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1.
Cells ; 9(12)2020 12 16.
Artigo em Inglês | MEDLINE | ID: mdl-33339337

RESUMO

Diet is a strong modifier of microbiome and mucosal microenvironment in the gut. Recently, components of western-type diets have been associated with metabolic and immune diseases. Here, we studied how high-sugar diet (HSD) consumption influences gut mucosal barrier and immune response under steady state conditions and in a mouse model of acute colitis. We found that HSD significantly increased gut permeability, spleen weight, and neutrophil levels in spleens of healthy mice. Subsequent dextran sodium sulfate administration led to severe colitis. In colon, HSD significantly promoted neutrophil infiltration and increased the levels of IL-6, IL-1ß, and TNF-α. Moreover, HSD-fed mice had significantly higher abundance of pathobionts, such as Escherichia coli and Candida, in fecal samples. Although germ-free mice colonized with microbiota of conventionally reared mice that consumed different diets had equally severe colitis, mice colonized with HSD microbiota showed markedly increased infiltration of neutrophils to the gut. The induction of colitis in Toll-like receptor 4 (TLR4)-deficient HSD-fed mice led to significantly milder colitis than in wild-type mice. In conclusion, our results suggested a significant role of HSD in disruption of barrier integrity and balanced mucosal and systemic immune response. In addition, these processes seemed to be highly influenced by resident potentially pathogenic microbiota or metabolites via the TLR4 signaling pathway.


Assuntos
Dieta , Microbioma Gastrointestinal , Inflamação/microbiologia , Inflamação/patologia , Monossacarídeos/efeitos adversos , Transdução de Sinais , Receptor 4 Toll-Like/metabolismo , Animais , Doença Crônica , Colite/genética , Colite/imunologia , Colite/patologia , Proteínas de Ligação a DNA/deficiência , Proteínas de Ligação a DNA/metabolismo , Sulfato de Dextrana , Fezes , Feminino , Regulação da Expressão Gênica , Imunidade nas Mucosas , Intestinos/patologia , Camundongos Endogâmicos BALB C , Permeabilidade , Índice de Gravidade de Doença , Linfócitos T/imunologia
2.
PLoS One ; 11(7): e0159539, 2016.
Artigo em Inglês | MEDLINE | ID: mdl-27434104

RESUMO

Psoriasis is a chronic inflammatory skin disease in which Th17 cells play a crucial role. Since indigenous gut microbiota influences the development and reactivity of immune cells, we analyzed the link among microbiota, T cells and the formation of psoriatic lesions in the imiquimod-induced murine model of psoriasis. To explore the role of microbiota, we induced skin inflammation in germ-free (GF), broad-spectrum antibiotic (ATB)-treated or conventional (CV) BALB/c and C57BL/6 mice. We found that both mice reared in GF conditions for several generations and CV mice treated with ATB were more resistant to imiquimod-induced skin inflammation than CV mice. The ATB treatment dramatically changed the diversity of gut bacteria, which remained stable after subsequent imiquimod application; ATB treatment resulted in a substantial increase in the order Lactobacillales and a significant decrease in Coriobacteriales and Clostridiales. Moreover, as compared to CV mice, imiquimod induced a lower degree of local and systemic Th17 activation in both GF and ATB-treated mice. These findings suggest that gut microbiota control imiquimod-induced skin inflammation by altering the T cell response.


Assuntos
Microbioma Gastrointestinal/fisiologia , Psoríase/imunologia , Psoríase/microbiologia , Pele/imunologia , Células Th17/imunologia , Actinobacteria/efeitos dos fármacos , Actinobacteria/fisiologia , Aminoquinolinas/farmacologia , Animais , Antibacterianos/farmacologia , Clostridiales/efeitos dos fármacos , Clostridiales/fisiologia , Modelos Animais de Doenças , Feminino , Microbioma Gastrointestinal/efeitos dos fármacos , Expressão Gênica , Vida Livre de Germes , Humanos , Imiquimode , Interleucina-17/genética , Interleucina-17/imunologia , Lactobacillales/efeitos dos fármacos , Lactobacillales/fisiologia , Ativação Linfocitária/efeitos dos fármacos , Camundongos , Camundongos Endogâmicos BALB C , Camundongos Endogâmicos C57BL , Membro 3 do Grupo F da Subfamília 1 de Receptores Nucleares/genética , Membro 3 do Grupo F da Subfamília 1 de Receptores Nucleares/imunologia , Psoríase/induzido quimicamente , Psoríase/patologia , Receptores de Antígenos de Linfócitos T gama-delta/genética , Receptores de Antígenos de Linfócitos T gama-delta/imunologia , Pele/efeitos dos fármacos , Pele/microbiologia , Pele/patologia , Especificidade da Espécie , Células Th17/efeitos dos fármacos , Células Th17/microbiologia
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