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学者姓名：李可
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Abstract ：
Emerging evidence suggest that C3aR plays important roles in homeostasis, host defense and disease. Although it is known that C3aR is protective in several models of acute bacterial infections, the role for C3aR in chronic infection is largely unknown. Here we show that C3aR is protective in experimental chronic pyelonephritis. Global C3aR deficient (C3ar(-/-)) mice had higher renal bacterial load, more pronounced renal histological lesions, increased renal apoptotic cell accumulation, tissue inflammation and extracellular matrix deposition following renal infection with uropathogenic E. coli (UPEC) strain IH11128, compared to WT control mice. Myeloid C3aR deficient (Lyz2-C3ar(-/-)) mice exhibited a similar disease phenotype to global C3ar(-/-) mice. Pharmacological treatment with a C3aR agonist reduced disease severity in experimental chronic pyelonephritis. Furthermore, macrophages of C3ar(-/-) mice exhibited impaired ability to phagocytose UPEC. Our data clearly demonstrate a protective role for C3aR against experimental chronic pyelonephritis, macrophage C3aR plays a major role in the protection, and C3aR is necessary for phagocytosis of UPEC by macrophages. Our observation that C3aR agonist curtailed the pathology suggests a therapeutic potential for activation of C3aR in chronic infection.
Keyword ：
C3aR chronic inflammation chronic pyelonephritis persistent infection phagocytosis renal fibrosis
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| GB/T 7714 | Zhao, Shu-Juan , Wu, Kun-Yi , Min, Xiao-Yun et al. Protective role for C3aR in experimental chronic pyelonephritis [J]. | FASEB JOURNAL , 2022 , 36 (11) . |
| MLA | Zhao, Shu-Juan et al. "Protective role for C3aR in experimental chronic pyelonephritis" . | FASEB JOURNAL 36 . 11 (2022) . |
| APA | Zhao, Shu-Juan , Wu, Kun-Yi , Min, Xiao-Yun , Wang, Chun-Xuan , Cao, Bo , Ma, Ning et al. Protective role for C3aR in experimental chronic pyelonephritis . | FASEB JOURNAL , 2022 , 36 (11) . |
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Abstract ：
Dopamine receptors are involved in several immunological diseases. We previously found that dopamine D3 receptor (D3R) on mast cells showed a high correlation with disease activity in patients with rheumatoid arthritis, but the mechanism remains largely elusive. In this study, a murine collagen-induced arthritis (CIA) model was employed in both DBA/1 mice and D3R knockout mice. Here, we revealed that D3R-deficient mice developed more severe arthritis than wild-type mice. D3R suppressed mast cell activation in vivo and in vitro via a Toll-like receptor 4 (TLR4)-dependent pathway. Importantly, D3R promoted LC3 conversion to accelerate ubiquitin-labeled TLR4 degradation. Mechanistically, D3R inhibited mTOR and AKT phosphorylation while enhancing AMPK phosphorylation in activated mast cells, which was followed by autophagy-dependent protein degradation of TLR4. In total, we found that D3R on mast cells alleviated inflammation in mouse rheumatoid arthritis through the mTOR/AKT/AMPK-LC3-ubiquitin-TLR4 signaling axis. These findings identify a protective function of D3R against excessive inflammation in mast cells, expanding significant insight into the pathogenesis of rheumatoid arthritis and providing a possible target for future treatment.
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| GB/T 7714 | Wang, Biao , Li, Xueyi , Li, Ming et al. Dopamine D3 receptor signaling alleviates mouse rheumatoid arthritis by promoting Toll-like receptor 4 degradation in mast cells [J]. | CELL DEATH & DISEASE , 2022 , 13 (3) . |
| MLA | Wang, Biao et al. "Dopamine D3 receptor signaling alleviates mouse rheumatoid arthritis by promoting Toll-like receptor 4 degradation in mast cells" . | CELL DEATH & DISEASE 13 . 3 (2022) . |
| APA | Wang, Biao , Li, Xueyi , Li, Ming , Geng, Yan , Wang, Na , Jin, Yaofeng et al. Dopamine D3 receptor signaling alleviates mouse rheumatoid arthritis by promoting Toll-like receptor 4 degradation in mast cells . | CELL DEATH & DISEASE , 2022 , 13 (3) . |
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Abstract ：
Emerging evidence suggests that signaling through the C3a anaphylatoxin receptor (C3aR) protects against various inflammation-related diseases. However, the role of C3aR in psoriasis remains unknown. The purpose of this study was to investigate the possible protective role of C3aR in psoriasis and to explore the underlying molecular mechanisms. We initially found that the psoriatic epidermis exhibited significantly decreased C3aR expression. C3aR showed protective roles in mouse models of imiquimod (IMQ)- and interleukin-23-induced psoriasis. Furthermore, increased epidermal thickness and keratin 6 (K6), K16, and K17 expression occurred in the ears and backs of C3aR(-/-) mice. Pharmacological treatment with a C3aR agonist ameliorated IMQ-induced psoriasiform lesions in mice and decreased the expression of K6, K16, and K17. Additionally, the signal transducer and activator of transcription 3 (STAT3) pathway participated in the protective function of C3aR. More importantly, the expression levels of K6, K16, and K17 in keratinocytes were all restored in HaCaT cells transfected with a C3aR-overexpression plasmid after treating them with colivelin (a STAT3 activator). Our findings demonstrate that C3aR protects against the development of psoriasis and suggest that C3aR confers protection by negatively regulating K6, K16, and K17 expression in a STAT3-dependent manner, thus inhibiting keratinocyte proliferation and helping reverse the pathogenesis of psoriasis.
Keyword ：
C3a anaphylatoxin receptor complement downregulation keratin proliferation psoriasis
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| GB/T 7714 | Qiao, Pei , Zhi, Dalong , Yu, Chen et al. Activation of the C3a anaphylatoxin receptor inhibits keratinocyte proliferation by regulating keratin 6, keratin 16, and keratin 17 in psoriasis [J]. | FASEB JOURNAL , 2022 , 36 (5) . |
| MLA | Qiao, Pei et al. "Activation of the C3a anaphylatoxin receptor inhibits keratinocyte proliferation by regulating keratin 6, keratin 16, and keratin 17 in psoriasis" . | FASEB JOURNAL 36 . 5 (2022) . |
| APA | Qiao, Pei , Zhi, Dalong , Yu, Chen , Zhang, Chen , Wu, Kunyi , Fang, Hui et al. Activation of the C3a anaphylatoxin receptor inhibits keratinocyte proliferation by regulating keratin 6, keratin 16, and keratin 17 in psoriasis . | FASEB JOURNAL , 2022 , 36 (5) . |
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Abstract ：
Our previous work using a murine model of pyelonephritis demonstrated that the C5a/C5aR1 axis plays a pathogenic role in acute kidney infection. In this study, we report that the C5a/C5aR1 axis also plays a pathogenic role in acute bladder infection. C5aR1-deficient mice had reduced bladder bacterial load and attenuated bladder tissue injury, which is associated with reduced expression of terminal alpha-mannosyl residues (Man) (a potential ligand for type 1 fimbriae of E. coli) at the luminal surface of the bladder epithelium and reduced early bacterial colonization of the bladder. In vitro, C5a stimulation enhanced mannose expression in and facilitated bacterial adhesion/colonization to human bladder epithelial cells. C5a stimulation also upregulated the activation of ERK1/2 and NF-kappa B signaling and gene expression of proinflammatory cytokines (i.e., Il6, Il1b, Cxcl1, Ccl2) in the epithelial cells, which could drive pro-inflammatory responses leading to tissue injury. Administration of the C5aR1 antagonist effectively reduced bladder bacterial load and tissue injury. Thus, our findings demonstrate a previously unknown pathogenic role for the C5a/C5aR1 axis in bladder infection and suggest that the C5a/C5aR1 axis-mediated upregulation of Man expression, enhancement of bacterial adhesion/colonization, and excessive inflammatory responses contribute to acute bladder infection. These findings improve our understanding of the pathogenesis of bladder infection with therapeutic implications for UTI.
Keyword ：
acute cystitis bacterial adhesion bladder inflammation C5a C5aR1 urinary tract infection
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| GB/T 7714 | Wu, Kun-Yi , Cao, Bo , Wang, Chun-Xuan et al. The C5a/C5aR1 Axis Contributes to the Pathogenesis of Acute Cystitis Through Enhancement of Adhesion and Colonization of Uropathogenic E. coli [J]. | FRONTIERS IN CELLULAR AND INFECTION MICROBIOLOGY , 2022 , 12 . |
| MLA | Wu, Kun-Yi et al. "The C5a/C5aR1 Axis Contributes to the Pathogenesis of Acute Cystitis Through Enhancement of Adhesion and Colonization of Uropathogenic E. coli" . | FRONTIERS IN CELLULAR AND INFECTION MICROBIOLOGY 12 (2022) . |
| APA | Wu, Kun-Yi , Cao, Bo , Wang, Chun-Xuan , Yang, Xue-Ling , Zhao, Shu-Juan , Diao, Teng-Yue et al. The C5a/C5aR1 Axis Contributes to the Pathogenesis of Acute Cystitis Through Enhancement of Adhesion and Colonization of Uropathogenic E. coli . | FRONTIERS IN CELLULAR AND INFECTION MICROBIOLOGY , 2022 , 12 . |
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Abstract ：
Objective The apoptotic signaling pathway is obviously disordered in systemic lupus erythematosus (SLE). Natural IgM (nIgM) is important in clearing apoptotic cells and preventing them from triggering deleterious autoimmunity. B-1 and innate-like B (ILBs) cells are the main nIgM producers. Human CD27(+)IgD(+) B cells (un-switched memory B cells) are considered ILBs. However, their functional properties in SLE remain undefined. Methods Peripheral blood sample of 50 SLE patients and 50 healthy controls were collected, and twelve SLE patients were assessed in a follow-up study. The amount of CD27(+)IgD(+) B cell in each population was analyzed by flow cytometry. The IgM and IL-10 levels of CD27(+)IgD(+) B cell were assessed by ELISPOT and qRT-PCR, respectively. SPSS 17.0 (SPSS, USA) was employed for data analysis. P < 0.05 indicated statistical significance. Result The amounts of CD27(+)IgD(+)B cell were significantly decreased in SLE patients than healthy control (P < 0.01). CD27(+)IgD(+)B cell amounts were positively correlated with WBC (r = 0.337, P =0 .017), platelet count (r = 0.396, P =0 .004), and serum C3 levels (r = 0.415, P =0 .003) and negatively correlated with serum creatinine levels (r= -0.285, P =0 .045), SLEDAI(r= -0.724, P =0 .000), and anti-d5DNA(r= -0.477, P = 0.000). The IgM and IL-10 levels of CD27(+)IgD(+)B in active SLE were decreased than healthy control (P < 0.001). Moreover, CD27(+)IgD(+)B cells are increased in SLE cases after treatment than before treatment (P <0 .001). Conclusion The amounts of CD27(+)IgD(+)B cell were significantly decreased in SLE patients compared with the healthy population, and CD27(+)IgD(+)B cell was verified to be correlated with clinical and immunological features in SLE patients.CD27(+)IgD(+)B cells had impaired function associated with IgM and IL-10 production in active SLE. Moreover, the amounts of CD27(+)IgD(+)B cells were recovered to the normal level in SLE cases with treatment-related disease remission.
Keyword ：
CD27(+)IgD(+) B cells Innate like B cells Natural IgM Systemic lupus erythematosus
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| GB/T 7714 | Zhang, Wei , Wang, Yong-Fu , Hu, Fan-Lei et al. Dysfunction of CD27(+)IgD(+)B cells correlates with aggravated systemic lupus erythematosus [J]. | CLINICAL RHEUMATOLOGY , 2022 , 41 (5) : 1551-1559 . |
| MLA | Zhang, Wei et al. "Dysfunction of CD27(+)IgD(+)B cells correlates with aggravated systemic lupus erythematosus" . | CLINICAL RHEUMATOLOGY 41 . 5 (2022) : 1551-1559 . |
| APA | Zhang, Wei , Wang, Yong-Fu , Hu, Fan-Lei , Lu, Fu-Ai , Wu, Tao , Feng, Yue-Lan et al. Dysfunction of CD27(+)IgD(+)B cells correlates with aggravated systemic lupus erythematosus . | CLINICAL RHEUMATOLOGY , 2022 , 41 (5) , 1551-1559 . |
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Objective Collectin 11 (CL-11) is a soluble C-type lectin, a mediator of innate immunity. Its role in autoimmune disorders is unknown. We undertook this study to determine the role of CL-11 in a mouse model of rheumatoid arthritis (RA). Methods A murine collagen-induced arthritis (CIA) model was used and combined two approaches, including gene deletion of Colec11 and treatment with recombinant CL-11 (rCL-11). Joint inflammation and tissue destruction, circulating levels of inflammatory cytokines, and adaptive immune responses were assessed in mice with CIA. Splenic CD11c+ cells were used to examine the influence of CL-11 on antigen-presenting cell (APC) function. Serum CL-11 levels in RA patients were also examined. Results Colec11(-/-) mice developed more severe arthritis than wild-type mice, as determined by disease incidence, clinical arthritis scores, and histopathology (P < 0.05). Disease severity was associated with significantly enhanced APC activation, Th1/Th17 responses, pathogenic IgG2a production and joint inflammation, as well as elevated circulating levels of inflammatory cytokines. In vitro analysis of CD11c+ cells revealed that CL-11 is critical for suppression of APC activation and function. Pharmacologic treatment of mice with rCL-11 reduced the severity of CIA in mice. Analysis of human blood samples revealed that serum CL-11 levels were lower in RA patients (n = 51) compared to healthy controls (n = 53). Reduction in serum CL-11 was inversely associated with the Disease Activity Score in 28 joints, erythrocyte sedimentation rate, and C-reactive protein level (P < 0.05). Conclusion Our findings demonstrate a novel role of CL-11 in protection against RA, suggesting that the underlying mechanism involves suppression of APC activation and subsequent T cell responses.
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| GB/T 7714 | Wang, Na , Wu, Weiju , Qiang, Cui et al. Protective Role of Collectin 11 in a Mouse Model of Rheumatoid Arthritis [J]. | ARTHRITIS & RHEUMATOLOGY , 2021 , 73 (8) : 1430-1440 . |
| MLA | Wang, Na et al. "Protective Role of Collectin 11 in a Mouse Model of Rheumatoid Arthritis" . | ARTHRITIS & RHEUMATOLOGY 73 . 8 (2021) : 1430-1440 . |
| APA | Wang, Na , Wu, Weiju , Qiang, Cui , Ma, Ning , Wu, Kunyi , Liu, Dan et al. Protective Role of Collectin 11 in a Mouse Model of Rheumatoid Arthritis . | ARTHRITIS & RHEUMATOLOGY , 2021 , 73 (8) , 1430-1440 . |
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Abstract ：
CD3(+)CD56(+)NKT-like cells are a rare population of lymphocytes that serve important roles in various types of immune-related diseases, and particularly in cancer. The complement system regulates inflammatory and immune responses by interacting with complement receptors expressed on a range of immune cells. However, whether CD3(+)CD56(+)NKT-like cells are regulated by the complement system has still not been definitively determined. In the present study, the expression of complement receptors and regulators in gated CD3(+)CD56(+)NKT-like cells isolated from human peripheral blood was assessed using PCR and flow cytometry. The results showed that human CD3(+)CD56(+)NKT-like cells expressed a range of complement receptors and regulators, such as CR3, C3aR, C5aR, C5L2, CD46 and CD55. Furthermore, the presence of complement component 3 (C3), a key component in complement activation in culture supernatant, mitigated the activity, IFN-gamma production and killing function of CD3(+)CD56(+)NKT-like cells. The present study provides evidences supporting the relationship between complement activation and functional modulation of CD3(+)CD56(+)NKT-like cells, expanding our knowledge of the complement regulatory network, and also highlighting a potential target for treatment of numerous immune-related diseases, particularly NKT cell-based tumor adoptive immunotherapy. (C) 2021 American Society for Histocompatibility and Immunogenetics. Published by Elsevier Inc. All rights reserved.
Keyword ：
C3 CD3(+)CD56(+)NKT Complement receptors Regulation
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| GB/T 7714 | Min, Xiao-Yun , Liu, Cheng-Fei , Cao, Bo et al. Human CD3(+)CD56(+)NKT-like cells express a range of complement receptors and C3 activation has negative effects on these cell activity and effector function [J]. | HUMAN IMMUNOLOGY , 2021 , 82 (9) : 625-633 . |
| MLA | Min, Xiao-Yun et al. "Human CD3(+)CD56(+)NKT-like cells express a range of complement receptors and C3 activation has negative effects on these cell activity and effector function" . | HUMAN IMMUNOLOGY 82 . 9 (2021) : 625-633 . |
| APA | Min, Xiao-Yun , Liu, Cheng-Fei , Cao, Bo , Zhang, Ting , Yang, Xiao , Ma, Ning et al. Human CD3(+)CD56(+)NKT-like cells express a range of complement receptors and C3 activation has negative effects on these cell activity and effector function . | HUMAN IMMUNOLOGY , 2021 , 82 (9) , 625-633 . |
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Abstract ：
Background and aim As a proinflammatory cytokine, tumor necrosis factor-like weak inducer of apoptosis (TWEAK) participates in the progression of renal fibrosis by binding to its receptor, fibroblast growth factor-inducible 14 (Fn14). However, the effect of Fn14 inhibition on tubular epithelial cell-mediated tubulointerstitial fibrosis remains unclear. This study aimed to elucidate the role of TWEAK/Fn14 interaction in the development of experimental tubulointerstitial fibrosis as well as the protective effect of Fn14 knockdown on proximal tubular epithelial cells. Methods A murine model of unilateral ureteral obstruction was constructed in both wild-type and Fn14-deficient BALB/c mice, followed by observation of the tubulointerstitial pathologies. Results Fn14 deficiency ameliorated the pathological changes, including inflammatory cell infiltration and cell proliferation, accompanied by reduced production of profibrotic factors and extracellular matrix deposition. In vitro experiments showed that TWEAK dose-dependently enhanced the expression of collagen I, fibronectin, and alpha-smooth muscle actin in proximal tubular epithelial cells. Interestingly, TWEAK also upregulated the expression levels of Notch1/Jagged1. Fn14 knockdown and Notch1/Jagged1 inhibition also mitigated the effect of TWEAK on these cells. Conclusions In conclusion, TWEAK/Fn14 signals contributed to tubulointerstitial fibrosis by acting on proximal tubular epithelial cells. Fn14 inhibition might be a therapeutic strategy for protecting against renal interstitial fibrosis.
Keyword ：
Fibroblast growth factor– Fn14 inducible 14 Proximal tubular epithelial cell Renal fibrosis Tumor necrosis factor-like weak inducer of apoptosis TWEAK Unilateral ureteral obstruction
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| GB/T 7714 | Luo, Mai , Liu, Mengmeng , Liu, Wei et al. Inhibition of fibroblast growth factor-inducible 14 attenuates experimental tubulointerstitial fibrosis and profibrotic factor expression of proximal tubular epithelial cells [J]. | INFLAMMATION RESEARCH , 2021 , 70 (5) : 553-568 . |
| MLA | Luo, Mai et al. "Inhibition of fibroblast growth factor-inducible 14 attenuates experimental tubulointerstitial fibrosis and profibrotic factor expression of proximal tubular epithelial cells" . | INFLAMMATION RESEARCH 70 . 5 (2021) : 553-568 . |
| APA | Luo, Mai , Liu, Mengmeng , Liu, Wei , Cui, Xiao , Zhai, Siyue , Gu, Hanjiang et al. Inhibition of fibroblast growth factor-inducible 14 attenuates experimental tubulointerstitial fibrosis and profibrotic factor expression of proximal tubular epithelial cells . | INFLAMMATION RESEARCH , 2021 , 70 (5) , 553-568 . |
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This study aimed to assess the association of coagulation-related indicators such as plasma fibrinogen (FIB), d-dimer, and fibrin degradation product (FDP) in rheumatoid arthritis (RA) with the disease activity. Data from 105 RA patients and 102 age- and gender-matched healthy controls were collected in the retrospective study. Disease activity score in 28 joints based on C-reactive protein (DAS28-CRP) was used to divide RA patients into low activity group (DAS28-CRP <= 2.7) and active group (DAS28-CRP > 2.7). Receiver operating characteristic (ROC) curve was applied to determine area under the curve (AUC). The association between plasma FIB, d-dimer, and FDP and DAS28-CRP was evaluated by spearman correlation. Logistical regression analysis was used to identify the independent variables associated with RA disease activity. RA patients showed higher levels of plasma FIB, d-dimer, and FDP than the controls (P < 0.01). Plasma FIB, d-dimer, and FDP were also increased in active groups of RA patients than those in inactive groups (P < 0.001). ROC curve analyses revealed that the AUC of d-dimer was higher than erythrocyte sedimentation rate (ESR) and rheumatoid factor (RF), and that of FDP was higher than RF in RA patients. In addition, the optimal cut-off value of plasma FIB, d-dimer, and FDP for RA diagnosis was 286 mg/dL, 470 mu g/L, and 1.45 mg/L, respectively. Spearman analysis showed that plasma FIB, d-dimer, and FDP were positively related with DAS28-CRP (P < 0.001) in RA patients. Logistical regression analysis showed that d-dimer (odds ratio 2.862, 95% confidence interval 1.851-5.426, P < 0.001) was an independent variable associated with RA disease activity. FIB, d-dimer, and FDP were increased in RA patients and positively correlated with the disease activity of RA. d-dimer may act as a novel inflammatory indice for indicating disease activity in RA patients.
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| GB/T 7714 | Xue, Li , Tao, Li , Li, Xueyi et al. Plasma fibrinogen, d-dimer, and fibrin degradation product as biomarkers of rheumatoid arthritis [J]. | SCIENTIFIC REPORTS , 2021 , 11 (1) . |
| MLA | Xue, Li et al. "Plasma fibrinogen, d-dimer, and fibrin degradation product as biomarkers of rheumatoid arthritis" . | SCIENTIFIC REPORTS 11 . 1 (2021) . |
| APA | Xue, Li , Tao, Li , Li, Xueyi , Wang, Yan , Wang, Biao , Zhang, Yanping et al. Plasma fibrinogen, d-dimer, and fibrin degradation product as biomarkers of rheumatoid arthritis . | SCIENTIFIC REPORTS , 2021 , 11 (1) . |
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Abstract ：
目的 探讨血清淀粉样蛋白A(SAA)在急性附睾炎中的诊断价值.方法 选取2018年3月至2019年9月商洛市中心医院收治的67例拟诊断为急性附睾炎患者(急性附睾炎组)作为研究对象,另选取同期在该院体检健康成年男性58例作为对照组,两组SAA、血白细胞计数(WBC)、尿WBC及C-反应蛋白(CRP)水平进行检测并比较各指标水平及其阳性率,分析SAA与CRP、血WBC及尿WBC相关性,利用受试者工作特征曲线(ROC曲线)分析SAA对急性附睾炎的诊断效能,以及比较急性附睾炎组治疗前及治疗7 d后各指标水平.结果 急性附睾炎组SAA、CRP、血WBC及尿WBC水平与对照组比较,差异均有统计学意义(P<0.05).急性附睾炎组SAA与CRP、血WBC及尿WBC水平呈正相关(r=0.792、0.816、0.429,P<0.05).急性附睾炎组SAA、CRP、血WBC及尿WBC的阳性率分别92.54％、74.17％、85.33％和61.49％.以SAA为变量绘制急性附睾炎的ROC曲线,ROC曲线下面积为0.932(P<0.05),95％可信区间为0.915～0.948.急性附睾炎治疗前SAA、CRP及血WBC水平与其治疗7 d后各指标水平比较,均明显下降,差异有统计学意义(P<0.05).结论 SAA检测对急性附睾炎患者的诊断具有重要应用价值.
Keyword ：
C-反应蛋白 白细胞计数 急性附睾炎 血清淀粉样蛋白
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| GB/T 7714 | 赵璇 , 李可 , 茹伯战 . 血清淀粉样蛋白A在急性附睾炎中的诊断价值研究 [J]. | 检验医学与临床 , 2020 , 17 (16) : 2344-2346,2349 . |
| MLA | 赵璇 et al. "血清淀粉样蛋白A在急性附睾炎中的诊断价值研究" . | 检验医学与临床 17 . 16 (2020) : 2344-2346,2349 . |
| APA | 赵璇 , 李可 , 茹伯战 . 血清淀粉样蛋白A在急性附睾炎中的诊断价值研究 . | 检验医学与临床 , 2020 , 17 (16) , 2344-2346,2349 . |
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