified recombinant protein. Significant expression of IL-33 was seen in mouse liver and lung tissues determined with the anti-IL-33. The production of the polyclonal antibody against IL-33 provides a good tool for studying the biofunctions of IL-33.
    Full-text · Article · Nov 2009 · BioMed Research International
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    ABSTRACT: Interleukin (IL)-33 is a recently described member of the IL-1 family and has been shown to induce production of T helper type 2 cytokines. In this study, an anti-IL-33 antibody was evaluated against pulmonary inflammation in mice sensitized and challenged with ovalbumin. The anti-IL-33 or a control antibody (150 microg/mouse) was given intraperitoneally as five doses before the sensitization and antigen challenge. Treatment with anti-IL-33 significantly reduced serum IgE secretion, the numbers of eosinophils and lymphocytes, and concentrations of IL-4, IL-5, and IL-13 in bronchoalveolar lavage fluid compared with administration of a control antibody. Histological examination of lung tissue demonstrated that anti-IL-33 significantly inhibited allergen-induced lung eosinophilic inflammation and mucus hypersecretion. Our data demonstrate for the first time that anti-IL-33 antibody can prevent the development of asthma in a mouse model and indicate that blockade of IL-33 may be a new therapeutic strategy for allergic asthma.
    No preview · Article · Jul 2009 · Biochemical and Biophysical Research Communications
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    Mingcai Li · Xiaojin Liu · Yanchun Zhou · Shao Bo Su
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    ABSTRACT: IFN-lambdas, including IFN-lambda1, IFN-lambda2, and IFN-lambda3, also known as IL-29, IL-28A, or IL-28B, are a newly described group of cytokines distantly related to the type I IFNs and IL-10 family members. The IFN-lambdaR complex consists of a unique ligand-binding chain, IFN-lambdaR1 (also designated IL-28Ralpha), and an accessory chain, IL-10R2, which is shared with receptors for IL-10-related cytokines. IFN-lambdas signal through the IFN-lambdaR and activate pathways of JAK-STATs and MAPKs to induce antiviral, antiproliferative, antitumor, and immune responses. In this review, we summarize recent findings about the biology of IFN-lambdas and their pathophysiological roles in viral infection, cancer, and immune responses of the innate and adaptive arms.
    Preview · Article · Apr 2009 · Journal of leukocyte biology