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Dig Liver Dis ; 48(1): 34-42, 2016 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-26493628

RESUMO

BACKGROUND: Krill oil is a marine derived oil rich in phospholipids, astaxanthin and omega-3 fatty acids. Several studies have found benefits of krill oil against oxidative and inflammatory damage. AIMS: We aimed at assessing the ability of krill oil to reduce intestinal inflammation by improving epithelial barrier integrity, increasing cell survival and reducing pathogenicity of adherent-invasive Escherichia coli. METHODS: CACO2 and HT29 cells were exposed to cytomix (TNFα and IFNγ) to induce inflammation and co-exposed to cytomix and krill oil. E-cadherin, ZO-1 and F-actin levels were analyzed by immunofluorescence to assess barrier integrity. Scratch test was performed to measure wound healing. Cell survival was analyzed by flow cytometry. Adherent-invasive Escherichia coli LF82 was used for adhesion/invasion assay. RESULTS: In inflamed cells E-cadherin and ZO-1 decreased, with loss of cell-cell adhesion, and F-actin polymerization increased stress fibres; krill oil restored initial conditions and improved wound healing, reduced bacterial adhesion/invasion in epithelial cells and survival within macrophages; krill oil reduced LF82-induced mRNA expression of pro-inflammatory cytokines. CONCLUSIONS: Krill oil improves intestinal barrier integrity and epithelial restitution during inflammation and controls bacterial adhesion and invasion to epithelial cells. Thus, krill oil may represent an innovative tool to reduce intestinal inflammation.


Assuntos
Aderência Bacteriana/efeitos dos fármacos , Sobrevivência Celular/efeitos dos fármacos , Euphausiacea , Ácidos Graxos Ômega-3/farmacologia , Viabilidade Microbiana/efeitos dos fármacos , RNA Mensageiro/efeitos dos fármacos , Actinas/metabolismo , Animais , Células CACO-2 , Caderinas/metabolismo , Adesão Celular/efeitos dos fármacos , Morte Celular/efeitos dos fármacos , Escherichia coli/patogenicidade , Escherichia coli/fisiologia , Infecções por Escherichia coli/imunologia , Células HT29 , Humanos , Interferon gama/farmacologia , Interleucina-8/genética , Interleucina-8/metabolismo , Camundongos , Células RAW 264.7 , Fator de Necrose Tumoral alfa/genética , Fator de Necrose Tumoral alfa/metabolismo , Fator de Necrose Tumoral alfa/farmacologia , Cicatrização/efeitos dos fármacos , Proteína da Zônula de Oclusão-1/metabolismo
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