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[PMID]:29441964
[Au] Autor:Kono Y; Miyoshi S; Fujita T
[Ti] Título:Dextran sodium sulfate alters cytokine production in macrophages .
[So] Source:Pharmazie;71(11):619-624, 2016 Nov 02.
[Is] ISSN:0031-7144
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:Macrophages have been assumed to have a crucial role in the development of inflammatory bowel disease (IBD). However, involvement of intestinal macrophages in IBD onset and functional alterations of macrophages during IBD development has not been clarified. We investigated the effect of exposure of compounds used in the induction of colitis in mice on the immune responses of peritoneal macrophages in mice. 2,4,6- trinitrobenzenesulfonic acid and oxazolone did not affect the production of interleukin (IL)-10 and IL-12 from lipopolysaccharide (LPS)-stimulated peritoneal macrophages from BALB/c mice. A significant increase in IL-10 secretion and decrease in IL-12 production from LPS-stimulated macrophages were observed upon exposure to dextran sodium sulfate (DSS). TNF-α production was enhanced significantly by exposure to DSS and LPS. The level of nitric-oxide production from macrophages was increased slightly by exposure to DSS and LPS. Expression of sphingosine kinase-1 and LIGHT (both of which are specific biomarkers of M2b macrophages) was observed in macrophages upon DSS exposure. Alteration of cytokine production in macrophages was observed upon DSS exposure in the absence of LPS stimulation. Peritoneal macrophages from C57BL/6 mice showed similar responses to peritoneal macrophages from BALB/c mice against DSS. These results suggest that DSS directs the immune response of macrophages towards the M2b phenotype.
[Mh] Termos MeSH primário: Citocinas/biossíntese
Sulfato de Dextrana/farmacologia
Macrófagos Peritoneais/metabolismo
[Mh] Termos MeSH secundário: Animais
Colite/induzido quimicamente
Colite/patologia
Feminino
Técnicas In Vitro
Interleucina-10/biossíntese
Interleucina-10/genética
Interleucina-12/biossíntese
Interleucina-12/genética
Lipopolissacarídeos/farmacologia
Macrófagos Peritoneais/efeitos dos fármacos
Camundongos
Camundongos Endogâmicos BALB C
Camundongos Endogâmicos C57BL
Óxido Nítrico/biossíntese
Fosfotransferases (Aceptor do Grupo Álcool)/biossíntese
Fosfotransferases (Aceptor do Grupo Álcool)/genética
Especificidade da Espécie
Membro 14 da Superfamília de Ligantes de Fatores de Necrose Tumoral/biossíntese
Membro 14 da Superfamília de Ligantes de Fatores de Necrose Tumoral/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cytokines); 0 (IL10 protein, mouse); 0 (Lipopolysaccharides); 0 (Tnfsf14 protein, mouse); 0 (Tumor Necrosis Factor Ligand Superfamily Member 14); 130068-27-8 (Interleukin-10); 187348-17-0 (Interleukin-12); 31C4KY9ESH (Nitric Oxide); 9042-14-2 (Dextran Sulfate); EC 2.7.1.- (Phosphotransferases (Alcohol Group Acceptor)); EC 2.7.1.- (sphingosine kinase)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180215
[St] Status:MEDLINE
[do] DOI:10.1691/ph.2016.6688


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[PMID]:29355546
[Au] Autor:Shen P; Zhang Z; He Y; Gu C; Zhu K; Li S; Li Y; Lu X; Liu J; Zhang N; Cao Y
[Ad] Endereço:College of Veterinary Medicine, Jilin University, Changchun 130062, People's Republic of China.
[Ti] Título:Magnolol treatment attenuates dextran sulphate sodium-induced murine experimental colitis by regulating inflammation and mucosal damage.
[So] Source:Life Sci;196:69-76, 2018 Mar 01.
[Is] ISSN:1879-0631
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Magnolol, the main and active ingredient of the Magnolia officinalis, has been widely used in traditional prescription to the human disorders. Magnolol has been proved to have several pharmacological properties including anti-bacterial, anti-oxidant and anti-inflammatory activities. However, the effects of magnolol on ulcerative colitis (UC) have not been reported. The aim of this study was to investigate the protective effects and mechanisms of magnolol on dextran sulphate sodium (DSS)-induced colitis in mice. The results showed that magnolol significantly alleviated DSS-induced body weight loss, disease activities index (DAI), colon length shortening and colonic pathological damage. In addition, magnolol restrained the expression of TNF-α, IL-1ß and IL-12 via the regulation of nuclear factor-κB (NF-κB) and Peroxisome proliferator-activated receptor-γ (PPAR-γ) pathways. Magnolol also enhanced the expression of ZO-1 and occludin in DSS-induced mice colonic tissues. These results showed that magnolol played protective effects on DSS-induced colitis and may be an alternative therapeutic reagent for colitis treatment.
[Mh] Termos MeSH primário: Compostos de Bifenilo/uso terapêutico
Colite Ulcerativa/induzido quimicamente
Colite Ulcerativa/tratamento farmacológico
Sulfato de Dextrana
Fármacos Gastrointestinais/uso terapêutico
Mucosa Intestinal/efeitos dos fármacos
Lignanas/uso terapêutico
[Mh] Termos MeSH secundário: Animais
Ceco/microbiologia
Colite Ulcerativa/patologia
Colo/patologia
Citocinas/biossíntese
Inflamação/fisiopatologia
Inflamação/prevenção & controle
Mediadores da Inflamação
Mucosa Intestinal/patologia
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Ocludina/antagonistas & inibidores
Ocludina/biossíntese
PPAR gama/efeitos dos fármacos
Perda de Peso/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biphenyl Compounds); 0 (Cytokines); 0 (Gastrointestinal Agents); 0 (Inflammation Mediators); 0 (Lignans); 0 (Occludin); 0 (PPAR gamma); 001E35HGVF (magnolol); 9042-14-2 (Dextran Sulfate)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180226
[Lr] Data última revisão:
180226
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180123
[St] Status:MEDLINE


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[PMID]:29366788
[Au] Autor:Yoshida K; Murayama MA; Shimizu K; Tang C; Katagiri N; Matsuo K; Fukai F; Iwakura Y
[Ad] Endereço:Center for Animal Disease Models, Research Institute for Biomedical Sciences (RIBS), Tokyo University of Science (TUS), Chiba, 278-0022, Japan; Department of Pharmaceutical Sciences, Graduate School of Pharmaceutical Sciences, TUS, Chiba, 278-0022, Japan.
[Ti] Título:IL-1R2 deficiency suppresses dextran sodium sulfate-induced colitis in mice via regulation of microbiota.
[So] Source:Biochem Biophys Res Commun;496(3):934-940, 2018 02 12.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Ulcerative colitis (UC) is an inflammatory disease of the colon. IL1R2, which encodes IL-1 receptor type 2 (IL-1R2), was reported as a risk gene for UC. To elucidate the roles of IL-1R2 in the development of colitis, we examined the development of dextran sodium sulfate-induced colitis, a mouse model for UC using Il1r2 mice. We found the severity score of colitis was milder in Il1r2 mice compared with wild-type (WT) mice when they were housed separately, however the severity score was similar when they were housed in a cage. In the separate housing condition, relative contents of Actinobacteria and Bacilli in feces of Il1r2 mice were lower than that of WT mice. Furthermore, IL-1ß induced the expression of antimicrobial peptides (AMPs) from colon. Thus, we show that IL-1R2 is harmful for the development of colitis, because IL-1R2 promotes the growth of proinflammatory intestinal microbiota by suppressing IL-1ß-induced AMP production.
[Mh] Termos MeSH primário: Peptídeos Catiônicos Antimicrobianos/imunologia
Colite/imunologia
Microbioma Gastrointestinal/imunologia
Receptores de Interleucina-1/imunologia
[Mh] Termos MeSH secundário: Animais
Colite/induzido quimicamente
Colite/patologia
Sulfato de Dextrana
Feminino
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Receptores de Interleucina-1/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antimicrobial Cationic Peptides); 0 (Receptors, Interleukin-1); 0 (interleukin-36 receptor, mouse); 9042-14-2 (Dextran Sulfate)
[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


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[PMID]:29236491
[Au] Autor:Hung TV; Suzuki T
[Ad] Endereço:Department of Biofunctional Science and Technology, Graduate School of Biosphere Science, Hiroshima University , Higashihiroshima 739-8528, Japan.
[Ti] Título:Short-Chain Fatty Acids Suppress Inflammatory Reactions in Caco-2 Cells and Mouse Colons.
[So] Source:J Agric Food Chem;66(1):108-117, 2018 Jan 10.
[Is] ISSN:1520-5118
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Short-chain fatty acids (SCFAs), such as acetate, propionate, and butyrate, play an important role in the maintenance of intestinal homeostasis. In the present study, anti-inflammatory effects of SCFAs were examined in human intestinal Caco-2 cells and mouse colonic cultures. Stimulation of Caco-2 cells with tumor necrosis factor (TNF)-α induced interleukin (IL)-8 (TNF-α, 17.1 ± 7.2 vs Control, 1.00 ± 0.26, P < 0.01) and IL-6 expression (TNF-α, 21.7 ± 10.0 vs Control, 1.00 ± 0.28, P < 0.01) through the activation of nuclear factor κB p65, spleen tyrosine kinase, and mitogen-activated protein kinase pathways. Pretreatment of cells with acetate (5 mM, IL-8 1.23 ± 0.40, IL-6 2.19 ± 0.92, P < 0.01 ), propionate (2.5 mM, IL-8 2.45 ± 2.10, IL-6 2.19 ± 0.92, P < 0.01), or butyrate (0.625 mM, IL-8 1.44 ± 0.70, IL-6 2.31 ± 0.32, P < 0.01) suppressed inflammatory responses induced by TNF-α. Pharmacological inhibition of monocarboxylate transporter (MCT)-1 attenuated the suppression of inflammatory signals by SCFAs. High expression levels of CXC motif chemokine ligand 2 (CXCL2, an IL-8 homologue, DSS, 31.7 ± 9.8 vs Control, 1.00 ± 0.70, P < 0.01) and IL-6 (DSS, 17.5 ± 7.2 vs Control, 1.00 ± 0.68, P < 0.01) were observed in BALB/c mouse colonic cultures exposed to dextran sodium sulfate, whereas treatments with mixtures of SCFAs decreased these elevated expression levels (CXCL2 4.14 ± 2.88, IL-6 0.58 ± 0.28, P < 0.01). Our results suggest that SCFAs transported by MCT-1 suppress TNF-α-induced inflammatory signaling in intestinal cells.
[Mh] Termos MeSH primário: Anti-Inflamatórios não Esteroides/farmacologia
Colite/tratamento farmacológico
Colo/efeitos dos fármacos
Ácidos Graxos Voláteis/farmacologia
[Mh] Termos MeSH secundário: Animais
Células CACO-2
Colite/induzido quimicamente
Colite/metabolismo
Colo/metabolismo
Colo/patologia
Citocinas/metabolismo
Sulfato de Dextrana/toxicidade
Seres Humanos
Interleucina-6/metabolismo
Interleucina-8/metabolismo
Masculino
Camundongos Endogâmicos BALB C
Proteínas/metabolismo
Fator de Necrose Tumoral alfa/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents, Non-Steroidal); 0 (Cytokines); 0 (Fatty Acids, Volatile); 0 (Interleukin-6); 0 (Interleukin-8); 0 (Proteins); 0 (Tumor Necrosis Factor-alpha); 9042-14-2 (Dextran Sulfate)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180215
[Lr] Data última revisão:
180215
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171214
[St] Status:MEDLINE
[do] DOI:10.1021/acs.jafc.7b04233


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[PMID]:28457855
[Au] Autor:Tan CW; Sam IC; Chong WL; Lee VS; Chan YF
[Ad] Endereço:Department of Medical Microbiology, Faculty of Medicine, University of Malaya, 50603 Kuala Lumpur, Malaysia. Electronic address: tancw86@gmail.com.
[Ti] Título:Polysulfonate suramin inhibits Zika virus infection.
[So] Source:Antiviral Res;143:186-194, 2017 07.
[Is] ISSN:1872-9096
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Zika virus (ZIKV) is an arthropod-borne flavivirus that causes newborn microcephaly and Guillian-Barré syndrome in adults. No therapeutics are available to treat ZIKV infection or other flaviviruses. In this study, we explored the inhibitory effect of glycosaminoglycans and analogues against ZIKV infection. Highly sulfated heparin, dextran sulfate and suramin significantly inhibited ZIKV infection in Vero cells. De-sulfated heparin analogues lose inhibitory effect, implying that sulfonate groups are critical for viral inhibition. Suramin, an FDA-approved anti-parasitic drug, inhibits ZIKV infection with 3-5 log PFU viral reduction with IC value of ∼2.5-5 µg/ml (1.93 µM-3.85 µM). A time-of-drug-addition study revealed that suramin remains potent even when administrated at 1-24 hpi. Suramin inhibits ZIKV infection by preventing viral adsorption, entry and replication. Molecular dynamics simulation revealed stronger interaction of suramin with ZIKV NS3 helicase than with the envelope protein. Suramin warrants further investigation as a potential antiviral candidate for ZIKV infection. Heparan sulfate (HS) is a cellular attachment receptor for multiple flaviviruses. However, no direct ZIKV-heparin interaction was observed in heparin-binding analysis, and downregulate or removal of cellular HS with sodium chlorate or heparinase I/III did not inhibit ZIKV infection. This indicates that cell surface HS is not utilized by ZIKV as an attachment receptor.
[Mh] Termos MeSH primário: Suramina/antagonistas & inibidores
Infecção pelo Zika virus/prevenção & controle
Zika virus/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Anticorpos Antivirais
Cercopithecus aethiops
Cloratos/farmacologia
DNA Helicases/metabolismo
Sulfato de Dextrana/antagonistas & inibidores
Flavivirus/efeitos dos fármacos
Glicosaminoglicanos/farmacologia
Heparina/análogos & derivados
Heparina/química
Heparina/farmacologia
Heparitina Sulfato/farmacologia
Concentração Inibidora 50
Camundongos
Simulação de Acoplamento Molecular
Simulação de Dinâmica Molecular
RNA Helicases/química
RNA Helicases/efeitos dos fármacos
Serina Endopeptidases/química
Serina Endopeptidases/efeitos dos fármacos
Suramina/administração & dosagem
Células Vero
Proteínas do Envelope Viral/metabolismo
Proteínas não Estruturais Virais/química
Proteínas não Estruturais Virais/efeitos dos fármacos
Internalização do Vírus/efeitos dos fármacos
Replicação Viral/efeitos dos fármacos
Zika virus/fisiologia
Infecção pelo Zika virus/virologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antibodies, Viral); 0 (Chlorates); 0 (Glycosaminoglycans); 0 (NS3 protein, flavivirus); 0 (Viral Envelope Proteins); 0 (Viral Nonstructural Proteins); 6032D45BEM (Suramin); 9005-49-6 (Heparin); 9042-14-2 (Dextran Sulfate); 9050-30-0 (Heparitin Sulfate); EC 3.4.21.- (Serine Endopeptidases); EC 3.6.4.- (DNA Helicases); EC 3.6.4.13 (RNA Helicases); T95DR77GMR (sodium chlorate)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:180213
[Lr] Data última revisão:
180213
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170502
[St] Status:MEDLINE


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[PMID]:29324769
[Au] Autor:Meers GK; Bohnenberger H; Reichardt HM; Lühder F; Reichardt SD
[Ad] Endereço:Institute for Cellular and Molecular Immunology, University Medical Center Goettingen, Göttingen, Germany.
[Ti] Título:Impaired resolution of DSS-induced colitis in mice lacking the glucocorticoid receptor in myeloid cells.
[So] Source:PLoS One;13(1):e0190846, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Inflammatory bowel disease (IBD) is a highly prevalent intestinal disorder for which no cure exists. Currently, the standard first-line treatment of IBD consists of systemic glucocorticoid (GC) application, even though therapy can be complicated by unresponsiveness or adverse effects. In view of the importance of macrophages and neutrophils for the pathogenesis of IBD we set out to define the relevance of these cell types as targets of GC using the mouse model of DSS-induced colitis. We found that the disease did not resolve in GRlysM mice lacking the GC receptor (GR) in myeloid cells after removal of the chemical insult. While clinical symptoms and tissue damage in the colon ameliorated again in GRflox mice, the disease further aggravated in GRlysM littermates. The observed difference coincided with an increased abundance of macrophages in inflammatory infiltrates in the colon of mutant mice whereas neutrophil and T cell numbers were similar. Concomitantly, systemic IL-6 secretion and mRNA levels of pro-inflammatory cytokines in the colon were elevated in GRlysM mice and gene expression of scavenger receptors and IL-10 was diminished. Taken together, our results reveal an important role of myeloid cells as targets of GC in DSS-induced colitis and probably in IBD in humans as well.
[Mh] Termos MeSH primário: Colite/imunologia
Células Mieloides/imunologia
Receptores de Glucocorticoides/deficiência
[Mh] Termos MeSH secundário: Animais
Colite/patologia
Colo/imunologia
Colo/patologia
Sulfato de Dextrana
Modelos Animais de Doenças
Interleucina-10/metabolismo
Interleucina-6/secreção
Mucosa Intestinal/imunologia
Mucosa Intestinal/patologia
Camundongos Endogâmicos C57BL
Camundongos Transgênicos
Células Mieloides/patologia
RNA Mensageiro/metabolismo
Receptores de Glucocorticoides/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (IL10 protein, mouse); 0 (Interleukin-6); 0 (RNA, Messenger); 0 (Receptors, Glucocorticoid); 0 (interleukin-6, mouse); 130068-27-8 (Interleukin-10); 9042-14-2 (Dextran Sulfate)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180206
[Lr] Data última revisão:
180206
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180112
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0190846


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[PMID]:29217385
[Au] Autor:Witaicenis A; de Oliveira ECS; Tanimoto A; Zorzella-Pezavento SFG; de Oliveira SL; Sartori A; Di Stasi LC
[Ad] Endereço:Universidade Estadual Paulista (UNESP), Institute of Biosciences, Department of Pharmacology, Câmpus Botucatu, SP, Brazil. Electronic address: aline.wit@ibb.unesp.br.
[Ti] Título:4-methylesculetin, a coumarin derivative, ameliorates dextran sulfate sodium-induced intestinal inflammation.
[So] Source:Chem Biol Interact;280:59-63, 2018 Jan 25.
[Is] ISSN:1872-7786
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:4-methylesculetin is one of the coumarin derivatives with great anti-oxidant and anti-inflammatory activities. Recent studies have shown that 4-methylesculetin has a promising potentiality to treat inflammatory diseases, especially those related to reactive oxygen species, as inflammatory bowel disease. Based on this, the present study aims to investigate the intestinal anti-inflammatory activity of 4-methylesculetin in dextran sulfate sodium (DSS) model. For this purpose, mice received DSS 5% for 5 days followed by 2 days of filtered tap water. Treated groups received orally 5 or 25 mg/kg of 4-methylesculetin daily since the first day. Macroscopic, microscopic and biochemical parameters were evaluated. 4-methylesculetin (25 mg/kg) improved microscopic parameters, decreased MPO activity, reduced the colonic levels of IL-6 and counteracted GSH depletion when compared with DSS-control group. Our results show the intestinal anti-inflammatory activity of 4-methylesculetin in DSS model, which is related to its antioxidant and anti-inflammatory properties. This way, 4-methylesculetin, is a new potential compound for treatment of both types of IBD.
[Mh] Termos MeSH primário: Colite/induzido quimicamente
Colo/efeitos dos fármacos
Cumarínicos/farmacologia
Sulfato de Dextrana
Umbeliferonas/farmacologia
[Mh] Termos MeSH secundário: Animais
Colite/patologia
Colite/prevenção & controle
Colo/metabolismo
Colo/patologia
Cumarínicos/química
Cumarínicos/uso terapêutico
Ensaio de Imunoadsorção Enzimática
Glutationa/metabolismo
Interleucina-17/análise
Interleucina-6/análise
Masculino
Camundongos
Peroxidase/metabolismo
Fator de Necrose Tumoral alfa/análise
Umbeliferonas/química
Umbeliferonas/uso terapêutico
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Coumarins); 0 (Interleukin-17); 0 (Interleukin-6); 0 (Tumor Necrosis Factor-alpha); 0 (Umbelliferones); 132H8N0A91 (4-methylesculetin); 9042-14-2 (Dextran Sulfate); EC 1.11.1.7 (Peroxidase); GAN16C9B8O (Glutathione)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180129
[Lr] Data última revisão:
180129
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171209
[St] Status:MEDLINE


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[PMID]:28747340
[Au] Autor:Bradford EM; Ryu SH; Singh AP; Lee G; Goretsky T; Sinh P; Williams DB; Cloud AL; Gounaris E; Patel V; Lamping OF; Lynch EB; Moyer MP; De Plaen IG; Shealy DJ; Yang GY; Barrett TA
[Ad] Endereço:Department of Internal Medicine, Ann & Robert H. Lurie Children's Hospital of Chicago, Northwestern University Feinberg School of Medicine, Chicago, IL 60611.
[Ti] Título:Epithelial TNF Receptor Signaling Promotes Mucosal Repair in Inflammatory Bowel Disease.
[So] Source:J Immunol;199(5):1886-1897, 2017 09 01.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:TNF plays an integral role in inflammatory bowel disease (IBD), as evidenced by the dramatic therapeutic responses in Crohn's disease (CD) patients induced by chimeric anti-TNF mAbs. However, treatment of CD patients with etanercept, a decoy receptor that binds soluble TNF, fails to improve disease. To explore this discrepancy, we investigated the role of TNF signaling in Wnt/ß-catenin-mediated intestinal stem cell and progenitor cell expansion in CD patients, human cells, and preclinical mouse models. We hypothesized that TNF exerts beneficial effects on intestinal epithelial cell (IEC) responses to injury. In CD patients, intestinal stem cell and progenitor cell Wnt/ß-catenin signaling correlates with inflammation status. TNF-deficient ( ) mice exhibited increased apoptosis, less IEC proliferation, and less Wnt signaling when stimulated with anti-CD3 mAb. Bone marrow (BM) chimera mice revealed that mucosal repair depended on TNF production by BM-derived cells and TNFR expression by radioresistant IECs. Wild-type→ BM chimera mice with chronic dextran sodium sulfate colitis exhibited delayed ulcer healing, more mucosal inflammation, and impaired Wnt/ß-catenin signaling, consistent with the hypothesis that epithelial TNFR signaling participates in mucosal healing. The direct effect of TNF on stem cells was demonstrated by studies of TNF-induced Wnt/ß-catenin target gene expression in murine enteroids and colonoid cultures and TNF-induced ß-catenin activation in nontransformed human NCM460 cells (TOPFlash) and mice (TOP-GAL). Together, these data support the hypothesis that TNF plays a beneficial role in enhancing Wnt/ß-catenin signaling during ulcer healing in IBD. These novel findings will inform clinicians and therapeutic chemists alike as they strive to develop novel therapies for IBD patients.
[Mh] Termos MeSH primário: Células-Tronco Adultas/fisiologia
Anticorpos Monoclonais/uso terapêutico
Colite/imunologia
Células Epiteliais/fisiologia
Doenças Inflamatórias Intestinais/imunologia
Mucosa Intestinal/fisiologia
Fator de Necrose Tumoral alfa/metabolismo
[Mh] Termos MeSH secundário: Animais
Anticorpos Monoclonais/metabolismo
Linhagem Celular
Sulfato de Dextrana
Seres Humanos
Doenças Inflamatórias Intestinais/terapia
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Receptores Tipo I de Fatores de Necrose Tumoral/genética
Receptores Tipo II do Fator de Necrose Tumoral/genética
Transdução de Sinais
Fator de Necrose Tumoral alfa/genética
Proteínas Wnt/metabolismo
Cicatrização
beta Catenina/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, U.S. GOV'T, NON-P.H.S.; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Antibodies, Monoclonal); 0 (Receptors, Tumor Necrosis Factor, Type I); 0 (Receptors, Tumor Necrosis Factor, Type II); 0 (Tumor Necrosis Factor-alpha); 0 (Wnt Proteins); 0 (beta Catenin); 9042-14-2 (Dextran Sulfate)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:180129
[Lr] Data última revisão:
180129
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170728
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1601066


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[PMID]:29261815
[Au] Autor:Bäcker V; Cheung FY; Siveke JT; Fandrey J; Winning S
[Ad] Endereço:Institut für Physiologie, Universität Duisburg-Essen, Essen, Germany.
[Ti] Título:Knockdown of myeloid cell hypoxia-inducible factor-1α ameliorates the acute pathology in DSS-induced colitis.
[So] Source:PLoS One;12(12):e0190074, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Inflammation and hypoxia are hallmarks of inflammatory bowel disease. Low oxygen levels activate hypoxia-inducible factors as central transcriptional regulators of cellular responses to hypoxia, particularly in myeloid cells where hypoxia-inducible factors control immune cell function and survival. Still, the role of myeloid hypoxia-inducible factor-1 during inflammatory bowel disease remains poorly defined. We therefore investigated the role of hypoxia-inducible factor-1 for myeloid cell function and immune response during colitis. Experimental colitis was induced by administration of 2.5% dextran sulfate sodium to mice with a conditional knockout of hypoxia-inducible factor-1α in myeloid cells and their wild type siblings. Murine colon tissue was examined by histologic analysis, immunohistochemistry, and quantitative polymerase chain reaction. Induction of experimental colitis increased levels of hypoxia and accumulation of hypoxia-inducible factor-1α positive cells in colon tissue of both treated groups. Myeloid hypoxia-inducible factor-1α knockout reduced weight loss and disease activity index when compared to wild type mice. Knockout mice displayed less infiltration of macrophages into intestinal mucosa and reduced mRNA expression of markers for dendritic cells and interleukin-17 secreting T helper cells. Expression of inflammatory and anti-inflammatory cytokines also showed a reduced and delayed induction in myeloid hypoxia-inducible factor-1α knockout mice. Our results show a disease promoting role of myeloid hypoxia-inducible factor-1 during intestinal inflammation. This might result from a hypoxia-inducible factor-1 dependent increase in pro-inflammatory interleukin-17 secreting T helper cells in the absence of obvious changes in regulatory T cells. In contrast, knockout mice appear to shift the balance to anti-inflammatory signals and cells resulting in milder intestinal inflammation.
[Mh] Termos MeSH primário: Colite/induzido quimicamente
Colite/patologia
Técnicas de Silenciamento de Genes
Subunidade alfa do Fator 1 Induzível por Hipóxia/metabolismo
Células Mieloides/metabolismo
Células Mieloides/patologia
[Mh] Termos MeSH secundário: Animais
Hipóxia Celular
Polaridade Celular
Colite/complicações
Colo/patologia
Citocinas/genética
Citocinas/metabolismo
Sulfato de Dextrana
Feminino
Hipóxia/complicações
Hipóxia/metabolismo
Hipóxia/patologia
Inflamação/complicações
Inflamação/patologia
Macrófagos/patologia
Camundongos Endogâmicos C57BL
Camundongos Knockout
RNA Mensageiro/genética
RNA Mensageiro/metabolismo
Linfócitos T Reguladores/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cytokines); 0 (Hypoxia-Inducible Factor 1, alpha Subunit); 0 (RNA, Messenger); 9042-14-2 (Dextran Sulfate)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180108
[Lr] Data última revisão:
180108
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171221
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0190074


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[PMID]:28456683
[Au] Autor:Qu C; Yuan ZW; Yu XT; Huang YF; Yang GH; Chen JN; Lai XP; Su ZR; Zeng HF; Xie Y; Zhang XJ
[Ad] Endereço:School of Chinese Materia Medica, Guangzhou University of Chinese Medicine, Guangzhou, Guangdong, PR China; Guangdong Provincial Key Laboratory of New Chinese Medicinal Development and Research, Guangzhou, Guangdong, PR China. Electronic address: qkc1012@163.com.
[Ti] Título:Patchouli alcohol ameliorates dextran sodium sulfate-induced experimental colitis and suppresses tryptophan catabolism.
[So] Source:Pharmacol Res;121:70-82, 2017 Jul.
[Is] ISSN:1096-1186
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Despite the increased morbidity of ulcerative colitis (UC) in recent years, available treatments remain unsatisfactory. Pogostemon cablin has been widely applied to treat a variety of gastrointestinal disorders in clinic for centuries, in which patchouli alcohol (PA, C H O) has been identified as the major active component. This study attempted to determine the bioactivity of PA on dextran sulfate sodium (DSS)-induced mice colitis and clarify the mechanism of action. Acute colitis was induced in mice by 3% DSS for 7 days. The mice were then given PA (10, 20 and 40mg/kg) or sulfasalazine (SASP, 200mg/kg) as positive control via oral administration for 7 days. At the end of study, animals were sacrificed and samples were collected for pathological and other analysis. In addition, a metabolite profiling and a targeted metabolite analysis, based on the Ultra-Performance Liquid Chromatography coupled with mass spectrometry (UPLC-MS) approach, were performed to characterize the metabolic changes in plasma. The results revealed that PA significantly reduced the disease activity index (DAI) and ameliorated the colonic injury of DSS mice. The levels of colonic MPO and cytokines involving TNF-α, IFN-γ, IL-1ß, IL-6, IL-4 and IL-10 also declined. Furthermore, PA improved the intestinal epithelial barrier by enhancing the level of colonic expression of the tight junction (TJ) proteins, for instance ZO-1, ZO-2, claudin-1 and occludin, and by elevating the levels of mucin-1 and mucin-2 mRNA. The study also demonstrated that PA inhibited the DSS-induced cell death signaling by modulating the apoptosis related Bax and Bcl-2 proteins and down-regulating the necroptosis related RIP3 and MLKL proteins. By comparison, up-regulation of IDO-1 and TPH-1 protein expression in DSS group was suppressed by PA, which was in line with the declined levels of kynurenine (Kyn) and 5-hydroxytryptophan (5-HTP) in plasma. The therapeutic effect of PA was evidently reduced when Kyn was given to mice. In summary, the study successfully demonstrated that PA ameliorated DSS-induced mice acute colitis by suppressing inflammation, maintaining the integrity of intestinal epithelial barrier, inhibiting cell death signaling, and suppressing tryptophan catabolism. The results provided valuable information and guidance for using PA in treatment of UC.
[Mh] Termos MeSH primário: Colite/induzido quimicamente
Colite/tratamento farmacológico
Colo/efeitos dos fármacos
Sulfato de Dextrana
Sesquiterpenos/uso terapêutico
Triptofano/metabolismo
[Mh] Termos MeSH secundário: Animais
Colite/metabolismo
Colite/patologia
Colo/metabolismo
Colo/patologia
Citocinas/análise
Masculino
Camundongos Endogâmicos BALB C
Pogostemon/química
Sesquiterpenos/química
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cytokines); 0 (Sesquiterpenes); 8DUH1N11BX (Tryptophan); 9042-14-2 (Dextran Sulfate); HHH8CPR1M2 (patchouli alcohol)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180105
[Lr] Data última revisão:
180105
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170501
[St] Status:MEDLINE



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