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[PMID]:29214791
[Au] Autor:Ahn MJ; Yu JE; Jeong J; Sim DW; Koh YI
[Ad] Endereço:Department of Internal Medicine, Chonnam National University Medical School, Gwangju, Korea.
[Ti] Título:A Case of Schnitzler's Syndrome without Monoclonal Gammopathy-Associated Chronic Urticaria Treated with Anakinra.
[So] Source:Yonsei Med J;59(1):154-157, 2018 Jan.
[Is] ISSN:1976-2437
[Cp] País de publicação:Korea (South)
[La] Idioma:eng
[Ab] Resumo:Chronic urticaria may often be associated with interleukin (IL)-1-mediated autoinflammatory disease, which should be suspected if systemic inflammation signs are present. Here, we report a case of Schnitzler's syndrome without monoclonal gammopathy treated successfully with the IL-1 receptor antagonist anakinra. A 69-year-old man suffered from a pruritic urticarial rash for 12 years. It became aggravated episodically and was accompanied by high fever, arthralgia, leukocytosis, and an elevated C-reactive protein and erythrocyte sedimentation rate. The episodes each lasted for over one week. Neutrophilic and eosinophilic inflammation was found on skin biopsy. However, serum and urine electrophoresis showed no evidence of monoclonal gammopathy. The cutaneous lesions were unresponsive to various kinds of anti-histamines, systemic glucocorticoids, colchicine, cyclosporine, dapsone, and methotrexate, which were administered over a span of 3 years immediately preceding successful treatment. A dramatic response, however, was observed after a daily administration of anakinra. This observation suggests that the correct diagnosis of this case is Schnitzler's syndrome without monoclonal gammopathy. For an adult patient with refractory chronic urticaria and systemic inflammation, Schnitzler's syndrome could be considered as a possible differential diagnosis. Although the typical form of Schnitzler's syndrome exhibits the presence of monoclonal gammopathy as a diagnostic criterion, monoclonal gammopathy may be absent in an atypical form. In such a situation, an IL-1 antagonist should be effective for the management of chronic urticaria.
[Mh] Termos MeSH primário: Proteína Antagonista do Receptor de Interleucina 1/uso terapêutico
Paraproteinemias/complicações
Síndrome de Schnitzler/tratamento farmacológico
Urticária/complicações
[Mh] Termos MeSH secundário: Idoso
Sedimentação Sanguínea
Proteína C-Reativa/metabolismo
Doença Crônica
Seres Humanos
Leucócitos/metabolismo
Masculino
Síndrome de Schnitzler/sangue
[Pt] Tipo de publicação:CASE REPORTS
[Nm] Nome de substância:
0 (Interleukin 1 Receptor Antagonist Protein); 9007-41-4 (C-Reactive Protein)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171208
[St] Status:MEDLINE
[do] DOI:10.3349/ymj.2018.59.1.154


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[PMID]:29390386
[Au] Autor:Nusshag C; Morath C; Zeier M; Weigand MA; Merle U; Brenner T
[Ad] Endereço:Department of Nephrology.
[Ti] Título:Hemophagocytic lymphohistiocytosis in an adult kidney transplant recipient successfully treated by plasmapheresis: A case report and review of the literature.
[So] Source:Medicine (Baltimore);96(50):e9283, 2017 Dec.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:RATIONALE: Hemophagocytic lymphohistiocytosis (HLH) is a life-threatening disease entity primarily described in children, but not less relevant in adults. It is characterized by a misdirected activation of the immune system, resulting in an uncontrolled cytokine release from macrophages and cytotoxic T-cells (CTLs). Primary HLH relies on a genetic predisposition, whereas secondary HLH develops in the context of infections, malignancies or autoimmune diseases. However, the awareness and therapeutic knowledge for HLH in adulthood is limited. Most therapy protocols are almost exclusively validated in pediatric cohorts and for primary HLH. Their transferability to adult individuals with mostly secondary HLH is doubtful. Especially the high liver and bone marrow toxicity of applied etoposide-based protocols is discussed controversially and connected to overwhelming infections and death. PATIENT CONCERN: A 51-year old, male, kidney transplant recipient was admitted to our center suffering from diarrhea, fever, nausea, hyponatremia, kidney graft failure, disorientation, progressive hemodynamic instability, and multiorgan failure. DIAGNOSES: Clinical and laboratory findings resembled those of a septic shock. Ferritin and soluble interleukin-2 receptor (sCD25) levels were disproportionally elevated. Only a mild hepatosplenomegaly was diagnosed in a CT scan. A T2-weighted, fluid-attenuated inversion recovery MRI showed marked, bilateral and periventricular white matter hyperintensities. The cerebrospinal fluid (CSF) analysis showed a moderately elevated protein content and cell count. There was no evidence of any bacterial, viral, or parasitic infection. The diagnosis of HLH was made. INTERVENTIONS & OUTCOMES: The patient was successfully treated by a combined approach consisting of plasma exchange (PE), corticosteroids, anakinra, and cyclosporine (CsA). LESSONS: HLH is an important differential diagnosis in critically ill patients. Its unspecific clinical picture complicates an early diagnosis and may be misclassified as sepsis. A combination of plasma exchange (PE), corticosteroids, anakinra, and cyclosporine (CsA) may be a promising and less toxic approach for HLH therapy in adults.
[Mh] Termos MeSH primário: Transplante de Rim
Linfo-Histiocitose Hemofagocítica/terapia
Plasmaferese
[Mh] Termos MeSH secundário: Corticosteroides/uso terapêutico
Antirreumáticos/uso terapêutico
Terapia Combinada
Ciclosporina/uso terapêutico
Diagnóstico Diferencial
Diagnóstico por Imagem
Seres Humanos
Imunossupressores/uso terapêutico
Proteína Antagonista do Receptor de Interleucina 1/uso terapêutico
Linfo-Histiocitose Hemofagocítica/etiologia
Masculino
Meia-Idade
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Adrenal Cortex Hormones); 0 (Antirheumatic Agents); 0 (Immunosuppressive Agents); 0 (Interleukin 1 Receptor Antagonist Protein); 83HN0GTJ6D (Cyclosporine)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180301
[Lr] Data última revisão:
180301
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:180203
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000009283


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[PMID]:29429508
[Au] Autor:Ezzedine K
[Ad] Endereço:Service de dermatologie, hôpital Henri-Mondor et EpiDermE, EA 7379, université Paris-Est Créteil Val-de-Marne, 94010, Créteil, France. Electronic address: haled.ezzedine@aphp.fr.
[Ti] Título:[What's new in dermatological therapy?]
[Ti] Título:Quoi de neuf en thérapeutique dermatologique ?.
[So] Source:Ann Dermatol Venereol;143 Suppl 3:S37-S42, 2016 Dec.
[Is] ISSN:0151-9638
[Cp] País de publicação:France
[La] Idioma:fre
[Ab] Resumo:Over the last year there has been major publications related to therapeutic trials in infectious dermatology, not only with regard to Herpes zoster subunit vaccine but also for the treatment of uncomplicated abscesses or scabies. In addition, biological treatments continue to be on the forefront, not only in the treatment of psoriasis but also in other chronic inflammatory dermatologic diseases such as atopic dermatitis and hidradenitis suppurativa, two diseases that significantly impact quality of life and for which there are to date, few therapeutic alternatives in moderate to severe forms. In addition, the treatment of cyclin-resistant papulopustular rosacea was also the subject of a large French controlled randomized controlled trial that could modify our therapeutic approach by the use of isotretinoin. Finally, the prevention of rashes induced by erlotinib with oral doxycyline is also part of this 2016 "what's new in dermatological therapeutics".
[Mh] Termos MeSH primário: Dermatopatias/tratamento farmacológico
[Mh] Termos MeSH secundário: Adalimumab/uso terapêutico
Antibacterianos/uso terapêutico
Anti-Inflamatórios/uso terapêutico
Anticorpos Monoclonais/uso terapêutico
Fármacos Dermatológicos/uso terapêutico
Dermatologia
Cloridrato de Erlotinib/uso terapêutico
Vacina contra Herpes Zoster
Seres Humanos
Proteína Antagonista do Receptor de Interleucina 1/uso terapêutico
Isotretinoína/uso terapêutico
Piperidinas/uso terapêutico
Inibidores de Proteínas Quinases/uso terapêutico
Pirimidinas/uso terapêutico
Pirróis/uso terapêutico
Dermatopatias/diagnóstico
Combinação Trimetoprima e Sulfametoxazol/uso terapêutico
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Anti-Bacterial Agents); 0 (Anti-Inflammatory Agents); 0 (Antibodies, Monoclonal); 0 (Dermatologic Agents); 0 (Herpes Zoster Vaccine); 0 (Interleukin 1 Receptor Antagonist Protein); 0 (Piperidines); 0 (Protein Kinase Inhibitors); 0 (Pyrimidines); 0 (Pyrroles); 0 (SAR231893); 8064-90-2 (Trimethoprim, Sulfamethoxazole Drug Combination); 87LA6FU830 (tofacitinib); DA87705X9K (Erlotinib Hydrochloride); EH28UP18IF (Isotretinoin); FYS6T7F842 (Adalimumab)
[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:180213
[St] Status:MEDLINE


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[PMID]:28468973
[Au] Autor:Tian T; Jin MQ; Dubin K; King SL; Hoetzenecker W; Murphy GF; Chen CA; Kupper TS; Fuhlbrigge RC
[Ad] Endereço:Department of Dermatology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115; ttian@partners.org Robert.Fuhlbrigge@childrenscolorado.org.
[Ti] Título:IL-1R Type 1-Deficient Mice Demonstrate an Impaired Host Immune Response against Cutaneous Vaccinia Virus Infection.
[So] Source:J Immunol;198(11):4341-4351, 2017 06 01.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The IL-1 superfamily of cytokines and receptors has been studied extensively. However, the specific roles of IL-1 elements in host immunity to cutaneous viral infection remain elusive. In this study, we applied vaccinia virus (VACV) by scarification to IL-1R1 knockout mice (IL-1R1 ) and found that these mice developed markedly larger lesions with higher viral genome copies in skin than did wild-type mice. The phenotype of infected IL-1R1 mice was similar to eczema vaccinatum, a severe side effect of VACV vaccination that may develop in humans with atopic dermatitis. Interestingly, the impaired cutaneous response of IL-1R1 mice did not reflect a systemic immune deficiency, because immunized IL-1R1 mice survived subsequent lethal VACV intranasal challenge, or defects of T cell activation or T cell homing to the site of inoculation. Histologic evaluation revealed that VACV infection and replication after scarification were limited to the epidermal layer of wild-type mice, whereas lack of IL-1R1 permitted extension of VACV infection into dermal layers of the skin. We explored the etiology of this discrepancy and determined that IL-1R1 mice contained significantly more macrophages and monocyte-derived dendritic cells in the dermis after VACV scarification. These cells were vulnerable to VACV infection and may augment the transmission of virus to adjacent skin, thus leading to larger skin lesions and satellite lesions in IL-1R1 mice. These results suggest new therapeutic strategies for treatment of eczema vaccinatum and inform assessment of risks in patients receiving IL-1 blocking Abs for treatment of chronic inflammatory disorders.
[Mh] Termos MeSH primário: Proteína Antagonista do Receptor de Interleucina 1/deficiência
Proteína Antagonista do Receptor de Interleucina 1/imunologia
Dermatopatias Infecciosas/imunologia
Pele/patologia
Vírus Vaccinia/imunologia
Vaccinia/imunologia
[Mh] Termos MeSH secundário: Administração Cutânea
Animais
Linfócitos T CD8-Positivos/imunologia
Proteína Antagonista do Receptor de Interleucina 1/genética
Erupção Variceliforme de Kaposi/imunologia
Erupção Variceliforme de Kaposi/fisiopatologia
Erupção Variceliforme de Kaposi/terapia
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Pele/anatomia & histologia
Pele/imunologia
Pele/virologia
Vacinação
Vírus Vaccinia/fisiologia
Replicação Viral
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Interleukin 1 Receptor Antagonist Protein)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:180131
[Lr] Data última revisão:
180131
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170505
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1500106


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[PMID]:28461572
[Au] Autor:Upadhyay K; Park JE; Yoon TW; Halder P; Kim YI; Metcalfe V; Talati AJ; English BK; Yi AK
[Ad] Endereço:Department of Pediatrics, The University of Tennessee Health Science Center, Memphis, TN 38163.
[Ti] Título:Group B Streptococci Induce Proinflammatory Responses via a Protein Kinase D1-Dependent Pathway.
[So] Source:J Immunol;198(11):4448-4457, 2017 06 01.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Group B streptococci (GBS) are one of the leading causes of life-threatening illness in neonates. Proinflammatory responses to GBS mediated through host innate immune receptors play a critical role in the disease manifestation. However, the mechanisms involved in proinflammatory responses against GBS, as well as the contribution of signaling modulators involved in host immune defense, have not been fully elucidated. In the present study, we investigated the role of protein kinase D (PKD)1 in the proinflammatory responses to GBS. We found that both live and antibiotic-killed GBS induce activation of PKD1 through a pathway that is dependent on the TLR signaling adaptor MyD88 and its downstream kinase IL-1R-associated kinase 1, but independent of TNFR-associated factor 6. Our studies using pharmacological PKD inhibitors and PKD1-knockdown macrophages revealed that PKD1 is indispensable for GBS-mediated activation of MAPKs and NF-κB and subsequent expression of proinflammatory mediators. Furthermore, systemic administration of a PKD inhibitor protects d-galactosamine-sensitized mice from shock-mediated death caused by antibiotic-killed GBS. These findings imply that PKD1 plays a critical regulatory role in GBS-induced proinflammatory reactions and sepsis, and inhibition of PKD1 activation together with antibiotic treatment in GBS-infected neonates could be an effective way to control GBS diseases.
[Mh] Termos MeSH primário: Inflamação/imunologia
Proteína Quinase C/metabolismo
Infecções Estreptocócicas/imunologia
Infecções Estreptocócicas/metabolismo
Streptococcus agalactiae/imunologia
[Mh] Termos MeSH secundário: Animais
Seres Humanos
Recém-Nascido
Proteína Antagonista do Receptor de Interleucina 1/imunologia
Proteína Antagonista do Receptor de Interleucina 1/metabolismo
Macrófagos/imunologia
Macrófagos/microbiologia
Camundongos
Fator 88 de Diferenciação Mieloide
NF-kappa B/metabolismo
Proteína Quinase C/antagonistas & inibidores
Proteína Quinase C/deficiência
Sepse/microbiologia
Transdução de Sinais
Fator de Necrose Tumoral alfa/biossíntese
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Il1rn protein, mouse); 0 (Interleukin 1 Receptor Antagonist Protein); 0 (Myeloid Differentiation Factor 88); 0 (NF-kappa B); 0 (Tumor Necrosis Factor-alpha); EC 2.7.10.- (protein kinase D); EC 2.7.11.13 (Protein Kinase C)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:180127
[Lr] Data última revisão:
180127
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1601089


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[PMID]:28448686
[Au] Autor:Gallentine WB; Shinnar S; Hesdorffer DC; Epstein L; Nordli DR; Lewis DV; Frank LM; Seinfeld S; Shinnar RC; Cornett K; Liu B; Moshé SL; Sun S; FEBSTAT Investigator Team
[Ad] Endereço:Department of Pediatrics (Neurology), Duke Children's Hospital, Durham, North Carolina, U.S.A.
[Ti] Título:Plasma cytokines associated with febrile status epilepticus in children: A potential biomarker for acute hippocampal injury.
[So] Source:Epilepsia;58(6):1102-1111, 2017 06.
[Is] ISSN:1528-1167
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: Our aim was to explore the association between plasma cytokines and febrile status epilepticus (FSE) in children, as well as their potential as biomarkers of acute hippocampal injury. METHODS: Analysis was performed on residual samples of children with FSE (n = 33) as part of the Consequences of Prolonged Febrile Seizures in Childhood study (FEBSTAT) and compared to children with fever (n = 17). Magnetic resonance imaging (MRI) was obtained as part of FEBSTAT within 72 h of FSE. Cytokine levels and ratios of antiinflammatory versus proinflammatory cytokines in children with and without hippocampal T2 hyperintensity were assessed as biomarkers of acute hippocampal injury after FSE. RESULTS: Levels of interleukin (IL)-8 and epidermal growth factor (EGF) were significantly elevated after FSE in comparison to controls. IL-1ß levels trended higher and IL-1RA trended lower following FSE, but did not reach statistical significance. Children with FSE were found to have significantly lower ratios of IL-1RA/IL-1ß and IL-1RA/IL-8. Specific levels of any one individual cytokine were not associated with FSE. However, lower ratios of IL-1RA/IL-1ß, IL-1RA/1L-6, and IL-1RA/ IL-8 were all associated with FSE. IL-6 and IL-8 levels were significantly higher and ratios of IL-1RA/IL-6 and IL-1RA/IL-8 were significantly lower in children with T2 hippocampal hyperintensity on MRI after FSE in comparison to those without hippocampal signal abnormalities. Neither individual cytokine levels nor ratios of IL-1RA/IL-1ß or IL-1RA/IL-8 were predictive of MRI changes. However, a lower ratio of IL-1RA/IL-6 was strongly predictive (odds ratio [OR] 21.5, 95% confidence interval [CI] 1.17-393) of hippocampal T2 hyperintensity after FSE. SIGNIFICANCE: Our data support involvement of the IL-1 cytokine system, IL-6, and IL-8 in FSE in children. The identification of the IL-1RA/IL-6 ratio as a potential biomarker of acute hippocampal injury following FSE is the most significant finding. If replicated in another study, the IL-1RA/IL-6 ratio could represent a serologic biomarker that offers rapid identification of patients at risk for ultimately developing mesial temporal lobe epilepsy (MTLE).
[Mh] Termos MeSH primário: Biomarcadores/sangue
Dano Encefálico Crônico/sangue
Citocinas/sangue
Hipocampo/diagnóstico por imagem
Hipocampo/fisiopatologia
Convulsões Febris/sangue
Estado Epiléptico/sangue
[Mh] Termos MeSH secundário: Dano Encefálico Crônico/diagnóstico por imagem
Criança
Pré-Escolar
Epilepsia do Lobo Temporal/sangue
Feminino
Seres Humanos
Lactente
Recém-Nascido
Proteína Antagonista do Receptor de Interleucina 1/sangue
Interleucina-1beta/sangue
Interleucina-6/sangue
Interleucina-8/sangue
Masculino
Fatores de Risco
Convulsões Febris/diagnóstico por imagem
Estado Epiléptico/diagnóstico por imagem
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Biomarkers); 0 (Cytokines); 0 (Interleukin 1 Receptor Antagonist Protein); 0 (Interleukin-1beta); 0 (Interleukin-6); 0 (Interleukin-8)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:180107
[Lr] Data última revisão:
180107
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170428
[St] Status:MEDLINE
[do] DOI:10.1111/epi.13750


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[PMID]:29223158
[Au] Autor:Esfahani M; Saidijam M; Goodarzi MT; Movahedian A; Najafi R
[Ad] Endereço:Isfahan University of Medical Sciences, School of Pharmacy and Pharmaceutical Sciences and Isfahan Pharmaceutical Sciences Research Center, Department of Clinical Biochemistry, Isfahan, Iran. Movahedian@pharm.mui.ac.ir.
[Ti] Título:Salusin-α Attenuates Inflammatory Responses in Vascular Endothelial Cells.
[So] Source:Biochemistry (Mosc);82(11):1314-1323, 2017 Nov.
[Is] ISSN:1608-3040
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Atherosclerosis accounts for numerous cardiovascular diseases, and cytokines have a critical role in acceleration or suppression of disease. Salusin-α presents a new class of bioactive peptides that can have anti-atherogenic properties. Therefore, the effects of salusin-α on the expression of some pro- and anti-inflammatory cytokines and on TNF-α-induced inflammatory responses in human umbilical vein endothelial cells (HUVECs) were examined. The involvement of the NF-κB pathway in effects of salusin-α in HUVECs was checked using Bay 11-7082 as an NF-κB inhibitor. The mRNA expression of pro-inflammatory cytokines including IL-6, IL-8, and IL-18 and anti-inflammatory cytokine IL-1Ra was assessed by real-time PCR. The protein levels of cytokines were measured by the ELISA method. Salusin-α suppressed both mRNA and protein expression of pro-inflammatory cytokines and induced mRNA and protein expression of IL-1Ra in HUVECs. Salusin-α suppressed TNF-α-induced inflammatory responses in HUVECs. The down-regulatory or up-regulatory effects of salusin-α on expression of cytokines could not be influenced by Bay 11-7082 pretreatment. Our findings indicate anti-inflammatory effects of salusin-α and suggest a novel peptide-based therapeutic strategy for atherosclerosis.
[Mh] Termos MeSH primário: Células Endoteliais/patologia
Inflamação/tratamento farmacológico
Peptídeos e Proteínas de Sinalização Intercelular/farmacologia
[Mh] Termos MeSH secundário: Anti-Inflamatórios/farmacologia
Aterosclerose/patologia
Células Cultivadas
Citocinas/análise
Citocinas/genética
Regulação da Expressão Gênica/efeitos dos fármacos
Células Endoteliais da Veia Umbilical Humana
Seres Humanos
Proteína Antagonista do Receptor de Interleucina 1/análise
Proteína Antagonista do Receptor de Interleucina 1/genética
NF-kappa B/metabolismo
RNA Mensageiro/análise
RNA Mensageiro/efeitos dos fármacos
Fator de Necrose Tumoral alfa/análise
Fator de Necrose Tumoral alfa/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents); 0 (Cytokines); 0 (Intercellular Signaling Peptides and Proteins); 0 (Interleukin 1 Receptor Antagonist Protein); 0 (NF-kappa B); 0 (RNA, Messenger); 0 (TOR2A protein, human); 0 (Tumor Necrosis Factor-alpha)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180103
[Lr] Data última revisão:
180103
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171211
[St] Status:MEDLINE
[do] DOI:10.1134/S0006297917110098


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[PMID]:28454880
[Au] Autor:Khandare AV; Bobade D; Deval M; Patil T; Saha B; Prakash D
[Ad] Endereço:National Centre for Cell Science [NCCS], Ganeshkhind, Pune 411007, India. Electronic address: ashwinvkhandare@gmail.com.
[Ti] Título:Expression of negative immune regulatory molecules, pro-inflammatory chemokine and cytokines in immunopathology of ECM developing mice.
[So] Source:Acta Trop;172:58-63, 2017 Aug.
[Is] ISSN:1873-6254
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:The pathological events in human cerebral malaria are mimicked in the experimental cerebral malaria (ECM) in Plasmodium berghei ANKA (PBA)-infected C57BL/6 mice. Although previously implied in ECM, the kinetics of cytokines and chemokines expression-an essential functional feature for defining causality in ECM development-remained untested. Herein, we characterized the immunopathological changes and the expression of negative immune regulatory molecules, cytokines and chemokines through asymptomatic (3days after infection, 3dpi), symptomatic (5dpi) and ECM (7dpi) stages in PBA-infected C57BL/6 mice. Parasitized RBCs were first detected in brain on 3dpi, edema and tissue alterations on 5dpi, and hemorrhages in different areas of brain on 7dpi. Increased cerebellar PD-1, CTLA-4 and LAG-3 expression and reduced hippocampal CXCL-4 expression on 3dpi were the first observed immunological changes. The negative immune regulatory molecules (PD-L1, CTLA-4), cytokines (TNF-α, sFAS-L), and chemokines (CXCL-10, MIP-1ß) transcript levels varied in different brain areas in symptomatic and ECM phases. By 5dpi, TNF-α, CXCL10 and MIP-1ß significantly increased in all brain parts studied; IL-1RA in whole brain, whereas CXCL4 reduced in hippocampus and cerebrum. By 7dpi, the hippocampal PD-1, CXCL4 and CTLA-4 expression decreased but the cerebral, cerebellar and hippocampal PD-L1 expression were elevated. TNF-α, CXCL10, MIP-1ß, PD-1, CTLA-4 and PD-L1 expression were up-regulated in different brain areas. The TNFR2, IFN-gamma receptor, Lymphotoxin-ß receptor and sFAS-L transcripts significantly increased in brain in ECM. Our data characterize key dynamic immunopathological changes in brain to imply relationship to ECM development.
[Mh] Termos MeSH primário: Malária Cerebral/imunologia
[Mh] Termos MeSH secundário: Animais
Antígeno CTLA-4/biossíntese
Quimiocinas/imunologia
Citocinas/biossíntese
Feminino
Seres Humanos
Fatores Imunológicos
Proteína Antagonista do Receptor de Interleucina 1/biossíntese
Camundongos
Camundongos Endogâmicos C57BL
Plasmodium berghei/imunologia
Fator de Necrose Tumoral alfa/biossíntese
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CTLA-4 Antigen); 0 (CTLA4 protein, human); 0 (Chemokines); 0 (Cytokines); 0 (Immunologic Factors); 0 (Interleukin 1 Receptor Antagonist Protein); 0 (Tumor Necrosis Factor-alpha)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171128
[Lr] Data última revisão:
171128
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170430
[St] Status:MEDLINE


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[PMID]:29023524
[Au] Autor:Mesa F; Lanza E; García L; Marfil-Alvarez R; Magan-Fernandez A
[Ad] Endereço:Periodontology Department, School of Dentistry, University of Granada, Granada, Spain.
[Ti] Título:Polymorphism IL-1RN rs419598 reduces the susceptibility to generalized periodontitis in a population of European descent.
[So] Source:PLoS One;12(10):e0186366, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Interleukin (IL) 1-ra is a potent endogenous competitive inhibitor of IL-α and ß and has an anti-inflammatory role. Study objectives were: 1) to assess the associations of IL-1RN genetic single nucleotide polymorphism (SNP) (rs419598) with generalized chronic periodontitis (GCP), generalized aggressive periodontitis (GAgP), and absence of periodontitis and 2) to assess its association with the load of five periodontopathogenic bacteria and periodontal clinical variables. A cross-sectional analytic study was conducted in 123 patients with GCP, 60 patients with GAgP, and 20 controls. Reverse hybridization PCR was used for genotyping analysis to detect SNPs in IL-1A (rs1800587), IL-1B (rs1143634), and IL-1RN (rs419598) genes and for determination of the load of five periodontopathogenic bacteria. The severity and extension of periodontitis were assessed. Multinomial logistic regression and mediated regression analyses were performed. Considering results for GCP and GAgP patients together, the presence of polymorphism in IL-1A and/or IL-1B gene was associated with a higher likelihood of periodontitis, (OR = 8.11; 95%CI [1.85-35.48]), but this likelihood was reduced when IL-1RN polymorphism was also present, (OR = 5.91; 95%CI [1.08-32.27]). IL-1RN polymorphism was significantly associated with lower counts of red complex bacteria, specifically Porphyromona gingivalis, Tannerella forsythia, and Prevotella intermedia, which were associated with improved clinical outcomes. The polymorphic expression of IL-1RN (rs419598) gene may be associated with a reduced susceptibility to GAgP and GCP in populations of European descent. This effect may be mediated by a decreased load of Porphyromona gingivalis, Tannerella forsythia, and Prevotella intermedia.
[Mh] Termos MeSH primário: Periodontite Crônica/genética
Grupo com Ancestrais do Continente Europeu/genética
Proteína Antagonista do Receptor de Interleucina 1/genética
[Mh] Termos MeSH secundário: Adulto
Periodontite Agressiva/genética
Periodontite Agressiva/microbiologia
Periodontite Agressiva/patologia
Alelos
Estudos de Casos e Controles
Periodontite Crônica/microbiologia
Periodontite Crônica/patologia
Estudos Transversais
Feminino
Genótipo
Seres Humanos
Interleucina-1alfa/genética
Interleucina-1beta/genética
Modelos Logísticos
Masculino
Meia-Idade
Polimorfismo de Nucleotídeo Único/genética
Porphyromonas gingivalis/genética
Porphyromonas gingivalis/isolamento & purificação
Porphyromonas gingivalis/fisiologia
Prevotella intermedia/genética
Prevotella intermedia/isolamento & purificação
Prevotella intermedia/fisiologia
RNA Ribossômico 16S/genética
RNA Ribossômico 16S/metabolismo
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Interleukin 1 Receptor Antagonist Protein); 0 (Interleukin-1alpha); 0 (Interleukin-1beta); 0 (RNA, Ribosomal, 16S)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171024
[Lr] Data última revisão:
171024
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171013
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0186366


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[PMID]:28941802
[Au] Autor:Valdivieso ÁG; Mori C; Clauzure M; Massip-Copiz M; Santa-Coloma TA
[Ad] Endereço:Institute for Biomedical Research (BIOMED, UCA-CONICET), Laboratory of Cellular and Molecular Biology, School of Medical Sciences, Pontifical Catholic University of Argentina (UCA) and The National Scientific and Technical Research Council of Argentina (CONICET), Buenos Aires, C1107AFF, Argentina.
[Ti] Título:CFTR modulates RPS27 gene expression using chloride anion as signaling effector.
[So] Source:Arch Biochem Biophys;633:103-109, 2017 Nov 01.
[Is] ISSN:1096-0384
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:In Cystic Fibrosis (CF), the impairment of the CFTR channel activity leads to a variety of alterations, including differential gene expression. However, the CFTR signaling mechanisms remain unclear. Recently, culturing IB3-1 CF cells under different intracellular Cl concentrations ([Cl ] ), we observed several Cl -dependent genes and further characterized one of them as RPS27. Thus, we hypothesized that Cl might act as a signaling effector for CFTR signaling. Here, to test this idea, we study RPS27 expression in T84 cells modulating the CFTR activity by using CFTR inhibitors. First, we observed that incubation of T84 cells with increasing concentrations of the CFTR inhibitors CFTR(inh)-172 or GlyH-101 determined a progressive increase in the relative [Cl ] (using the Cl fluorescent probe SPQ). The [Cl ] rise was concomitant with a dose-dependent down-regulation of RPS27. These results imply that CFTR inhibition produce Cl accumulation and that RPS27 expression can be modulated by CFTR inhibition. Therefore, Cl behaves as a signaling effector for CFTR in the modulation of RPS27 expression. In addition, the IL-1ß receptor antagonist IL1RN or the JNK inhibitor SP600125, both restored the down-regulation of RPS27 induced by CFTRinh-172, implying a role of autocrine IL-1ß and JNK signaling downstream of Cl in RPS27 modulation.
[Mh] Termos MeSH primário: Cloretos/metabolismo
Regulador de Condutância Transmembrana em Fibrose Cística/genética
Células Epiteliais/metabolismo
Metaloproteínas/genética
Proteínas Nucleares/genética
Proteínas de Ligação a RNA/genética
Proteínas Ribossômicas/genética
Transdução de Sinais
[Mh] Termos MeSH secundário: Antracenos/farmacologia
Comunicação Autócrina
Benzoatos/farmacologia
Linhagem Celular Tumoral
Regulador de Condutância Transmembrana em Fibrose Cística/antagonistas & inibidores
Regulador de Condutância Transmembrana em Fibrose Cística/metabolismo
Células Epiteliais/citologia
Células Epiteliais/efeitos dos fármacos
Corantes Fluorescentes/metabolismo
Regulação da Expressão Gênica
Glicina/análogos & derivados
Glicina/farmacologia
Seres Humanos
Hidrazinas/farmacologia
Proteína Antagonista do Receptor de Interleucina 1/farmacologia
Interleucina-1beta/antagonistas & inibidores
Interleucina-1beta/genética
Interleucina-1beta/metabolismo
Transporte de Íons/efeitos dos fármacos
MAP Quinase Quinase 4/antagonistas & inibidores
MAP Quinase Quinase 4/genética
MAP Quinase Quinase 4/metabolismo
Metaloproteínas/metabolismo
Proteínas Nucleares/metabolismo
Inibidores de Proteínas Quinases/farmacologia
Proteínas de Ligação a RNA/metabolismo
Proteínas Ribossômicas/metabolismo
Tiazolidinas/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (3-((3-trifluoromethyl)phenyl)-5-((3-carboxyphenyl)methylene)-2-thioxo-4-thiazolidinone); 0 (Anthracenes); 0 (Benzoates); 0 (CFTR protein, human); 0 (Chlorides); 0 (Fluorescent Dyes); 0 (Hydrazines); 0 (IL1B protein, human); 0 (IL1RN protein, human); 0 (Interleukin 1 Receptor Antagonist Protein); 0 (Interleukin-1beta); 0 (Metalloproteins); 0 (N-(2-naphthalenyl)-((3,5-dibromo-2,4-dihydroxyphenyl)methylene)glycine hydrazide); 0 (Nuclear Proteins); 0 (Protein Kinase Inhibitors); 0 (RNA-Binding Proteins); 0 (RPS27 protein, human); 0 (Ribosomal Proteins); 0 (Thiazolidines); 126880-72-6 (Cystic Fibrosis Transmembrane Conductance Regulator); 1TW30Y2766 (pyrazolanthrone); EC 2.7.12.2 (MAP Kinase Kinase 4); TE7660XO1C (Glycine)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171031
[Lr] Data última revisão:
171031
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170925
[St] Status:MEDLINE



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