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  1 / 3656 MEDLINE  
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PMID:28456012
Autor:Alizadeh A; Dyck SM; Kataria H; Shahriary GM; Nguyen DH; Santhosh KT; Karimi-Abdolrezaee S
Endereço:Regenerative Medicine Program, Department of Physiology and Pathophysiology, Spinal Cord Research Centre, University of Manitoba, Winnipeg, Manitoba, R3E 0J9, Canada.
Título:Neuregulin-1 positively modulates glial response and improves neurological recovery following traumatic spinal cord injury.
Fonte:Glia; 65(7):1152-1175, 2017 Jul.
ISSN:1098-1136
País de publicação:United States
Idioma:eng
Resumo:Spinal cord injury (SCI) results in glial activation and neuroinflammation, which play pivotal roles in the secondary injury mechanisms with both pro- and antiregeneration effects. Presently, little is known about the endogenous molecular mechanisms that regulate glial functions in the injured spinal cord. We previously reported that the expression of neuregulin-1 (Nrg-1) is acutely and chronically declined following traumatic SCI. Here, we investigated the potential ramifications of Nrg-1 dysregulation on glial and immune cell reactivity following SCI. Using complementary in vitro approaches and a clinically-relevant model of severe compressive SCI in rats, we demonstrate that immediate delivery of Nrg-1 (500 ng/day) after injury enhances a neuroprotective phenotype in inflammatory cells associated with increased interleukin-10 and arginase-1 expression. We also found a decrease in proinflammatory factors including IL-1ß, TNF-α, matrix metalloproteinases (MMP-2 and 9) and nitric oxide after injury. In addition, Nrg-1 modulates astrogliosis and scar formation by reducing inhibitory chondroitin sulfate proteoglycans after SCI. Mechanistically, Nrg-1 effects on activated glia are mediated through ErbB2 tyrosine phosphorylation in an ErbB2/3 heterodimer complex. Furthermore, Nrg-1 exerts its effects through downregulation of MyD88, a downstream adaptor of Toll-like receptors, and increased phosphorylation of Erk1/2 and STAT3. Nrg-1 treatment with the therapeutic dosage of 1.5 µg/day significantly improves tissue preservation and functional recovery following SCI. Our findings for the first time provide novel insights into the role and mechanisms of Nrg-1 in acute SCI and suggest a positive immunomodulatory role for Nrg-1 that can harness the beneficial properties of activated glia and inflammatory cells in recovery following SCI.
Tipo de publicação: JOURNAL ARTICLE
Nome de substância:0 (Culture Media, Conditioned); 0 (Glial Fibrillary Acidic Protein); 0 (Lipopolysaccharides); 0 (Neuregulin-1); 130068-27-8 (Interleukin-10); EC 3.5.3.1 (Arginase); EC 3.5.3.1 (arginase I, rat)


  2 / 3656 MEDLINE  
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PMID:29427649
Autor:Blagojevic V; Kovacevic-Jovanovic V; Curuvija I; Petrovic R; Vujnovic I; Vujic V; Stanojevic S
Endereço:Immunology Research Centre "Branislav Jankovic", Institute of Virology, Vaccines and Sera "Torlak", Belgrade, Serbia. Electronic address: sstanojevic@torlak.rs.
Título:Rat strain differences in peritoneal immune cell response to selected gut microbiota: A crossroad between tolerance and autoimmunity?
Fonte:Life Sci; 197:147-157, 2018 Mar 15.
ISSN:1879-0631
País de publicação:Netherlands
Idioma:eng
Resumo:AIMS: Some gut commensals can be protective, whereas others are implicated as necessary for development of inflammatory/autoimmune diseases. Peritoneal immune cells may play an important role in promoting autoimmunity in response to gut microbiota. This study investigated the phenotype and the function of peritoneal immune cells in the autoimmunity-resistant Albino Oxford (AO), and the autoimmunity-prone Dark Agouti (DA) rat strains upon stimulation with their own colonic E. coli or Enterococcus. MAIN METHODS: Rats were intraperitoneally injected with their own E. coli or Enterococcus. Peritoneal cells isolated two days later were tested for nitric oxide (NO) and cytokine production, and for arginase and myeloperoxidase (MPO) activity. The phenotype of cells was determined using flow cytometry. KEY FINDINGS: While the Enterococcus injection did not affect the composition of peritoneal cells in AO rats, the E. coli treatment increased the percentages of activated CD11b HIS48 neutrophils, and decreased the proportion of resident (CD11b HIS48 , CD163 + CD86+) and anti-inflammatory CD68 + CD206+ macrophages. E. coli increased the production of NO and urea, but preserved their ratio in cells from AO rats. Conversely, both E. coli and Enterococcus diminished the proportion of resident and anti-inflammatory macrophages, increased the proportion of activated neutrophils, and induced inflammatory polarization of peritoneal cells in DA rats. However, injection of E. coli maintained the ratio of typical CD11b HIS48 neutrophils in DA rats, which correlated with the sustained MPO activity. SIGNIFICANCE: The rat strain differences in peritoneal cell response to own commensal microbiota may contribute to differential susceptibility to inflammatory/autoimmune diseases.
Tipo de publicação: JOURNAL ARTICLE
Nome de substância:0 (Cytokines); 31C4KY9ESH (Nitric Oxide); EC 1.11.1.7 (Peroxidase); EC 3.5.3.1 (Arginase)


  3 / 3656 MEDLINE  
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PMID:28464918
Autor:Lam SK; Li YY; Xu S; Leung LL; U KP; Zheng YF; Cheng PN; Ho JC
Endereço:Division of Respiratory Medicine, Department of Medicine, The University of Hong Kong, Queen Mary Hospital, Pokfulam, SAR, Hong Kong.
Título:Growth suppressive effect of pegylated arginase in malignant pleural mesothelioma xenografts.
Fonte:Respir Res; 18(1):80, 2017 May 02.
ISSN:1465-993X
País de publicação:England
Idioma:eng
Resumo:BACKGROUND: Malignant pleural mesothelioma (MPM) is a difficult-to-treat global disease. Pegylated arginase (BCT-100) has recently shown anti-tumor effects in hepatocellular carcinoma, acute myeloid leukemia and melanoma. This study aims to investigate the effects of PEG-BCT-100 in MPM. METHODS: A panel of 5 mesothelioma cell lines (H28, 211H, H226, H2052 and H2452) was used to study the in vitro effects of BCT-100 by crystal violet staining. The in vivo effects of BCT-100 were studied using 211H and H226 nude mice xenografts. Protein expression (argininosuccinate synthetase, ornithine transcarbamylase, cleaved PARP, cleaved caspase 3, cyclins (A2, D3, E1 and H), CDK4 and Ki67) and arginine concentration were evaluated by Western blot and ELISA respectively. Cellular localization of BCT-100 was detected by immunohistochemistry and immunoflorescence. TUNEL assay was used to identify cellular apoptotic events. RESULTS: Argininosuccinate synthetase was expressed in H28, H226, and H2452 cells as well as 211H and H266 xenografts. Ornithine transcarbamylase was undetectable in all cell lines and xenograft models. BCT-100 reduced in vitro cell viability (IC values at 13-24 mU/ml, 72 h) across different cell lines and suppressed tumor growth in both 211H and H226 xenograft models. BCT-100 (60 mg/kg) significantly suppressed tumor growth (p < 0.01) with prolonged median survival (p < 0.01) in both xenograft models. Combining BCT-100 with pemetrexed or cisplatin conferred no additional benefits over single agents. Serum and intratumoral arginine levels were effectively decreased by BCT-100, associated with cytosolic accumulation of BCT-100 within tumor cells. Apoptosis (PARP cleavage in 211H xenografts; Bcl-2 downregulation, and cleavage of PARP and caspase 3 in H226 xenografts; positive TUNEL staining in both) and G1 arrest (downregulation of cyclin A2, D3, E1 and CDK4 in 211H xenografts; suppression of cyclin A2, E1, H and CDK4 in H226 xenografts) were evident with BCT-100 treatment. Furthermore, proliferative factor Ki67 was downregulated in BCT-100 treatments arms. CONCLUSIONS: BCT-100 suppressed tumor growth with prolonged median survival partially mediated by intratumoral arginine depletion resulting in apoptosis and G1 arrest in mesothelioma xenograft models. The findings provide scientific evidence to support further clinical development of BCT-100 in treatment of MPM.
Tipo de publicação: JOURNAL ARTICLE
Nome de substância:0 (Antineoplastic Agents); 30IQX730WE (Polyethylene Glycols); EC 3.5.3.1 (Arginase)


  4 / 3656 MEDLINE  
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PMID:29443755
Autor:Cai X; Yu D; Xie Y; Zhou H
Endereço:Department of Pediatrics, West China Second University Hospital.
Título:Argininemia as a cause of severe chronic stunting and partial growth hormone deficiency (PGHD): A case report.
Fonte:Medicine (Baltimore); 97(7):e9880, 2018 Feb.
ISSN:1536-5964
País de publicação:United States
Idioma:eng
Resumo:RATIONALE: Argininemia is an autosomal recessive inherited disorder of the urea cycle. Because of its atypical symptoms in early age, diagnosis can be delayed until the typical chronic manifestations - including spastic diplegia, deterioration in cognitive function, and epilepsy - appear in later childhood. PATIENT CONCERNS: A Chinese boy initially presented with severe stunting and partial growth hormone deficiency (PGHD) at 3 years old and was initially treated with growth hormone replacement therapy. Seven years later (at 10 years old), he presented with spastic diplegia, cognitive function lesions, epilepsy, and peripheral neuropathy. DIAGNOSES: Ultimately, the patient was diagnosed with argininemia with homozygous mutation (c.32T>C) of the ARG1 gene at 10 years old. Blood tests showed mildly elevated blood ammonia and creatine kinase, and persistently elevated bilirubin. INTERVENTIONS: Protein intake was limited to 0.8 g/kg/day, citrulline (150-200 mg [kg d]) was prescribed. OUTCOMES: The patient's mental state and vomiting had improved after 3 months treatment. At 10 years and 9 month old, his height and weight had reached 121cm and 22kg, respectively, but his spastic diplegia symptoms had not improved. LESSONS: This case demonstrates that stunting and PGHD that does not respond to growth hormone replacement therapy might hint at inborn errors of metabolism (IEM). IEM should also be considered in patients with persistently elevated bilirubin with or without abnormal liver transaminase, as well as elevated blood ammonia and creatine kinase, in the absence of hepatic disease.
Tipo de publicação: CASE REPORTS; JOURNAL ARTICLE
Nome de substância:9002-72-6 (Growth Hormone); EC 3.5.3.1 (Arginase); RFM9X3LJ49 (Bilirubin)


  5 / 3656 MEDLINE  
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PMID:28458349
Autor:Matsutani T; Tamura K; Kutsukake M; Matsuda A; Tachikawa E; Uchida E
Endereço:Department of Gastrointestinal and Hepato-Biliary-Pancreatic Surgery, Nippon Medical School.
Título:Impact of Pioglitazone on Macrophage Dynamics in Adipose Tissues of Cecal Ligation and Puncture-Treated Mice.
Fonte:Biol Pharm Bull; 40(5):638-644, 2017.
ISSN:1347-5215
País de publicação:Japan
Idioma:eng
Resumo:Pioglitazone improves sepsis-induced organ injury accompanied with anti-inflammatory effects on visceral adipose tissue. However, its action in adipose immune cells remains to be ascertained. We investigated the effects of pioglitazone on visceral adipose macrophage population and polarisation in cecal ligation and puncture (CLP)-induced sepsis mice. Eight-week-old male mice were assigned to 3 groups: 1) sham-operated group, 2) CLP group, or 3) pioglitazone-treated CLP group. Pioglitazone (10 mg/kg) was injected intraperitonally for 7 d and CLP surgery was performed. Visceral adipose tissues were collected 24 h after the surgery. mRNA expression of several macrophage markers (inducible nitric oxide synthase (iNOS) for M1, arginase1 (Arg1) and interleukin (IL)-10 for M2, CD163 and F4/80 for mature macrophages) and inflammatory adipokines (IL-6, monocyte chemoattractant protein-1: MCP-1) was quantified by real-time RT-PCR. Tissue sections were subjected to the immunohistochemical analysis and the terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labeling (TUNEL) assay. CLP significantly enhanced Arg1, IL-10 and iNOS mRNA expressions as compared with the sham group, and pioglitazone significantly increased the mRNA level of CD163 and F4/80 in CLP mice. Expression of IL-6 and MCP-1 stimulated by CLP was reduced by pioglitazone treatment. Increased CD11b/c- and CD163-positive cells as well as apoptotic cells were observed in the CLP group and the pioglitazone-treated group. The data indicate that M1/M2 macrophage activation of visceral adipose tissues is induced in CLP-induced mice, and the function of macrophages recruited from surrounding organs may be modulated by pioglitazone treatment.
Tipo de publicação: JOURNAL ARTICLE
Nome de substância:0 (Adipokines); 0 (Biomarkers); 0 (Ccl2 protein, mouse); 0 (Chemokine CCL2); 0 (Hypoglycemic Agents); 0 (IL10 protein, mouse); 0 (Thiazolidinediones); 130068-27-8 (Interleukin-10); EC 3.5.3.1 (Arg1 protein, mouse); EC 3.5.3.1 (Arginase); X4OV71U42S (pioglitazone)


  6 / 3656 MEDLINE  
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PMID:29191699
Autor:Nieto-Meneses R; Castillo R; Hernández-Campos A; Maldonado-Rangel A; Matius-Ruiz JB; Trejo-Soto PJ; Nogueda-Torres B; Dea-Ayuela MA; Bolás-Fernández F; Méndez-Cuesta C; Yépez-Mulia L
Endereço:Departamento de Parasitología, ENCB-IPN, 11340 Mexico City, Mexico; Unidad de Investigación Médica en Enfermedades Infecciosas y Parasitarias-Pediatría, Instituto Mexicano del Seguro Social, 06720 Mexico City, Mexico.
Título:In vitro activity of new N-benzyl-1H-benzimidazol-2-amine derivatives against cutaneous, mucocutaneous and visceral Leishmania species.
Fonte:Exp Parasitol; 184:82-89, 2018 Jan.
ISSN:1090-2449
País de publicação:United States
Idioma:eng
Resumo:The identification of specific therapeutic targets and the development of new drugs against leishmaniasis are urgently needed, since chemotherapy currently available for its treatment has several problems including many adverse side effects. In an effort to develop new antileishmanial drugs, in the present study a series of 28 N-benzyl-1H-benzimidazol-2-amine derivatives was synthesized and evaluated in vitro against Leishmania mexicana promastigotes. Compounds 7 and 8 with the highest antileishmanial activity (micromolar) and lower cytotoxicity than miltefosine and amphotericin B were selected to evaluate their activity against L. braziliensis 9and L. donovani, species causative of mucocutaneous and visceral leishmaniasis, respectively. Compound 7 showed significantly higher activity against L. braziliensis promastigotes than compound 8 and slightly lower than miltefosine. Compounds 7 and 8 had IC values in the micromolar range against the amastigote of L. mexicana and L. braziliensis. However, both compounds did not show better activity against L. donovani than miltefosine. Compound 8 showed the highest SI against both parasite stages of L. mexicana. In addition, compound 8 inhibited 68.27% the activity of recombinant L. mexicana arginase (LmARG), a therapeutic target for the treatment of leishmaniasis. Docking studies were also performed in order to establish the possible mechanism of action by which this compound exerts its inhibitory effect. Compound 8 shows promising potential for the development of more potent antileishmanial benzimidazole derivatives.
Tipo de publicação: JOURNAL ARTICLE
Nome de substância:0 (Antiprotozoal Agents); 0 (Benzimidazoles); 107-73-3 (Phosphorylcholine); 53EY29W7EC (miltefosine); 7XU7A7DROE (Amphotericin B); EC 3.5.3.1 (Arginase)


  7 / 3656 MEDLINE  
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PMID:28464218
Autor:Köstlin N; Vogelmann M; Spring B; Schwarz J; Feucht J; Härtel C; Orlikowsky TW; Poets CF; Gille C
Endereço:Department of Neonatology, Tübingen University Children's Hospital, Tübingen, Germany.
Título:Granulocytic myeloid-derived suppressor cells from human cord blood modulate T-helper cell response towards an anti-inflammatory phenotype.
Fonte:Immunology; 152(1):89-101, 2017 09.
ISSN:1365-2567
País de publicação:England
Idioma:eng
Resumo:Infections are a leading cause of perinatal morbidity and mortality. The outstandingly high susceptibility to infections early in life is mainly attributable to the compromised state of the neonatal immune system. One important difference to the adult immune system is a bias towards T helper type 2 (Th2) responses in newborns. However, mechanisms regulating neonatal T-cell responses are incompletely understood. Granulocytic myeloid-derived suppressor cells (GR-MDSC) are myeloid cells with a granulocytic phenotype that suppress various functions of other immune cells and accumulate under physiological conditions during pregnancy in maternal and fetal blood. Although it has been hypothesized that GR-MDSC accumulation during fetal life could be important for the maintenance of maternal-fetal tolerance, the influence of GR-MDSC on the immunological phenotype of neonates is still unclear. Here, we investigated the impact of GR-MDSC isolated from cord blood (CB-MDSC) on the polarization of Th cells. We demonstrate that CB-MDSC inhibit Th1 responses and induced Th2 responses and regulatory T (Treg) cells. Th1 inhibition was cell-contact dependent and occurred independent of other cell types, while Th2 induction was mediated independently of cell contact through expression of ArgI and reactive oxygen species by CB-MDSC and partially needed the presence of monocytes. Treg cell induction by CB-MDSC also occurred cell-contact independently but was partially mediated through inducible nitric oxide synthase. These results point towards a role of MDSC in regulating neonatal immune responses. Targeting MDSC function in neonates could be a therapeutic opportunity to improve neonatal host defence.
Tipo de publicação: JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
Nome de substância:0 (Reactive Oxygen Species); EC 1.14.13.39 (NOS2 protein, human); EC 1.14.13.39 (Nitric Oxide Synthase Type II); EC 3.5.3.1 (Arginase); EC 3.5.3.1 (arginase I, human)


  8 / 3656 MEDLINE  
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PMID:29253854
Autor:Abdossamadi Z; Seyed N; Zahedifard F; Taheri T; Taslimi Y; Montakhab-Yeganeh H; Badirzadeh A; Vasei M; Gharibzadeh S; Rafati S
Endereço:Department of Immunotherapy and Leishmania Vaccine Research, Pasteur institute of Iran, Tehran, Iran.
Título:Human Neutrophil Peptide 1 as immunotherapeutic agent against Leishmania infected BALB/c mice.
Fonte:PLoS Negl Trop Dis; 11(12):e0006123, 2017 12.
ISSN:1935-2735
País de publicação:United States
Idioma:eng
Resumo:Human Neutrophil Peptide 1 (HNP1) produced by neutrophils, is a well-known antimicrobial peptide which plays a role both in innate as well as in adaptive immunity and is under intensive investigation as a potential therapeutic agent. Previous in vitro experiments have indicated the leishmaniacidal effect of recombinant HNP1 on Leishmania major (L. major) promastigotes and amastigotes. In the current study, we further extended the idea to explore the remedial effect of HNP1 in the two modalities of peptide therapy (folded HNP1) and gene therapy in L. major infected BALB/c mice. To this end, mice in five different groups received synthetic folded HNP1 (G1), pcDNA-HNP1-EGFP (G2), pcDNA-EGFP (G3), Amphotericin B (G4) and PBS (G5), which was started three weeks after infection for three consecutive weeks. Footpad swelling was monitored weekly and a day after the therapy ended, IFN-γ, IL-4, IL-10, IL-6 and nitric oxide produced by splenocytes were analyzed together with the parasite load in draining lymph nodes. Arginase activity and dermal histopathological changes were also analyzed in the infected footpads. We demonstrated that both therapeutic approaches effectively induced Th1 polarization and restricted parasite burden. It can control disease progression in contrast to non-treated groups. However, pcDNA-HNP1-EGFP is more promising in respect to parasite control than folded HNP1, but less effective than AmB treatment. We concluded with the call for a future approach, that is, a DNA-based expression of HNP1 combined with AmB as it can improve the leishmaniacidal efficacy.
Tipo de publicação: JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
Nome de substância:0 (Cytokines); 0 (Recombinant Proteins); 0 (Trypanocidal Agents); 0 (alpha-Defensins); 0 (enhanced green fluorescent protein); 0 (human neutrophil peptide 1); 147336-22-9 (Green Fluorescent Proteins); 31C4KY9ESH (Nitric Oxide); 7XU7A7DROE (Amphotericin B); EC 3.5.3.1 (Arginase)


  9 / 3656 MEDLINE  
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PMID:29180488
Autor:Lin A; Liang F; Thompson EA; Vono M; Ols S; Lindgren G; Hassett K; Salter H; Ciaramella G; Loré K
Endereço:Immunology and Allergy Unit, Department of Medicine, Karolinska Institutet, Karolinska University Hospital Solna, 171 76 Stockholm, Sweden.
Título:Rhesus Macaque Myeloid-Derived Suppressor Cells Demonstrate T Cell Inhibitory Functions and Are Transiently Increased after Vaccination.
Fonte:J Immunol; 200(1):286-294, 2018 01 01.
ISSN:1550-6606
País de publicação:United States
Idioma:eng
Resumo:Myeloid-derived suppressor cells (MDSCs) are major regulators of T cell responses in several pathological conditions. Whether MDSCs increase and influence T cell responses in temporary inflammation, such as after vaccine administration, is unknown. Using the rhesus macaque model, which is critical for late-stage vaccine testing, we demonstrate that monocytic (M)-MDSCs and polymorphonuclear (PMN)-MDSCs can be detected using several of the markers used in humans. However, whereas rhesus M-MDSCs lacked expression of CD33, PMN-MDSCs were identified as CD33 low-density neutrophils. Importantly, both M-MDSCs and PMN-MDSCs showed suppression of T cell proliferation in vitro. The frequency of circulating MDSCs rapidly and transiently increased 24 h after vaccine administration. M-MDSCs infiltrated the vaccine injection site, but not vaccine-draining lymph nodes. This was accompanied by upregulation of genes relevant to MDSCs such as arginase-1, IDO1, PDL1, and IL-10 at the injection site. MDSCs may therefore play a role in locally maintaining immune balance during vaccine-induced inflammation.
Tipo de publicação: JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
Nome de substância:0 (B7-H1 Antigen); 0 (Indoleamine-Pyrrole 2,3,-Dioxygenase); 0 (Influenza Vaccines); 0 (Sialic Acid Binding Ig-like Lectin 3); 130068-27-8 (Interleukin-10); EC 3.5.3.1 (Arginase); EC 3.5.3.1 (arginase I, human)


  10 / 3656 MEDLINE  
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PMID:28747341
Autor:Suwanpradid J; Shih M; Pontius L; Yang B; Birukova A; Guttman-Yassky E; Corcoran DL; Que LG; Tighe RM; MacLeod AS
Endereço:Department of Dermatology, Duke University, Durham, NC 27710.
Título:Arginase1 Deficiency in Monocytes/Macrophages Upregulates Inducible Nitric Oxide Synthase To Promote Cutaneous Contact Hypersensitivity.
Fonte:J Immunol; 199(5):1827-1834, 2017 09 01.
ISSN:1550-6606
País de publicação:United States
Idioma:eng
Resumo:The innate immune components that modulate allergic contact hypersensitivity (CHS) responses are poorly defined. Using human skin from contact dermatitis patients and a mouse model of CHS, we find that hapten allergens disrupt the Arginase1 (Arg1) and inducible NO synthase (iNOS) dynamic in monocytes/macrophages (mono/MΦ), which renders those cells ineffectual in suppressing skin inflammation. Mice lacking Arg1 in MΦ develop increased CHS characterized by elevated ear thickening, mono/MΦ-dominated dermal inflammation, and increased iNOS and IL-6 expression compared with control mice. Treatment of Arg1 ; LysMCre mice with a selective NOS inhibitor or knockout of , encoding iNOS, significantly ameliorates CHS. Our findings suggest a critical role for Arg1 in mono/MΦ in suppressing CHS through dampening expression. These results support that increasing Arg1 may be a potential therapeutic avenue in treating allergic contact dermatitis.
Tipo de publicação: JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
Nome de substância:0 (Allergens); 0 (Haptens); 0 (Interleukin-6); EC 1.14.13.39 (Nitric Oxide Synthase Type II); EC 1.14.13.39 (Nos2 protein, mouse); EC 3.5.3.1 (Arg1 protein, mouse); EC 3.5.3.1 (Arginase); EC 3.5.3.1 (arginase I, human)



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