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[PMID]:29386429
[Au] Autor:Uno K
[Ad] Endereço:Faculty of Pharmacy, Chiba Institute of Science.
[Ti] Título:[Pathogenic Mechanism and Diagnostic Testing for Drug Allergies].
[So] Source:Yakugaku Zasshi;138(2):151-167, 2018.
[Is] ISSN:1347-5231
[Cp] País de publicação:Japan
[La] Idioma:jpn
[Ab] Resumo: Three stages of the pathogenic mechanism of drug allergies can be considered: antigen formation, immune reaction and inflammation/disorder reaction. Drugs are thought to form 4 types of antigens: drug only, polymers, drug-carrier conjugates, and metabolite-carrier complexes. Antigens are recognized by B cell receptors and T cell receptors. Helper T cells (Th) are differentiated into four subsets, namely, Th1, Th2, Th17 and regulatory T cells (Treg). Th1 produces interleukin (IL)-2 and interferon (IFN)-γ, and activates macrophages and cytotoxic T cells (Tc). Macrophages induce type IV allergies, and Tc lead to serious type IV allergies. On the other hand, Th2 produces IL-4, IL-5, and IL-6, etc., and activates B cells. B cells produce IgE antibodies, and the IgE antibody affects mast cells and induces type I allergies. Activated eosinophil leads to the chronic state of type I allergy. Diagnostic testing for allergenic drugs is necessary for patients with drug allergies. Because in vivo diagnostic tests for allergenic drugs are associated with a risk and burden to the patient, in vitro allergy tests are recommended to identify allergenic drugs. In allergy tests performed in vitro, cytological tests are more effective than serological tests, and the leukocyte migration test (LMT) presently has the highest efficacy. An LMT-chamber is better than LMT-agarose in terms of usability and sensitivity, and it can detect about 80% of allergenic drugs.
[Mh] Termos MeSH primário: Ensaios de Migração de Leucócitos
Hipersensibilidade a Drogas/diagnóstico
Hipersensibilidade a Drogas/imunologia
[Mh] Termos MeSH secundário: Antígenos/imunologia
Linfócitos B/imunologia
Citocinas/metabolismo
Eosinófilos/imunologia
Seres Humanos
Imunoglobulina E
Macrófagos/imunologia
Mastócitos/imunologia
Receptores de Antígenos de Linfócitos B/imunologia
Receptores de Antígenos de Linfócitos T/imunologia
Sensibilidade e Especificidade
Subpopulações de Linfócitos T/imunologia
Linfócitos T Auxiliares-Indutores/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Antigens); 0 (Cytokines); 0 (Receptors, Antigen, B-Cell); 0 (Receptors, Antigen, T-Cell); 37341-29-0 (Immunoglobulin E)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180228
[Lr] Data última revisão:
180228
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180202
[St] Status:MEDLINE
[do] DOI:10.1248/yakushi.17-00174-1


  2 / 25866 MEDLINE  
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[PMID]:27779084
[Au] Autor:Bonadonna P; Bonifacio M; Zanotti R
[Ad] Endereço:Allergy Unit, Azienda Ospedaliera Universitaria Integrata di Verona, Piazzale Stefani 1, 37126, Verona, Italy.
[Ti] Título:Mast Cell Disorders In Drug Hypersensitivity.
[So] Source:Curr Pharm Des;22(45):6862-6869, 2016.
[Is] ISSN:1873-4286
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Mastocytosis is a clonal disease characterized by proliferation and accumulation of mast cells (MC) in different tissues, preferentially skin and bone marrow, leading to a wide variety of clinical manifestations, mainly caused by the inappropriate release of MC mediators. As a consequence, patients with mastocytosis may experience symptoms due to massive MC activation and release of mediators. Anaphylaxis is the most frequent manifestation of this phenomenon. Drugs are possible triggers of anaphylaxis in patients with mastocytosis, even though the association between mastocytosis and drug anaphylaxis does not appear to be as strong as anaphylaxis after hymenoptera sting; nevertheless, MC disorders might be ruled out in cases of severe systemic reactions to drugs. Moreover, the risk of perioperative anaphylaxis in adults appears high, mainly in patients with indolent systemic mastocytosis regardless of skin involvement. Such risk is probably lower in patients who have never experienced anaphylaxis and/or have tolerated previous general anaesthesia. However, data published about drug anaphylaxis in patients with MC disorders are scanty and currently it is not possible to provide clear recommendations.
[Mh] Termos MeSH primário: Anafilaxia/imunologia
Hipersensibilidade a Drogas/imunologia
Mastócitos/imunologia
Mastócitos/patologia
Mastocitose/patologia
[Mh] Termos MeSH secundário: Anafilaxia/diagnóstico
Anafilaxia/epidemiologia
Hipersensibilidade a Drogas/diagnóstico
Hipersensibilidade a Drogas/epidemiologia
Seres Humanos
Mastócitos/efeitos dos fármacos
Mastocitose/diagnóstico
Mastocitose/epidemiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Em] Mês de entrada:1712
[Cu] Atualização por classe:180227
[Lr] Data última revisão:
180227
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161026
[St] Status:MEDLINE
[do] DOI:10.2174/1381612822666160928121857


  3 / 25866 MEDLINE  
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[PMID]:29370173
[Au] Autor:Benedé S; Berin MC
[Ad] Endereço:Jaffe Food Allergy Institute, Icahn School of Medicine at Mount Sinai, New York, NY, United States of America.
[Ti] Título:Mast cell heterogeneity underlies different manifestations of food allergy in mice.
[So] Source:PLoS One;13(1):e0190453, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Food can trigger a diverse array of symptoms in food allergic individuals from isolated local symptoms affecting skin or gut to multi-system severe reactions (systemic anaphylaxis). Although we know that gastrointestinal and systemic manifestations of food allergy are mediated by tissue mast cells (MCs), it is not clear why allergen exposure by the oral route can result in such distinct clinical manifestations. Our aim was to assess the contribution of mast cell subsets to different manifestations of food allergy. We used two common models of IgE-mediated food allergy, one resulting in systemic anaphylaxis and the other resulting in acute gastrointestinal symptoms, to study the immune basis of allergic reactions. We used responders and non-responders in each model system, as well as naïve controls to identify the association of mast cell activation with clinical reactivity rather than sensitization. Systemic anaphylaxis was uniquely associated with activation of connective tissue mast cells (identified by release of mouse mast cell protease (MMCP) -7 into the serum) and release of histamine, while activation of mucosal mast cells (identified by release of MMCP-1 in the serum) did not correlate with symptoms. Gastrointestinal manifestations of food allergy were associated with an increase of MMCP-1-expressing mast cells in the intestine, and evidence of both mucosal and connective tissue mast cell activation. The data presented in this paper demonstrates that mast cell heterogeneity is an important contributor to manifestations of food allergy, and identifies the connective tissue mast cell subset as key in the development of severe systemic anaphylaxis.
[Mh] Termos MeSH primário: Hipersensibilidade Alimentar/imunologia
Mastócitos/imunologia
[Mh] Termos MeSH secundário: Animais
Trato Gastrointestinal/imunologia
Liberação de Histamina
Técnicas Imunoenzimáticas
Mastócitos/enzimologia
Camundongos
Camundongos Endogâmicos BALB C
Camundongos Endogâmicos C3H
Reação em Cadeia da Polimerase em Tempo Real
Triptases/sangue
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
EC 3.4.21.59 (Tpsab1 protein, mouse); EC 3.4.21.59 (Tryptases)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180222
[Lr] Data última revisão:
180222
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180126
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0190453


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[PMID]:29254289
[Au] Autor:Gerges Geagea A; Rizzo M; Eid A; Hajj Hussein I; Zgheib Z; Zeenny MN; Jurjus R; Uzzo ML; Spatola GF; Bonaventura G; Leone A; Massaad-Massade L; Jurjus A
[Ad] Endereço:Department of Anatomy, Cell Biology and Physiological Sciences, Faculty of Medicine, American University of Beirut, Beirut, Lebanon.
[Ti] Título:Tea catechins induce crosstalk between signaling pathways and stabilize mast cells in ulcerative colitis.
[So] Source:J Biol Regul Homeost Agents;31(4):865-877, 2017 Oct-Dec.
[Is] ISSN:0393-974X
[Cp] País de publicação:Italy
[La] Idioma:eng
[Ab] Resumo:It is well documented that nutraceuticals, in general, and Green tea catechins, in particular, possess a potential therapeutic value in inflammatory bowel diseases (IBD) due to their anti-oxidative and anti-inflammatory effects. This study aimed to investigate the possible mechanism of action of catechins in a rat model of colitis induced by 2.4.6 trinitrobenzene sulfonic acid (TNBS). Thirty-five young adult Sprague-Dawley rats were divided into four groups: normal control (n=5), catechins (n=9), TNBS (n=9) and TNBS plus catechins (n=12) treated. Catechin in the form of Epigallocatechin-3-gallate (EGCG) was administered daily by intraperitoneal injection, 1 week before the induction date of UC. Biopsies of the descending colon were collected on days 3, 10 and 17, and partly frozen for molecular studies or fixed for light microscopy. The status of intestinal tissue alterations and mast cells number were also assessed, as well as the mRNA expressions of IL-6, TNF-a and NF-kB, and determination of ROS expression. Histological data depicted a significant amelioration in the TNBS- and EGCG-treated rats compared to the non-treated animals. Catechin expressed strong anti-inflammatory and anti-oxidant effects, ameliorated ulcerative colitis and stabilized mast cells. The mechanism of action occurred basically through the NF-kB pathway and possibly through a crosstalk with other pathways.
[Mh] Termos MeSH primário: Anti-Inflamatórios/farmacologia
Antioxidantes/farmacologia
Catequina/análogos & derivados
Colite/tratamento farmacológico
Colo/efeitos dos fármacos
Transdução de Sinais/efeitos dos fármacos
Chá/química
[Mh] Termos MeSH secundário: Animais
Anti-Inflamatórios/isolamento & purificação
Antioxidantes/isolamento & purificação
Catequina/isolamento & purificação
Catequina/farmacologia
Colite/induzido quimicamente
Colite/imunologia
Colite/patologia
Colo/imunologia
Colo/patologia
Regulação da Expressão Gênica
Interleucina-6/genética
Interleucina-6/imunologia
Masculino
Mastócitos/efeitos dos fármacos
Mastócitos/imunologia
Mastócitos/patologia
NF-kappa B/genética
NF-kappa B/imunologia
Ratos
Ratos Sprague-Dawley
Espécies Reativas de Oxigênio/imunologia
Espécies Reativas de Oxigênio/metabolismo
Ácido Trinitrobenzenossulfônico
Fator de Necrose Tumoral alfa/genética
Fator de Necrose Tumoral alfa/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents); 0 (Antioxidants); 0 (Interleukin-6); 0 (NF-kappa B); 0 (Reactive Oxygen Species); 0 (Tea); 0 (Tumor Necrosis Factor-alpha); 8R1V1STN48 (Catechin); 8T3HQG2ZC4 (Trinitrobenzenesulfonic Acid); BQM438CTEL (epigallocatechin gallate)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180222
[Lr] Data última revisão:
180222
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171220
[St] Status:MEDLINE


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[PMID]:29254286
[Au] Autor:Robuffo I; Toniato E; Tettamanti L; Mastrangelo F; Ronconi G; Frydas I; Caraffa A; Kritas SK; Conti P
[Ad] Endereço:Institute of Molecular Genetics, CNR, Sede di Chieti, Italy.
[Ti] Título:Mast cell in innate immunity mediated by proinflammatory and antiinflammatory IL-1 family members.
[So] Source:J Biol Regul Homeost Agents;31(4):837-842, 2017 Oct-Dec.
[Is] ISSN:0393-974X
[Cp] País de publicação:Italy
[La] Idioma:eng
[Ab] Resumo:Innate immunity consists of physical and chemical barriers which provide the early defense against infections. Innate immunity orchestrates the defense of the host with cellular and biochemical proteins. Mast cells (MCs) are involved in innate and adaptive immunity and are the first line of defense which generates multiple inflammatory cytokines/chemokines in response to numerous antigens. MC-activated antigen receptor Fc-RI provokes a number of important biochemical pathways with secretion of numerous vasoactive, chemoattractant and inflammatory compounds which participate in allergic and inflammatory diseases. MCs can also be activated by Th1 cytokines and generate pre-formed and de novo inflammatory mediators, including TNF. IL-37 is an anti-inflammatory cytokine which binds IL-18R-alpha chain and reduces the production of inflammatory IL-1 family members. IL-37 down-regulates innate immunity by inhibiting macrophage response and its accumulation and reduces the cytokines that mediate inflammatory diseases. Here, we discuss the relationship between MCs, innate immunity, and pro-inflammatory and anti-inflammatory cytokines.
[Mh] Termos MeSH primário: Inflamação/imunologia
Interleucina-1/imunologia
Macrófagos/imunologia
Mastócitos/imunologia
Receptores de Interleucina-1/imunologia
[Mh] Termos MeSH secundário: Imunidade Adaptativa
Linfócitos B/imunologia
Linfócitos B/patologia
Comunicação Celular
Regulação da Expressão Gênica
Seres Humanos
Imunidade Inata
Inflamação/genética
Inflamação/patologia
Interleucina-1/genética
Subunidade alfa de Receptor de Interleucina-18/genética
Subunidade alfa de Receptor de Interleucina-18/imunologia
Peptídeos e Proteínas de Sinalização Intracelular/genética
Peptídeos e Proteínas de Sinalização Intracelular/imunologia
Macrófagos/patologia
Mastócitos/patologia
Receptores de Interleucina-1/genética
Transdução de Sinais
Linfócitos T/imunologia
Linfócitos T/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (FcRI protein, human); 0 (IL18R1 protein, human); 0 (IL37 protein, human); 0 (Interleukin-1); 0 (Interleukin-18 Receptor alpha Subunit); 0 (Intracellular Signaling Peptides and Proteins); 0 (Receptors, Interleukin-1)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180222
[Lr] Data última revisão:
180222
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171220
[St] Status:MEDLINE


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[PMID]:28744120
[Au] Autor:Chakraborty S; Kar N; Kumari L; De A; Bera T
[Ad] Endereço:Laboratory of Nanomedicine, Department of Pharmaceutical Technology, Jadavpur University, Kolkata, West Bengal, India.
[Ti] Título:Inhibitory effect of a new orally active cedrol-loaded nanostructured lipid carrier on compound 48/80-induced mast cell degranulation and anaphylactic shock in mice.
[So] Source:Int J Nanomedicine;12:4849-4868, 2017.
[Is] ISSN:1178-2013
[Cp] País de publicação:New Zealand
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Type I hypersensitivity is an allergic reaction characterized by the overactivity of the immune system provoked by normally harmless substances. Glucocorticoids, anti-histamines, or mast cell stabilizers are the choices of treatment for type I hypersensitivity. Even though these drugs have the anti-allergic effect, they can have several side effects in prolong use. Cedrol is the main bioactive compound of with anti-tumor, anti-oxidative, and platelet-activating factor inhibiting properties. METHODS: In this study, the preparation and anti-anaphylactic effect of cedrol-loaded nanostructured lipid carriers (NLCs) were evaluated. NLCs were prepared using Compritol 888 ATO and triolein as lipid phase and vitamin E d-α-tocopherylpolyethyleneglycol 1000 succinate, soya lecithin, and sodium deoxycholate as nanoparticle stabilizers. RESULTS: The average diameter of cedrol-NLCs (CR-NLCs) was 71.2 nm (NLC-C ) and 91.93 nm (NLC-C ). The particle had negative zeta potential values of -31.9 mV (NLC-C ) and -44.5 mV (NLC-C ). Type I anaphylactoid reaction in the animal model is significantly reduced by cedrol and cedrol-NLC. This in vivo activity of cedrol resulted that cedrol suppressed compound 48/80-induced peritoneal mast cell degranulation and histamine release from mast cells. Furthermore, compound 48/80-evoked Ca uptake into mast cells was reduced in a dose-dependent manner by cedrol and cedrol-NLC. Studies confirmed that the inhibition of type I anaphylactoid response in vivo in mice and compound 48/80-induced mast cell activation in vitro are greatly enhanced by the loading of cedrol into the NLCs. The safety of cedrol and CR-NLC was evaluated as selectivity index (SI) with prednisolone and cromolyn sodium as positive control. SI of CR-NLC-C was found to be 11.5-fold greater than both prednisolone and cromolyn sodium. CONCLUSION: Administration of CR-NLC 24 hours before the onset of anaphylaxis can prevent an anaphylactoid reaction. NLCs could be a promising vehicle for the oral delivery of cedrol to protect anaphylactic reactions.
[Mh] Termos MeSH primário: Anafilaxia/tratamento farmacológico
Portadores de Fármacos/química
Mastócitos/efeitos dos fármacos
Nanoestruturas/administração & dosagem
Terpenos/administração & dosagem
[Mh] Termos MeSH secundário: Administração Oral
Animais
Degranulação Celular/efeitos dos fármacos
Relação Dose-Resposta a Droga
Portadores de Fármacos/administração & dosagem
Ácidos Graxos
Feminino
Liberação de Histamina/efeitos dos fármacos
Lipídeos/administração & dosagem
Lipídeos/química
Masculino
Mastócitos/fisiologia
Camundongos Endogâmicos BALB C
Nanopartículas/química
Nanoestruturas/química
Terpenos/farmacologia
Trioleína/química
Vitamina E/química
p-Metoxi-N-metilfenetilamina/efeitos adversos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Drug Carriers); 0 (Fatty Acids); 0 (Lipids); 0 (Terpenes); 122-32-7 (Triolein); 1406-18-4 (Vitamin E); 18641-57-1 (glyceryl behenate); 4091-50-3 (p-Methoxy-N-methylphenethylamine); 63ZM9703BO (cedrol); O03S90U1F2 (tocophersolan)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180222
[Lr] Data última revisão:
180222
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170727
[St] Status:MEDLINE
[do] DOI:10.2147/IJN.S132114


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[PMID]:29262347
[Au] Autor:Harris NL; Loke P
[Ad] Endereço:Global Health Institute, École Polytechnique Fédérale de Lausanne, Lausanne 1015, Switzerland. Electronic address: nicola.harris@epfl.ch.
[Ti] Título:Recent Advances in Type-2-Cell-Mediated Immunity: Insights from Helminth Infection.
[So] Source:Immunity;47(6):1024-1036, 2017 Dec 19.
[Is] ISSN:1097-4180
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Type-2-cell-mediated immune responses play a critical role in mediating both host-resistance and disease-tolerance mechanisms during helminth infections. Recently, type 2 cell responses have emerged as major regulators of tissue repair and metabolic homeostasis even under steady-state conditions. In this review, we consider how studies of helminth infection have contributed toward our expanding cellular and molecular understanding of type-2-cell-mediated immunity, as well as new areas such as the microbiome. By studying how these successful parasites form chronic infections without overt pathology, we are gaining additional insights into allergic and inflammatory diseases, as well as normal physiology.
[Mh] Termos MeSH primário: Helmintíase/imunologia
Imunidade Celular
Macrófagos/imunologia
Nematoides/imunologia
Células Th2/imunologia
Trematódeos/imunologia
[Mh] Termos MeSH secundário: Animais
Citocinas/genética
Citocinas/imunologia
Células Epiteliais/imunologia
Células Epiteliais/parasitologia
Regulação da Expressão Gênica/imunologia
Helmintíase/genética
Helmintíase/parasitologia
Homeostase/imunologia
Interações Hospedeiro-Parasita/imunologia
Seres Humanos
Macrófagos/parasitologia
Mastócitos/imunologia
Mastócitos/parasitologia
Microbiota/imunologia
Células Th2/parasitologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Cytokines)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:180221
[Lr] Data última revisão:
180221
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171221
[St] Status:MEDLINE


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[PMID]:28467354
[Au] Autor:Pal S; Meininger CJ; Gashev AA
[Ad] Endereço:Department of Medical Physiology, College of Medicine, Texas A&M University Health Science Center, Temple, TX 76504, USA. spal@medicine.tamhsc.edu.
[Ti] Título:Aged Lymphatic Vessels and Mast Cells in Perilymphatic Tissues.
[So] Source:Int J Mol Sci;18(5), 2017 May 03.
[Is] ISSN:1422-0067
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:This review provides a comprehensive summary of research on aging-associated alterations in lymphatic vessels and mast cells in perilymphatic tissues. Aging alters structure (by increasing the size of zones with low muscle cell investiture), ultrastructure (through loss of the glycocalyx), and proteome composition with a concomitant increase in permeability of aged lymphatic vessels. The contractile function of aged lymphatic vessels is depleted with the abolished role of nitric oxide and an increased role of lymphatic-born histamine in flow-dependent regulation of lymphatic phasic contractions and tone. In addition, aging induces oxidative stress in lymphatic vessels and facilitates the spread of pathogens from these vessels into perilymphatic tissues. Aging causes the basal activation of perilymphatic mast cells, which, in turn, restricts recruitment/activation of immune cells in perilymphatic tissues. This aging-associated basal activation of mast cells limits proper functioning of the mast cell/histamine/NF-κB axis that is essential for the regulation of lymphatic vessel transport and barrier functions as well as for both the interaction and trafficking of immune cells near and within lymphatic collecting vessels. Cumulatively, these changes play important roles in the pathogenesis of alterations in inflammation and immunity associated with aging.
[Mh] Termos MeSH primário: Envelhecimento/fisiologia
Imunidade/imunologia
Inflamação/imunologia
Vasos Linfáticos/fisiologia
Tecido Linfoide/fisiologia
[Mh] Termos MeSH secundário: Animais
Histamina/metabolismo
Seres Humanos
Mastócitos/metabolismo
Camundongos
NF-kappa B/metabolismo
Ratos
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (NF-kappa B); 820484N8I3 (Histamine)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180221
[Lr] Data última revisão:
180221
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170504
[St] Status:MEDLINE


  9 / 25866 MEDLINE  
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[PMID]:29351747
[Au] Autor:Park SM; Min BG; Jung JY; Jegal KH; Lee CW; Kim KY; Kim YW; Choi YW; Cho IJ; Ku SK; Kim SC
[Ad] Endereço:College of Korean Medicine, Daegu Haany University, Gyeongsan, 38610, Republic of Korea.
[Ti] Título:Combination of Pelargonium sidoides and Coptis chinensis root inhibits nuclear factor kappa B-mediated inflammatory response in vitro and in vivo.
[So] Source:BMC Complement Altern Med;18(1):20, 2018 Jan 19.
[Is] ISSN:1472-6882
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Pelargonium sidoides (PS) and Coptis chinensis root (CR) have traditionally been used to treat various diseases, including respiratory and gastrointestinal infections, dysmenorrhea, and hepatic disorders. The present study was conducted to evaluate the anti-inflammatory effects of a combination of PS and CR in vitro and in vivo. METHODS: The in vitro effects of PS + CR on the induction of inflammation-related proteins were evaluated in lipopolysaccharide (LPS)-stimulated RAW 264.7 cells. The levels of nitric oxide (NO) and of inflammatory cytokines and prostaglandin E (PGE ) were measured using the Griess reagent and enzyme-linked immunosorbent assay (ELISA) methods, respectively. The expression of inflammation-related proteins was confirmed by Western blot. Additionally, the effects of PS + CR on paw edema volume, skin thickness, and numbers of infiltrated inflammatory cells, mast cells, COX-2-, iNOS-, and TNF-α-immunoreactive cells in dorsum and ventrum pedis skin were evaluated in a rat model of carrageenan (CA)-induced paw edema. RESULTS: PS + CR significantly reduced production of NO, PGE and three pro-inflammatory cytokines (tumor necrosis factor-α (TNF-α), interleukin (IL)-1ß, and IL-6) and also decreased levels of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2). Treatment with PS + CR significantly reduced the protein expression levels of LPS-stimulated nuclear factor kappa B (NF-κB) and phosphorylated inhibitor of NF-κB (p-I-κBα). Additionally, PS + CR significantly inhibited the increases in paw swelling, skin thickness, infiltrated inflammatory cells, mast cell degranulation, COX-2-, iNOS-, and TNF-α-immunoreactive cells in the rat model of CA-induced acute edematous paw. CONCLUSIONS: These results demonstrate that PS + CR exhibits anti-inflammatory properties through decreasing the production of pro-inflammatory mediators (NO, PGE , TNF-α, IL-1ß, and IL-6), suppressing NF-κB signaling in LPS-induced RAW 264.7 cells. Additionally, the results of the CA-induced rat paw edema assay revealed an anti-edema effect of PS + CR. Furthermore, it is suggested that PS + CR also inhibits acute edematous inflammation by suppressing mast cell degranulation and inflammatory mediators (COX-2, iNOS, and TNF-α). Thus, PS + CR may be a potential candidate for the treatment of various inflammatory diseases, and it may also contribute to a better understanding of the molecular mechanisms underlying inflammatory response regulation.
[Mh] Termos MeSH primário: Coptis/química
Inflamação/metabolismo
NF-kappa B/metabolismo
Pelargonium/química
Extratos Vegetais/química
Extratos Vegetais/farmacologia
Raízes de Plantas/química
[Mh] Termos MeSH secundário: Animais
Citocinas/metabolismo
Edema/metabolismo
Expressão Gênica/efeitos dos fármacos
Masculino
Mastócitos/efeitos dos fármacos
Camundongos
Óxido Nítrico/metabolismo
Células RAW 264.7
Ratos
Ratos Sprague-Dawley
Pele/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cytokines); 0 (NF-kappa B); 0 (Plant Extracts); 31C4KY9ESH (Nitric Oxide)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180216
[Lr] Data última revisão:
180216
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180121
[St] Status:MEDLINE
[do] DOI:10.1186/s12906-018-2088-x


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[PMID]:28471519
[Au] Autor:Hughes EL; Becker F; Flower RJ; Buckingham JC; Gavins FNE
[Ad] Endereço:Centre for Brain Sciences, Department of Medicine, Imperial College London, London, W12 0NN, UK.
[Ti] Título:Mast cells mediate early neutrophil recruitment and exhibit anti-inflammatory properties via the formyl peptide receptor 2/lipoxin A receptor.
[So] Source:Br J Pharmacol;174(14):2393-2408, 2017 Jul.
[Is] ISSN:1476-5381
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND AND PURPOSE: In recent years, studies have focused on the resolution of inflammation, which can be achieved by endogenous anti-inflammatory agonists such as Annexin A1 (AnxA1). Here, we investigated the effects of mast cells (MCs) on early LPS-induced neutrophil recruitment and the involvement of the AnxA1-formyl peptide receptor 2/ALX (FPR2/ALX or lipoxin A receptor) pathway. EXPERIMENTAL APPROACH: Intravital microscopy (IVM) was used to visualize and quantify the effects of LPS (10 µg per mouse i.p.) on murine mesenteric cellular interactions. Furthermore, the role that MCs play in these inflammatory responses was determined in vivo and in vitro, and effects of AnxA1 mimetic peptide Ac2-26 were assessed. KEY RESULTS: LPS increased both neutrophil endothelial cell interactions within the mesenteric microcirculation and MC activation (determined by IVM and ruthenium red dye uptake), which in turn lead to the early stages of neutrophil recruitment. MC recruitment of neutrophils could be blocked by preventing the pro-inflammatory activation (using cromolyn sodium) or enhancing an anti-inflammatory phenotype (using Ac2-26) in MCs. Furthermore, MCs induced neutrophil migration in vitro, and MC stabilization enhanced the release of AnxA1 from neutrophils. Pharmacological approaches (such as the administration of FPR pan-antagonist Boc2, or the FPR2/ALX antagonist WRW4) revealed neutrophil FPR2/ALX to be important in this process. CONCLUSIONS AND IMPLICATIONS: Data presented here provide evidence for a role of MCs, which are ideally positioned in close proximity to the vasculature, to act as sentinel cells in neutrophil extravasation and resolution of inflammation via the AnxA1-FPR2/ALX pathway.
[Mh] Termos MeSH primário: Anti-Inflamatórios/farmacologia
Mastócitos/efeitos dos fármacos
Mastócitos/metabolismo
Infiltração de Neutrófilos/efeitos dos fármacos
Receptores de Formil Peptídeo/metabolismo
[Mh] Termos MeSH secundário: Animais
Anexina A1/química
Anexina A1/farmacologia
Anti-Inflamatórios/química
Cromolina Sódica/química
Cromolina Sódica/farmacologia
Células Endoteliais/efeitos dos fármacos
Microscopia Intravital
Lipopolissacarídeos/química
Lipopolissacarídeos/farmacologia
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Neutrófilos/efeitos dos fármacos
Peptídeos/química
Peptídeos/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Annexin A1); 0 (Anti-Inflammatory Agents); 0 (Fpr1 protein, mouse); 0 (Lipopolysaccharides); 0 (Peptides); 0 (Receptors, Formyl Peptide); 0 (annexin A1 peptide (2-26)); 0 (formyl peptide receptor 2, mouse); Q2WXR1I0PK (Cromolyn Sodium)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180216
[Lr] Data última revisão:
180216
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170505
[St] Status:MEDLINE
[do] DOI:10.1111/bph.13847



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