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Antiviral activity of Bifidobacterium adolescentis SPM1605 against Coxsackievirus B3.

ABSTRACT: Bifidobacteria are considered one of the most beneficial probiotics and have been widely studied for their effects against specific pathogens. The present study investigated the antiviral activity of probiotics isolated from Koreans against Coxsackievirus B3 (CVB3). The effect of probiotic isolates against CVB3 was measured by the plaque assay and cellular toxicity of bifidobacteria in HeLa cells was measured using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. Among 13 probiotic isolates, 3 Bifidobacterium adolescentis, 2 Bifidobacterium longum and 1 Bifidobacterium pseudocatenulatum had an antiviral effect against CVB3, while the others did not show such effect. B. adolescentis SPM1605 showed the greatest inhibitory properties against CVB3. When the threshold cycle (CT) values for the treated B. adolescentis SPM1605 samples were compared to the results for the non-treated samples, it was shown that the amplified viral sequences from the CVB3 had their copy number lowered by B. adolescentis SPM1605. Moreover, the gene expression in infected HeLa cells was also inhibited by 50%. The results suggest that B. adolescentis SPM1605 suppresses CVB3 and could be used as an alternative therapy against infectious diseases caused by coxsackieviruses.

SUBMITTER: Kim MJ

PROVIDER: S-EPMC4433936 | biostudies-other | 2014 Jul

REPOSITORIES: biostudies-other

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Project description:BACKGROUND: Cardiac fibrogenesis in the late stage of viral myocarditis causing contractile dysfunction and ventricular dilatation, is a major pathogenic factor for the progression of myocarditis to serious cardiovascular diseases including dilated cardiomyopathy (DCM) and congestive heart failure (HF). Recent studies indicate that regulatory T cells (Tregs) are involved in the fibrotic process of liver and lung fibosis. However, the role of Tregs in the development of viral myocarditis-caused cardiac fibrosis and their therapeutic potential remains unclear. METHODOLOGY/PRINCIPAL FINDINGS: Myocardial fibrosis was induced in BALB/c mice by intraperitoneal injection of Coxsackievirus B3 (CVB3) assessed by picrosirius red staining and detection of expression levels of collagen I, matrix metalloproteinase-1 (MMP-1), matrix metalloproteinase-3 (MMP-3) and tissue inhibitor of metalloproteinase-1 (TIMP-1). Myocardial Treg frequency was down-regulated during the course of viral myocarditis and a negative correlation with the severity of cardiac fibrosis was found. To explore the role of Tregs in CVB-induced cardiac fibrosis, Treg was in vivo depleted by injecting anti-CD25 mAb which resulted in aggravation of cardiac fibrosis. In consistent with that, after adoptive transfer of isolated Tregs into mice, significant amelioration of CVB3-induced cardiac fibrosis was confirmed. Interleukin-10 (IL-10) neutralizing antibodies were used in vivo and in vitro to explore the molecular mechanism of the therapeutic effect of Treg. It was found that administration of anti-IL-10 mAb after Treg transfer abrogated Treg's treating effect and the inhibition of Treg on collagen production by cardiac fibroblasts was mediated mainly through IL-10. CONCLUSION/SIGNIFICANCE: Our data suggested that Tregs have a protective role in the fibrotic process of CVB3-induced cardiac fibrosis via secreting IL-10 and might provide an alternative option for the future treatment of cardiac fibrosis.

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Antiviral activity of Bifidobacterium adolescentis SPM1605 against Coxsackievirus B3.

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