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[PMID]: 29524423
[Au] Autor:Lee JH; Jeon YD; Lee YM; Kim DK
[Ad] Address:Department of Immunology and Institute for Medical Sciences, Chonbuk National University Medical School, Jeonju, Jeollabuk-do 54907, Republic of Korea.
[Ti] Title:The suppressive effect of puerarin on atopic dermatitis-like skin lesions through regulation of inflammatory mediators in vitro and in vivo.
[So] Source:Biochem Biophys Res Commun;, 2018 Mar 07.
[Is] ISSN:1090-2104
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Atopic dermatitis (AD) is one of the common inflammatory immune disorders. Puerarin is the main isoflavonoid obtained from the root of Pueraria lobata and has been known have ameliorative effects on diverse inflammatory diseases. However, the effects of puerarin on AD have not been uncovered. 2,4-dinitrochlorobenzene (DNCB) was used to induce atopic dermatitis(AD)-like skin lesions on BALB/c mice for 17 days. Further, the BALB/c mice were orally administered puerarin. Puerarin ameliorated DNCB-induced AD-like symptoms in the mice by regulating skin thickness, degranulation of mast cells, and serum immunoglobulin E (IgE). Human keratinocytes (HaCaT cells) were also used to clarify the effects of puerarin on the secretion of pro-inflammatory cytokines. Puerarin inhibited the secretion of inflammatory cytokines and chemokines. The aim of this study was to investigate the protective and alleviative effect of puerarin on AD in vitro and in vivo. The results in this study indicated that puerarin ameliorates AD-like skin lesion and skin inflammation via regulation of various atopic and inflammatory mediators. Therefore, puerarin might be useful in treating AD and other skin diseases.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  2 / 65643 MEDLINE  
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[PMID]: 29517616
[Au] Autor:Robertson MJ; Stamatkin CW; Pelloso D; Weisenbach J; Prasad NK; Safa AR
[Ad] Address:Lymphoma Program and Bone Marrow and Stem Cell Transplantation Program, Department of Medicine, Division of Hematology/Oncology.
[Ti] Title:A Dose-escalation Study of Recombinant Human Interleukin-18 in Combination With Ofatumumab After Autologous Peripheral Blood Stem Cell Transplantation for Lymphoma.
[So] Source:J Immunother;, 2018 Mar 06.
[Is] ISSN:1537-4513
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Interleukin-18 (IL-18) is an immunostimulatory cytokine that augments antibody-dependent cellular cytotoxicity mediated by human natural killer cells against antibody-coated lymphoma cells in vitro and that has antitumor activity in animal models. Ofatumumab is a CD20 monoclonal antibody with activity against human B-cell lymphomas. A phase I study of recombinant human (rh) IL-18 given with ofatumumab was undertaken in patients with CD20 lymphoma who had undergone high-dose chemotherapy and autologous peripheral blood stem cell transplantation. Cohorts of 3 patients were given intravenous infusions of ofatumumab 1000 mg weekly for 4 weeks with escalating doses of rhIL-18 as a intravenous infusion weekly for 8 consecutive weeks. Nine male patients with CD20 lymphomas were given ofatumumab in combination with rhIL-18 at doses of 3, 10, and 30 µg/kg. No unexpected or dose-limiting toxicities were observed. The mean reduction from predose levels in the number of peripheral blood natural killer cells after the first rhIL-18 infusion was 91%, 96%, and 97% for the 3, 10, and 30 µg/kg cohorts, respectively. Serum concentrations of interferon-γ and chemokines transiently increased following IL-18 dosing. rhIL-18 can be given in biologically active doses by weekly infusions in combination with ofatumumab after peripheral blood stem cell transplantation to patients with lymphoma. A maximum tolerated dose of rhIL-18 plus ofatumumab was not determined. Further studies of rhIL-18 and CD20 monoclonal antibodies in B-cell malignancies are warranted.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:Publisher
[do] DOI:10.1097/CJI.0000000000000220

  3 / 65643 MEDLINE  
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[PMID]: 29503445
[Au] Autor:Yang J; Zhang S; Zhang L; Xie X; Wang H; Jie Z; Gu M; Yang JY; Cheng X; Sun SC
[Ad] Address:Department of Immunology, The University of Texas MD Anderson Cancer Center, Houston TX 77030, USA.
[Ti] Title:Lymphatic endothelial cells regulate B-cell homing to lymph nodes via a NIK-dependent mechanism.
[So] Source:Cell Mol Immunol;, 2018 Mar 05.
[Is] ISSN:2042-0226
[Cp] Country of publication:China
[La] Language:eng
[Ab] Abstract:B cells home to the lymph nodes (LNs) via high endothelial venules (HEVs) under the guidance of chemokines, particularly CXCL13. However, as CXCL13 is not directly made in HEVs, the molecular mechanism mediating B-cell homing to LNs has remained unclear. We show here that nuclear factor (NF)-κB-inducing kinase (NIK), a kinase mediating activation of the noncanonical NF-κB pathway, functions in lymphatic endothelial cells (LECs) to regulate B-cell homing to LNs. LEC-conditional deletion of NIK in mice did not affect the integrity or global function of lymphatic vessels but caused a severe reduction in the frequency of B cells in LNs. The LEC-specific NIK deficiency did not affect the survival of B cells or the frequency of B cells in the spleen. B-cell adoptive transfer studies revealed that the LEC-specific NIK deletion impairs the ability of LNs to recruit B cells. We further show that NIK mediates expression of the chemokines CXCL13 and CCL19 in LECs. Although CCL19 is also expressed in blood endothelial cells (BECs), CXCL13 is not produced in BECs. These results suggest that NIK regulates naive B-cell homing to LNs via mediating production of the B-cell homing chemokine CXCL13 in LECs.Cellular and Molecular Immunology advance online publication, 5 March 2018; doi:10.1038/cmi.2017.167.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:Publisher
[do] DOI:10.1038/cmi.2017.167

  4 / 65643 MEDLINE  
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[PMID]: 29471085
[Au] Autor:Zhu H; Lu X; Ling L; Li H; Ou Y; Shi X; Lu Y; Zhang Y; Chen D
[Ad] Address:Department of Microbiological and Biochemical Pharmacy, School of Pharmacy, Fudan University, Shanghai, China.
[Ti] Title:Houttuynia cordata polysaccharides ameliorate pneumonia severity and intestinal injury in mice with influenza virus infection.
[So] Source:J Ethnopharmacol;218:90-99, 2018 Feb 19.
[Is] ISSN:1872-7573
[Cp] Country of publication:Ireland
[La] Language:eng
[Ab] Abstract:ETHNOPHARMACOLOGICAL RELEVANCE: Hottuynia cordata is an important traditional Chinese medicine for the treatment of respiratory diseases including bacterial and viral infections. Polysaccharides isolated from Houttuynia cordata (HCP), as its main ingredients, have been demonstrated to ameliorate the LPS-induced acute lung injury in mice. The study aimed to determine the protective effects of HCP on multiple organ injury in influenza A virus (IAV) H1N1 infected mice and its primary mechanisms in anti-inflammation and immune regulation. MATERIALS AND METHODS: Mice were inoculated with IAV H1N1 and then treated with 20 or 40 mg/kg/d of HCP for survival test and acute lung-gut injury test. RESULTS: The treatment with HCP resulted in an increase in the survival rate of H1N1 infected mice and the protection from lung and intestine injury, accompanied with the reduced virus replication. HCP markedly decreased the concentration of pulmonary proinflammatory cytokines/chemokines and the number of intestinal goblet cells, and strengthened the intestinal physical and immune barrier, according to the increase of sIgA and tight junction protein (ZO-1) in intestine. At the same time, the inhibition of inflammation in lung and gut was related to the suppressing of the expression of TLR4 and p-NFκB p65 in lung. CONCLUSIONS: These results indicated that HCP ameliorated lung and intestine injury induced by IAV attack. The mechanisms were associated with inhibition of inflammation, protection of intestinal barrier and regulation of mucosal immunity, which may be related to the regulation of gut-lung axis. As an alternative medicine, HCP may have clinical potential to treat IAV infection in human beings.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  5 / 65643 MEDLINE  
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[PMID]: 29432913
[Au] Autor:Ren X; Liu W; Liu Y
[Ad] Address:Department of Infectious Diseases Medicine, Cangzhou Central Hospital, 16 Xinhua West Road, Cangzhou, 061001, China. Electronic address: renxiaojuan888@163.com.
[Ti] Title:Effects of fluconazole on the clinical outcome and immune response in fungal co-infected tuberculosis patients.
[So] Source:Microb Pathog;117:148-152, 2018 Feb 09.
[Is] ISSN:1096-1208
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:With overuse of the broad-spectrum antibiotics, the pulmonary fungal infection increasingly becomes the most common complication associated with senile pulmonary tuberculosis (TB) and attracts intensive attentions from clinicians. Here we presented the retrospective analysis of impact of fluconazole treatment on the clinical outcome and immune response in fungal co-infected tuberculosis patients. A randomized, double-blind, placebo-controlled trial of fluconazole (100 mg per day for consecutive weeks) in fungal-positive senile tuberculosis patients was conducted in our hospital. Peripheral eosinophil counts were computed by the automatic hematology analyzer. The secretory inflammatory cytokines interferon (IFN)-γ, tumor necrosis factor (TNF)-α and chemokines chemokine C-X-C motif ligand (CXCL)9, CXCL10, CXCL11 were determined with enzyme-linked immunosorbent assay kits. The peripheral T helper 1 cells (Th1) and regulatory T cells (Treg) population were analyzed by flow cytometry. None of significant difference in respect to baseline TB score was observed between placebo and fluconazole groups. Administration of fluconazole significantly stimulated eosinophils population and secretion of inflammatory cytokines IFN-γ and TNF-α. Simultaneously, the peripheral Th1% and chemokines including CXCL9, CSCL10, CXCL11 were markedly induced in response to fluconazole treatment. Fungal infection significantly affected host immunity during tuberculosis which was effectively reversed by fluconazole treatment.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  6 / 65643 MEDLINE  
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[PMID]: 29524043
[Au] Autor:Xin H; Cao Y; Shao ML; Zhang W; Zhang CB; Wang JT; Liang LC; Shao WW; Qi YL; Li Y; Zhang ZY; Yang Z; Sun YH; Zhang PX; Jia LL; Wang WQ
[Ad] Address:Department of Laboratory Medicine, The First Affiliated Hospital, Jiamusi University, Jiamusi, 154002, Heilongjiang, China.
[Ti] Title:Chemokine CXCL3 mediates prostate cancer cells proliferation, migration and gene expression changes in an autocrine/paracrine fashion.
[So] Source:Int Urol Nephrol;, 2018 Mar 09.
[Is] ISSN:1573-2584
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:INTRODUCTION: We have previously indicated that CXCL3 was upregulated in the tissues of prostate cancer, and exogenous administration of CXCL3 played a predominant role in the tumorigenicity of prostate cancer cells. In the present study, we further explored the role and the underlying mechanism of CXCL3 overexpression in the oncogenic potential of prostate cancer in an autocrine/paracrine fashion. METHODS: CXCL3-overexpressing prostate cancer cell line PC-3 and immortalized prostate stromal cell line WPMY-1 were established by gene transfection. CCK-8, transwell assays and growth of tumor xenografts were conducted to characterize the effects of CXCL3 on PC-3 cells' proliferation and migration. Western blotting was conducted to test whether CXCL3 could affect the expression of tumorigenesis-associated genes. RESULTS: The results showed that CXCL3 overexpression in PC-3 cells and the PC-3 cells treated with the supernatants of CXCL3-transfected WPMY-1 cells stimulated the proliferation and migration of PC-3 cells in vitro and in a nude mouse xenograft model. Western blotting revealed higher levels of p-ERK, Akt and Bcl-2 and lower levels of Bax in the tumor xenografts transplanted with CXCL3-transfected PC-3 cells. Moreover, the tumor xenografts derived from the PC-3 cells treated with supernatants of CXCL3-transfected WPMY-1 cells showed higher expression of ERK, Akt and Bcl-2 and lower expression of Bax. CONCLUSIONS: These findings suggest that CXCL3 autocrine/paracrine pathways are involved in the development of prostate cancer by regulating the expression of the target genes that are related to the progression of malignancies.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher
[do] DOI:10.1007/s11255-018-1818-9

  7 / 65643 MEDLINE  
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[PMID]: 29523540
[Au] Autor:Terra M; Oberkampf M; Fayolle C; Rosenbaum P; Guillerey C; Dadaglio G; Leclerc C
[Ad] Address:Immunology, Institut Pasteur.
[Ti] Title:Tumor-derived TGF-ß alters the ability of plasmacytoid dendritic cells to respond to innate immune signaling.
[So] Source:Cancer Res;, 2018 Mar 09.
[Is] ISSN:1538-7445
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:A growing number of observations has suggested that plasmacytoid dendritic cells (pDC) play a critical role in tumor biology. In patients, infiltration of tumors by pDC generally correlates with a poor prognosis, suggesting that pDC may play an important role in the host-tumor relationship. Here we analyze the influence of pDC in solid tumor development using two different tumor models: TC-1 and B16-OVA. Phenotypic and functional gene profiling analysis of tumor-associated pDC showed that the tumor microenvironment affected their activation status and ability to produce cytokines and chemokines. In addition, tumor cells secreted factors that inhibit the ability of pDC to produce type I IFN. Among the various cytokines and chemokines produced by the tumor cells, we demonstrate that TGF-ß is the main factor responsible for this inhibition. Using a mouse model deficient for pDCs, we also show that pDCs promote TC-1 tumor growth and that NK cells and regulatory T cells are involved in the protumoral effect of pDCs. Overall, our results evidence the crosstalk among pDCs, NK and regulatory T cells in the promotion of tumor growth and their role in the development of anti-tumor immune responses.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  8 / 65643 MEDLINE  
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[PMID]: 29522761
[Au] Autor:Bryson TD; Gu X; Khalil RM; Khan S; Zhu L; Xu J; Peterson E; Yang XP; Harding P
[Ad] Address:Hypertension & Vascular Research Division, Dept. of Internal Medicine, USA; Dept. of Physiology, Wayne State University School of Medicine, USA.
[Ti] Title:Overexpression of prostaglandin E2 EP4 receptor improves cardiac function after myocardial infarction.
[So] Source:J Mol Cell Cardiol;, 2018 Mar 06.
[Is] ISSN:1095-8584
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:BACKGROUND: Prostaglandin E2 (PGE ) signals through 4 separate G-protein coupled receptor sub-types to elicit a variety of physiologic and pathophysiological effects. We recently reported that PGE via its EP3 receptor could reduce cardiac contractility of isolated myocytes and the working heart preparation. We thus hypothesized that there is an imbalance in the EP3/EP4 ratio towards EP3 in the failing heart and that overexpression of EP4 in a mouse model of heart failure would improve cardiac function. METHODS AND RESULTS: Our hypothesis was tested in a mouse model of myocardial infarction (MI) with the use of AAV9-EP4 driven by the myosin heavy chain promoter to overexpress EP4 in the cardiac myocytes. Echocardiography was performed to assess cardiac function. We found that overexpression of EP4 improved shortening fraction (p = 0.0025), ejection fraction (p = 0.0003), and reduced left ventricular dimension at systole (p = 0.0013). Overexpression of EP4 also significantly reduced indices of cardiac hypertrophy and interstitial collagen fraction. Animals treated with AAV9-EP4 also had a significant decrease in TNFα mRNA expression and in the number of macrophages and T cells migrated post MI coupled with a reduction in the expression of iNOS. CONCLUSION: Overexpression of EP4 improves cardiac function post MI. This may be mediated through reductions in adverse cardiac remodeling or via inhibition of cytokine/chemokine production.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:Publisher

  9 / 65643 MEDLINE  
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[PMID]: 29492713
[Au] Autor:Becorpi A; Campisciano G; Zanotta N; Tredici Z; Guaschino S; Petraglia F; Pieralli A; Sisti G; De Seta F; Comar M
[Ad] Address:Section of Gynecology and Obstetrics, Department of Woman and Child Health, Careggi University Hospital, Largo Brambilla 3, 50144, Florence, Italy.
[Ti] Title:Fractional CO laser for genitourinary syndrome of menopause in breast cancer survivors: clinical, immunological, and microbiological aspects.
[So] Source:Lasers Med Sci;, 2018 Mar 01.
[Is] ISSN:1435-604X
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:The composition of vaginal microbiome in menopause and cancer survivor women changes dramatically leading to genitourinary syndrome of menopause (GSM) in up to 70% of patients. Recent reports suggest that laser therapy may be valuable as a not hormonal therapeutic modality. The aim of the present study was to evaluate the effects of fractional CO laser treatment on the vaginal secretory pathway of a large panel of immune mediators, usually implicated in tissue remodeling and inflammation, and on microbiome composition in postmenopausal breast cancer survivors. The Ion Torrent PGM platform and the Luminex Bio-Plex platform were used for microbiome and immune factor analysis. The significant reduction of clinical symptoms and the non-significant changes in vaginal microbiome support the efficacy and safety of laser treatment. Moreover, the high remodeling status in vaginal epithelium is demonstrated by the significant changes in inflammatory and modulatory cytokine patterns. Laser therapy can be used for the treatment of GSM symptoms and does not show any adverse effects. However, further studies will be needed to clarify its long-term efficacy and other effects.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher
[do] DOI:10.1007/s10103-018-2471-3

  10 / 65643 MEDLINE  
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[PMID]: 29410057
[Au] Autor:Pan GJ; Rayner BS; Zhang Y; van Reyk DM; Hawkins CL
[Ad] Address:Heart Research Institute, 7 Eliza Street, Newtown, NSW 2042, Australia; School of Life Sciences, University of Technology Sydney, PO Box 123, Broadway, NSW 2007, Australia.
[Ti] Title:A pivotal role for NF-κB in the macrophage inflammatory response to the myeloperoxidase oxidant hypothiocyanous acid.
[So] Source:Arch Biochem Biophys;642:23-30, 2018 Mar 15.
[Is] ISSN:1096-0384
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Atherosclerosis is characterised by the infiltration of macrophages at sites of inflammation within the vessel wall and the release of myeloperoxidase (MPO), which forms hypochlorous acid (HOCl) and hypothiocyanous acid (HOSCN). HOCl is a damaging oxidant implicated in the development of atherosclerosis. Preferential formation of HOSCN occurs under conditions where thiocyanate ions are elevated, as is the case in smokers. HOSCN reacts selectively with thiols, which can result in more enzyme inactivation and damage than HOCl at susceptible sites, which may contribute to atherosclerosis in smokers. In this study, we show that exposure of macrophages to HOSCN results in a time- and dose-dependent increase in the mRNA expression and release of pro-inflammatory cytokines and chemokines, including monocyte chemotactic protein 1, tumour necrosis factor alpha, and interleukins 6, 8 and 1ß. At high oxidant concentrations (>200 µM), a significant loss of cellular thiols and increased cell death is observed. HOSCN-induced cytokine/chemokine expression and cell death were decreased on pharmacological inhibition of nuclear factor kappa B. These data highlight a pathway by which HOSCN could promote inflammation and the development of atherosclerosis, in the presence of supra-physiological levels of the precursor thiocyanate, which are achievable by cigarette smoking.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:In-Data-Review


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