Database : MEDLINE
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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 / 63497 MEDLINE  
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[PMID]: 29501537
[Au] Autor:Ribatti D
[Ad] Address:Department of Basic Medical Sciences, Neurosciences and Sensory Organs, University of Bari Medical School, Bari, Italy; National Cancer Institute "Giovanni Paolo II", Bari, Italy. Electronic address: domenico.ribatti@uniba.it.
[Ti] Title:A new role of mast cells in arteriogenesis.
[So] Source:Microvasc Res;118:57-60, 2018 Mar 05.
[Is] ISSN:1095-9319
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Arteriogenesis is defined as the growth of functional collateral arteries from pre-existing arterio-arteriolar anastomoses. The role of mast cells in arteriogenesis is largely unexplored. Recent evidences suggest that mast cells together with other inflammatory cells, including monocytes-macrophages, lymphocytes, NK cells and endothelial precursor cells (EPCs) may be involved in this process. This review article analyzes the literature concerning this new aspect of biological activity of mast cells.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  3 / 63497 MEDLINE  
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[PMID]: 29523718
[Au] Autor:Mondillo C; Varela ML; Abiuso AMB; Vázquez R
[Ad] Address:C Mondillo, Laboratorio de Endocrinología Molecular y Transducción de Señales, Instituto de Biologia y Medicina Experimental, Ciudad de Buenos Aires, Argentina carolina.mondillo@gmail.com.
[Ti] Title:Potential negative effects of anti-histamines on male reproductive function.
[So] Source:Reproduction;, 2018 Mar 09.
[Is] ISSN:1741-7899
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Histamine (HA) is a pleiotropic biogenic amine synthesized exclusively by histidine decarboxylase (HDC) in most mammalian tissues. The literature on the role of HA within the male gonad has expanded over the last years, attracting attention to potential unexpected side-effects of anti-histamines on testicular function. In this regard, HA receptors (HRH1, HRH2 and HRH4) have been described in Leydig cells of different species, including human. Via these receptors, HA has been reported to trigger positive or negative interactions with the LH/hCG signaling pathway depending upon its concentration, thereby contributing to the local control of testicular androgen levels. It should then be considered that anti-histamines may affect testicular homeostasis by increasing or decreasing steroid production. Additionally, HRH1 and HRH2 receptors are present in peritubular and germ cells, and HRH2 antagonists have been found to negatively affect peritubular cells and reduce sperm viability. The potential negative impact of anti-histamines on male reproduction becomes even more dramatic if we consider that HA has also been associated with human sexual behavior and penile erection. What is more, although testicular mast cells are the major source of locally produced HA, recent studies have described HDC expression in macrophages, Leydig cells and germ cells, revealing the existence of multiple sources of HA within the testis. Undoubtedly, the more we learn about the testicular histaminergic system, the more opportunities there will be for rational design of drugs aimed at treating HA-related pathologies, with minimum or nule negative impact on fertility.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  4 / 63497 MEDLINE  
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[PMID]: 29523597
[Au] Autor:Colombo MP; Jachetti E; Cancila V; Rigoni A; Bongiovanni L; Cappetti B; Belmonte B; Enriquez C; Casalini P; Ostano P; Frossi B; Sangaletti S; Chiodoni C; Chiorino G; Pucillo CE; Tripodo C
[Ad] Address:Molecular Immunology Unit, Department of Research, Fondazione IRCCS Istituto Nazionale dei Tumori mariopaolo.colombo@istitutotumori.mi.it.
[Ti] Title:Cross-Talk between Myeloid-Derived Suppressor Cells and Mast Cells Mediates Tumor-Specific Immunosuppression in Prostate Cancer.
[So] Source:Cancer Immunol Res;, 2018 Mar 09.
[Is] ISSN:2326-6074
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Immunotherapy, including the use of checkpoint inhibitors, is a potent therapeutic approach for some cancers, but has limited success with prostate tumors, in which immune suppression is instigated by the tumor. The immunosuppressive capacity of mast cells, which promote adenocarcinoma development in the prostate, prompted our investigation on whether mast cells promote tolerance to SV40 Large-T antigen, the transforming oncogene in transgenic adenocarcinoma of the mouse prostate (TRAMP) mice. The incidence of adenocarcinoma was reduced in the offspring of a cross between TRAMP mice and mast cell-deficient KitWsh mice. TRAMP mice are tolerant to the SV40 Large T antigen, which is otherwise immunogenic in normal syngeneic B6 mice. Genetic ablation of mast cells in TRAMP mice restored their ability to mount a tumor-specific cytotoxic T-cell response. In KitWsh-TRAMP mice, the restored T-cell immunity correlated with the reduced activity of polymorphonuclear myeloid-derived suppressor cells (PMN-MDSCs), along with their reduced expression of Arg1, Nos2 and Stat3. Having found that CD40L-expressing mast cells can interact in vivo with CD40-expressing PMN-MDSC, we then determined that only KitWsh-TRAMP mice reconstituted with mast cells expressing CD40L could restore PMN-MDSCs suppressive functions, T cell unresponsiveness and adenocarcinoma development. Thus mast cells have an immunoregulatory effect on PMN-MDSCs activity through CD40L-CD40 interaction, favoring immunosuppression and tumor onset. In prostate cancer patients, in silico analyses correlated poor clinical outcomes with high expression of genes related to mast cells and PMN-MDSCs.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  5 / 63497 MEDLINE  
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[PMID]: 29522843
[Au] Autor:Suto H; Nambu A; Morita H; Yamaguchi S; Numata T; Yoshizaki T; Shimura E; Arae K; Asada Y; Motomura K; Kaneko M; Abe T; Matsuda A; Iwakura Y; Okumura K; Saito H; Matsumoto K; Sudo K; Nakae S
[Ad] Address:Atopy Research Center, Juntendo University, Tokyo.
[Ti] Title:IL-25 enhances Th17 cell-mediated contact dermatitis by promoting IL-1ß production by dermal dendritic cells.
[So] Source:J Allergy Clin Immunol;, 2018 Mar 06.
[Is] ISSN:1097-6825
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:BACKGROUND: As well as thymic stromal lymphopoietin (TSLP) and IL-33, IL-25 is known to induce Th2 cytokine production by various cell types-including Th2 cells, Th9 cells, invariant NKT cells and group 2 innate lymphoid cells-involved in Th2-type immune responses. Since both Th2-type and Th17-type cells/cytokines are crucial for contact hypersensitivity (CHS), IL-25 may contribute to this by enhancing Th2-type immune responses. However, the precise role of IL-25 in the pathogenesis of FITC-induced CHS is poorly understood. OBJECTIVE: We investigated the contribution of IL-25 to CHS using Il25 mice. METHODS: CHS was evaluated by measurement of ear skin thickness in mice after FITC-painting. Skin dendritic cell (DC) migration, hapten-specific Th cell differentiation and detection of IL-1ß-producing cells were determined by flow cytometry, ELISA and immunohistochemistry, respectively. RESULTS: In contrast to TSLP, we found that IL-25 was not essential for skin DC migration or hapten-specific Th cell differentiation in the sensitization phase of CHS. Unexpectedly, mast cell- and non-immune cell-derived IL-25 was important for hapten-specific Th17 cell-, rather than Th2 cell-, mediated inflammation in the elicitation phase of CHS by enhancing Th17-related, but not Th2-related, cytokines in the skin. In particular, IL-1ß produced by dermal DCs in response to IL-25 was crucial for hapten-specific Th17 cell activation, contributing to induction of local inflammation in the elicitation phase of CHS. CONCLUSION: Our results identify a novel IL-25 inflammatory pathway involved in induction of Th17, but not Th2, cell-mediated CHS. IL-25 neutralization may be a potential approach for treatment of CHS.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:Publisher

  6 / 63497 MEDLINE  
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[PMID]: 29454616
[Au] Autor:Liu S; Sahid MNA; Takemasa E; Maeyama K; Mogi M
[Ad] Address:Department of Pharmacology, Graduate School of Medicine, Ehime University, Toon, Ehime 791-0295, Japan. Electronic address: liussmzk@ehime-u.ac.jp.
[Ti] Title:Zoledronate modulates intracellular vesicle trafficking in mast cells via disturbing the interaction of myosinVa/Rab3a and sytaxin4/VAMP7.
[So] Source:Biochem Pharmacol;151:18-25, 2018 Feb 15.
[Is] ISSN:1873-2968
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Nitrogen-containing bisphosphonates (NBPs) have been widely used as bone anti-resorptive drugs for the treatment of osteoclast-dependent bone disorders. Zoledronate is currently the most potent NBP, and has potential as an inhibitor of farnesyl pyrophosphate synthase. The present study was undertaken to elucidate the possible effects of zoledronate on FcεRI-dependent mast cell activity in vitro, which is essential for in maintaining homeostasis of the gastrointestinal mucosa. Treatment with zoledronate significantly diminished exocytosis of mast cells, which was reflected by a decrease of FcεRI-dependent histamine release compared to that in vehicle-treated mast cells. Our single-vesicle monitoring and biochemical results suggested that zoledronate modulates intracellular formation of the myosinVa/Rab3a complex and syntaxin4/VAMP7 complex, which are critical in vesicle motility, and therefore disturbs exocytosis via suppression of the velocity of intracellular vesicles and inhibition of membrane fusion. Our findings imply that oral administration of zoledronate could modulate mucosal immune function by blocking mast cell function, and this risk should be of concern in the clinical usage of NBPs.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:Publisher

  7 / 63497 MEDLINE  
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[PMID]: 29431352
[Au] Autor:Popova OA; Khatuaev RO
[Ti] Title:[Radiosensitivity of morphoenzymological structural elements of the jejunum mucous membrane in chronodynamics of the impact of electromagnetic fields impulses].
[So] Source:Gig Sanit;95(10):974-6, 2016.
[Is] ISSN:0016-9900
[Cp] Country of publication:Russia (Federation)
[La] Language:rus
[Ab] Abstract:Results of numerous researches have revealed that most sensitive to electromagnetic radiations are the nervous, endocrine and cardiovascular systems of an organism, however, the analysis of literary data confirms also the direct involvement of organs of the intestinal system in physiological, and not seldom, and the pathological program of the response of an organism to the action of extreme factors. In the experiment executed on white laboratory male rats by ourselves there was studied the grade of the radiosensitivity of morphoenzymological structural elements of jejunum mucous membrane after 5, 7 and 10 months of chronic influence of electromagnetic fields impulses with a density of induced currents 0.37; 0.7; 0.8; 2.7 kA/m and frequency of impulses 50, 100 and 500 in a week irrespective of their divisibility of ultrashort duration of 15 a 40 ns. Scientific value and novelty of results is concluded in revealed multiple linear relationships between indices of electromagneticfields (duration of the impact, density of induced currents, periodicity of impulses and the dynamics of the studied indices of a morphofunctional condition of a jejunum mucous membrane). Besides that, there was found the critical population to indices of electromagneticfields impulses parameters - the jejunum mast cells differing in hypersensitivity and dependence on duration of influence and density of induced currents revealed, at that their bioeffects were unidirectional.
[Mh] MeSH terms primary: Electromagnetic Fields/adverse effects
Intestinal Mucosa
Jejunum
[Mh] MeSH terms secundary: Animals
Electromagnetic Radiation/classification
Intestinal Mucosa/pathology
Intestinal Mucosa/physiopathology
Intestinal Mucosa/radiation effects
Jejunum/pathology
Jejunum/physiopathology
Jejunum/radiation effects
Male
Models, Animal
Radiation Tolerance
Rats
Time Factors
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[Js] Journal subset:IM
[Da] Date of entry for processing:180213
[St] Status:MEDLINE

  8 / 63497 MEDLINE  
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[PMID]: 29358324
[Au] Autor:Isobe M; Izawa K; Sugiuchi M; Sakanishi T; Kaitani A; Takamori A; Maehara A; Matsukawa T; Takahashi M; Yamanishi Y; Oki T; Uchida S; Uchida K; Ando T; Maeda K; Nakano N; Yagita H; Takai T; Ogawa H; Okumura K; Kitamura T; Kitaura J
[Ad] Address:From the Atopy (Allergy) Research Center, Juntendo University Graduate School of Medicine, 2-1-1 Hongo, Bunkyo-ku, Tokyo 113-8421.
[Ti] Title:The CD300e molecule in mice is an immune-activating receptor.
[So] Source:J Biol Chem;293(10):3793-3805, 2018 Mar 09.
[Is] ISSN:1083-351X
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:CD300 molecules (CD300s) belong to paired activating and inhibitory receptor families, which mediate immune responses. Human CD300e (hCD300e) is expressed in monocytes and myeloid dendritic cells and transmits an immune-activating signal by interacting with DNAX-activating protein 12 (DAP12). However, the CD300e ortholog in mice (mCD300e) is poorly characterized. Here, we found that mCD300e is also an immune-activating receptor. We found that mCD300e engagement triggers cytokine production in mCD300e-transduced bone marrow-derived mast cells (BMMCs). Loss of DAP12 and another signaling protein, FcRγ, did not affect surface expression of transduced mCD300e, but abrogated mCD300e-mediated cytokine production in the BMMCs. Co-immunoprecipitation experiments revealed that mCD300e physically interacts with both FcRγ and DAP12, suggesting that mCD300e delivers an activating signal via these two proteins. Binding and reporter assays with the mCD300e extracellular domain identified sphingomyelin as a ligand of both mCD300e and hCD300e. Notably, the binding of sphingomyelin to mCD300e stimulated cytokine production in the transduced BMMCs in an FcRγ- and DAP12-dependent manner. Flow cytometric analysis with an mCD300e-specific Ab disclosed that mCD300e expression is highly restricted to CD115 Ly-6C peripheral blood monocytes, corresponding to CD14 CD16 human nonclassical and intermediate monocytes. Loss of FcRγ or DAP12 lowered the surface expression of endogenous mCD300e in the CD115 Ly-6C monocytes. Stimulation with sphingomyelin failed to activate the CD115 Ly-6C mouse monocytes, but induced hCD300e-mediated cytokine production in the CD14 CD16 human monocytes. Taken together, these observations indicate that mCD300e recognizes sphingomyelin and thereby regulates nonclassical and intermediate monocyte functions through FcRγ and DAP12.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1801
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:In-Data-Review
[do] DOI:10.1074/jbc.RA117.000696

  9 / 63497 MEDLINE  
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[PMID]: 29520592
[Au] Autor:Belin-Rauscent A; Lacoste J; Hermine O; Moussy A; Everitt BJ; Belin D
[Ad] Address:Department of Psychology, University of Cambridge, Downing Street, Cambridge, CB2 3EB, UK.
[Ti] Title:Decrease of cocaine, but not heroin, self-administration and relapse by the tyrosine kinase inhibitor masitinib in male Sprague Dawley rats.
[So] Source:Psychopharmacology (Berl);, 2018 Mar 08.
[Is] ISSN:1432-2072
[Cp] Country of publication:Germany
[La] Language:eng
[Ab] Abstract:RATIONALE: Accumulating evidence shows that cocaine, and also heroin, influence several tyrosine kinases, expressed in neurons and in non-neuronal populations such as microglia, astrocytes and mast-cells. Drug-induced activation of mast cells both triggers inflammatory processes in the brain mediated by the glial cells they activate, and facilitates histamine release which may directly influence the dopamine system. Thus, by triggering the activation and degranulation of mast cells dependent on the tyrosine kinase c-kit and Fyn, the latter being also involved in NMDA-dependent synaptic plasticity, cocaine and heroin may indirectly influence the neural mechanisms that mediate their reinforcing properties. Masitinib, a novel tyrosine kinase inhibitor with high selectivity for c-Kit, Fyn and Lyn, may alter the aberrant consequences of the activation of these tyrosine kinases by cocaine and heroin. OBJECTIVE: We investigated in rats the effect of a chronic oral treatment with masitinib (20 mg/kg) on the reinforcing and motivational properties of self-administered cocaine (250 µg/infusion) and heroin (40 µg/infusion). METHODS: Three different cohorts of rats were trained instrumentally to respond for cocaine, heroin or food under continuous reinforcement. In each group, we assessed the influence of chronic daily treatment with masitinib on the maintenance of instrumental responding and intake and the motivation for the reinforcer. Thus, masitinib and vehicle-treated rats were challenged to adapt to high behavioural demand, to respond under a progressive ratio schedule of reinforcement and to reinstate instrumental responding after extinction and/or abstinence. RESULTS: Masitinib selectively decreased cocaine intake, the motivation for cocaine and the subsequent propensity to respond for cocaine under extinction, while having no effect on instrumental responding for heroin or food. CONCLUSION: The present findings suggest masitinib, a drug with proven efficacy in CNS disorders, could represent a novel treatment for cocaine addiction provided its influence on the reinforcing and incentive properties of the drug is confirmed.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:Publisher
[do] DOI:10.1007/s00213-018-4865-0

  10 / 63497 MEDLINE  
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[PMID]: 29518425
[Au] Autor:Lazarinis N; Bood J; Gomez C; Kolmert J; Lantz AS; Gyllfors P; Davis A; Wheelock CE; Dahlén SE; Dahlén B
[Ad] Address:Division of Respiratory Medicine and Allergy, Department of Medicine, Karolinska University Hospital Huddinge, Stockholm, Sweden. Electronic address: nikolaos.lazarinis@ki.se.
[Ti] Title:Leukotriene E induces airflow obstruction and mast cell activation via the CysLT receptor.
[So] Source:J Allergy Clin Immunol;, 2018 Mar 05.
[Is] ISSN:1097-6825
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:BACKGROUND: Leukotriene E (LTE ) is the final active metabolite among the cysteinyl leukotrienes (CysLTs). Animal studies have identified a distinct LTE receptor, suggesting that current CysLT receptor antagonists may provide incomplete inhibition of CysLT responses. OBJECTIVE: We tested this hypothesis by assessing the influence of the CysLT antagonist montelukast on responses induced by inhalation of LTE in asthmatic subjects. METHODS: Fourteen subjects with mild intermittent asthma and two subjects with aspirin exacerbated respiratory disease (AERD) received montelukast 20 mg bid and placebo for 5-7 days in a randomized, double blind, crossover study (NCT01841164). The provocative dose of LTE causing 20% fall in FEV (PD ) was determined at the end of each treatment period by a rising dose challenge. Measurements included lipid mediators in urine and sputum cells 4 hours post LTE challenge. RESULTS: Montelukast completely blocked the LTE induced bronchoconstriction. Despite tolerating at least 10 times higher dose of LTE after montelukast, there was no difference in the percentage of eosinophils in sputum. The urinary excretion of all major lipid mediators increased after the LTE inhalation. Montelukast blocked the release of the mast cell product prostaglandin (PG) D , as well as the release of PGF , and thromboxane, but not the increased excretion of PGE and its metabolites nor isoprostanes. CONCLUSION: Leukotriene E induces airflow obstruction and mast cell activation via the CysLT receptor. CLINICAL IMPLICATIONS: Clinically available leukotriene antagonists protect against the airway obstruction and the pro-inflammatory effects of the terminal cysteinyl-leukotriene LTE
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180308
[Lr] Last revision date:180308
[St] Status:Publisher


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